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Erschienen in: Tumor Biology 12/2014

01.12.2014 | Review

EGFR inhibitors and autophagy in cancer treatment

verfasst von: Jie Cui, Yun-Feng Hu, Xie-Min Feng, Tao Tian, Ya-Huan Guo, Jun-Wei Ma, Ke-Jun Nan, Hong-Yi Zhang

Erschienen in: Tumor Biology | Ausgabe 12/2014

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Abstract

Epidermal growth factor receptor (EGFR) inhibitor treatment is a strategy for cancer therapy. However, innate and acquired resistance is a major obstacle of the efficacy. Autophagy is a self-digesting process in cells, which is considered to be associated with anti-cancer drug resistance. The activation of EGFR can regulate autophagy through multiple signal pathways. EGFR inhibitors can induce autophagy, but the specific function of the induction of autophagy by EGFR inhibitors remains biphasic. On the one hand, autophagy induced by EGFR inhibitors acts as a cytoprotective response in cancer cells, and autophagy inhibitors can enhance the cytotoxic effects of EGFR inhibitors. On the other hand, a high level of autophagy after treatment of EGFR inhibitors can also result in autophagic cell death lacking features of apoptosis, and the combination of EGFR inhibitors with an autophagy inducer might be beneficial. Thus, autophagy regulation represents a promising approach for improving the efficacy of EGFR inhibitors in the treatment of cancer patients.
Literatur
1.
Zurück zum Zitat De Duve C, Wattiaux R. Functions of lysosomes. Annu Rev Physiol. 1966;28:435–92.PubMed De Duve C, Wattiaux R. Functions of lysosomes. Annu Rev Physiol. 1966;28:435–92.PubMed
2.
Zurück zum Zitat Klionsky DJ. Autophagy revisited: a conversation with Christian de Duve. Autophagy. 2008;4(6):740–3.PubMed Klionsky DJ. Autophagy revisited: a conversation with Christian de Duve. Autophagy. 2008;4(6):740–3.PubMed
4.
Zurück zum Zitat Hu YL, Jahangiri A, Delay M, Aghi MK. Tumor cell autophagy as an adaptive response mediating resistance to treatments like anti-angiogenic therapy. Cancer Res. 2012;72(17):4294–9.PubMedPubMedCentral Hu YL, Jahangiri A, Delay M, Aghi MK. Tumor cell autophagy as an adaptive response mediating resistance to treatments like anti-angiogenic therapy. Cancer Res. 2012;72(17):4294–9.PubMedPubMedCentral
5.
Zurück zum Zitat Martin DE, Hall MN. The expanding TOR signaling network. Curr Opin Cell Biol. 2005;17(2):158–66.PubMed Martin DE, Hall MN. The expanding TOR signaling network. Curr Opin Cell Biol. 2005;17(2):158–66.PubMed
6.
Zurück zum Zitat Sonenberg N, Hay N. Upstream and downstream of mTOR. Genes Dev. 2004;18:1926–45.PubMed Sonenberg N, Hay N. Upstream and downstream of mTOR. Genes Dev. 2004;18:1926–45.PubMed
7.
Zurück zum Zitat Dowling R, Topisirovic I, Fonseca B, Sonenberg N. Dissecting the role of mTOR: lessons from mTOR inhibitors. Biochim Biophys Acta. 1804;2010:433–9. Dowling R, Topisirovic I, Fonseca B, Sonenberg N. Dissecting the role of mTOR: lessons from mTOR inhibitors. Biochim Biophys Acta. 1804;2010:433–9.
8.
Zurück zum Zitat Alers S, Löffler AS, Wesselborg S, Stork B. Role of AMPK-mTOR-Ulk1/2 in the regulation of autophagy: cross talk, shortcuts, and feedbacks. Mol Cell Biol. 2012;32(1):2–11.PubMedPubMedCentral Alers S, Löffler AS, Wesselborg S, Stork B. Role of AMPK-mTOR-Ulk1/2 in the regulation of autophagy: cross talk, shortcuts, and feedbacks. Mol Cell Biol. 2012;32(1):2–11.PubMedPubMedCentral
9.
Zurück zum Zitat Pattingre S, Espert L, Biard-Piechaczyk M, Codogno P. Regulation of macroautophagy by mTOR and Beclin 1 complexes. Biochimie. 2008;90(2):313–23.PubMed Pattingre S, Espert L, Biard-Piechaczyk M, Codogno P. Regulation of macroautophagy by mTOR and Beclin 1 complexes. Biochimie. 2008;90(2):313–23.PubMed
10.
Zurück zum Zitat Fu LL, Cheng Y, Liu B. Beclin-1: autophagic regulator and therapeutic target in cancer. Int J Biochem Cell Biol. 2013;45(5):921–4.PubMed Fu LL, Cheng Y, Liu B. Beclin-1: autophagic regulator and therapeutic target in cancer. Int J Biochem Cell Biol. 2013;45(5):921–4.PubMed
11.
Zurück zum Zitat Zinzalla V, Stracka D, Oppliger W, Hall MN. Activation of mTORC2 by association with the ribosome. Cell. 2011;144:757–68.PubMed Zinzalla V, Stracka D, Oppliger W, Hall MN. Activation of mTORC2 by association with the ribosome. Cell. 2011;144:757–68.PubMed
12.
Zurück zum Zitat Li L, Chen Y, Gibson SB. Starvation-induced autophagy is regulated by mitochondrial reactive oxygen species leading to AMPK activation. Cell Signal. 2013;25(1):50–65.PubMed Li L, Chen Y, Gibson SB. Starvation-induced autophagy is regulated by mitochondrial reactive oxygen species leading to AMPK activation. Cell Signal. 2013;25(1):50–65.PubMed
14.
Zurück zum Zitat Shimizu S, Kanaseki T, Mizushima N, Mizuta T, Arakawa-Kobayashi S, Thompson CB, et al. Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes. Nat Cell Biol. 2004;6(12):1221–8.PubMed Shimizu S, Kanaseki T, Mizushima N, Mizuta T, Arakawa-Kobayashi S, Thompson CB, et al. Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes. Nat Cell Biol. 2004;6(12):1221–8.PubMed
15.
Zurück zum Zitat Yu L, Alva A, Su H, Dutt P, Freundt E, Welsh S, et al. Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8. Science. 2004;304(5676):1500–2.PubMed Yu L, Alva A, Su H, Dutt P, Freundt E, Welsh S, et al. Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8. Science. 2004;304(5676):1500–2.PubMed
16.
Zurück zum Zitat Kubisch J, Türei D, Földvári-Nagy L, Dunai ZA, Zsákai L, Varga ML, et al. Complex regulation of autophagy in cancer—integrated approaches to discover the networks that hold a double-edged sword. Semin Cancer Biol. 2013;23(4):252–61.PubMed Kubisch J, Türei D, Földvári-Nagy L, Dunai ZA, Zsákai L, Varga ML, et al. Complex regulation of autophagy in cancer—integrated approaches to discover the networks that hold a double-edged sword. Semin Cancer Biol. 2013;23(4):252–61.PubMed
17.
Zurück zum Zitat Sui X, Chen R, Wang Z, Huang Z, Kong N, Zhang M, et al. Autophagy and chemotherapy resistance: a promising therapeutic target for cancer treatment. Cell Death Dis. 2013;4:e838.PubMedPubMedCentral Sui X, Chen R, Wang Z, Huang Z, Kong N, Zhang M, et al. Autophagy and chemotherapy resistance: a promising therapeutic target for cancer treatment. Cell Death Dis. 2013;4:e838.PubMedPubMedCentral
18.
Zurück zum Zitat Wells A. EGF receptor. Int J Biochem Cell Biol. 1999;31(6):637–43.PubMed Wells A. EGF receptor. Int J Biochem Cell Biol. 1999;31(6):637–43.PubMed
19.
Zurück zum Zitat Vogt PK, Gymnopoulos M, Hart JR. PI3-kinase and cancer: changing accents. Curr Opin Genet Dev. 2009;19(1):12–7.PubMedPubMedCentral Vogt PK, Gymnopoulos M, Hart JR. PI3-kinase and cancer: changing accents. Curr Opin Genet Dev. 2009;19(1):12–7.PubMedPubMedCentral
20.
Zurück zum Zitat Yuan TL, Cantley LC. PI3K pathway alterations in cancer: variations on a theme. Oncogene. 2008;27(41):5497–510.PubMedPubMedCentral Yuan TL, Cantley LC. PI3K pathway alterations in cancer: variations on a theme. Oncogene. 2008;27(41):5497–510.PubMedPubMedCentral
21.
Zurück zum Zitat Shaw RJ, Cantley LC. Ras, PI(3)K and mTOR signalling controls tumour cell growth. Nature. 2006;441(7092):424–30.PubMed Shaw RJ, Cantley LC. Ras, PI(3)K and mTOR signalling controls tumour cell growth. Nature. 2006;441(7092):424–30.PubMed
22.
Zurück zum Zitat Wang RC, Wei Y, An Z, Zou Z, Xiao G, Bhagat G, et al. Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation. Science. 2012;338(6109):956–9.PubMedPubMedCentral Wang RC, Wei Y, An Z, Zou Z, Xiao G, Bhagat G, et al. Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation. Science. 2012;338(6109):956–9.PubMedPubMedCentral
23.
Zurück zum Zitat Santi SA, Lee H. Ablation of Akt2 induces autophagy through cell cycle arrest, the downregulation of p70S6K, and the deregulation of mitochondria in MDA-MB231 cells. PLoS One. 2011;6(1):e14614.PubMedPubMedCentral Santi SA, Lee H. Ablation of Akt2 induces autophagy through cell cycle arrest, the downregulation of p70S6K, and the deregulation of mitochondria in MDA-MB231 cells. PLoS One. 2011;6(1):e14614.PubMedPubMedCentral
24.
Zurück zum Zitat Wei Y, Zou Z, Becker N, Anderson M, Sumpter R, Xiao G, et al. EGFR-mediated Beclin 1 phosphorylation in autophagy suppression, tumor progression, and tumor chemoresistance. Cell. 2013;154(6):1269–84.PubMedPubMedCentral Wei Y, Zou Z, Becker N, Anderson M, Sumpter R, Xiao G, et al. EGFR-mediated Beclin 1 phosphorylation in autophagy suppression, tumor progression, and tumor chemoresistance. Cell. 2013;154(6):1269–84.PubMedPubMedCentral
25.
Zurück zum Zitat Furuta S, Hidaka E, Ogata A, Yokota S, Kamata T. Ras is involved in the negative control of autophagy through the class I PI3-kinase. Oncogene. 2004;23(22):3898–904.PubMed Furuta S, Hidaka E, Ogata A, Yokota S, Kamata T. Ras is involved in the negative control of autophagy through the class I PI3-kinase. Oncogene. 2004;23(22):3898–904.PubMed
26.
Zurück zum Zitat Ogier-Denis E, Pattingre S, El Benna J, Codogno P. Erk1/2-dependent phosphorylation of Galpha-interacting protein stimulates its GTPase accelerating activity and autophagy in human colon cancer cells. J Biol Chem. 2000;275(50):39090–5.PubMed Ogier-Denis E, Pattingre S, El Benna J, Codogno P. Erk1/2-dependent phosphorylation of Galpha-interacting protein stimulates its GTPase accelerating activity and autophagy in human colon cancer cells. J Biol Chem. 2000;275(50):39090–5.PubMed
27.
Zurück zum Zitat Pattingre S, Bauvy C, Codogno P. Amino acids interfere with the ERK1/2-dependent control of macroautophagy by controlling the activation of Raf-1 in human colon cancer HT-29 cells. J Biol Chem. 2003;278(19):16667–74.PubMed Pattingre S, Bauvy C, Codogno P. Amino acids interfere with the ERK1/2-dependent control of macroautophagy by controlling the activation of Raf-1 in human colon cancer HT-29 cells. J Biol Chem. 2003;278(19):16667–74.PubMed
28.
Zurück zum Zitat Corcelle E, Nebout M, Bekri S, Gauthier N, Hofman P, Poujeol P, et al. Disruption of autophagy at the maturation step by the carcinogen lindane is associated with the sustained mitogen-activated protein kinase/extracellular signal-regulated kinase activity. Cancer Res. 2006;66(13):6861–70.PubMed Corcelle E, Nebout M, Bekri S, Gauthier N, Hofman P, Poujeol P, et al. Disruption of autophagy at the maturation step by the carcinogen lindane is associated with the sustained mitogen-activated protein kinase/extracellular signal-regulated kinase activity. Cancer Res. 2006;66(13):6861–70.PubMed
29.
Zurück zum Zitat Stevens C, Lin Y, Harrison B, Burch L, Ridgway RA, Sansom O, et al. Peptide combinatorial libraries identify TSC2 as a death-associated protein kinase (DAPK) death domain-binding protein and reveal a stimulatory role for DAPK in mTORC1 signaling. J Biol Chem. 2009;284(1):334–44.PubMed Stevens C, Lin Y, Harrison B, Burch L, Ridgway RA, Sansom O, et al. Peptide combinatorial libraries identify TSC2 as a death-associated protein kinase (DAPK) death domain-binding protein and reveal a stimulatory role for DAPK in mTORC1 signaling. J Biol Chem. 2009;284(1):334–44.PubMed
30.
Zurück zum Zitat Weihua Z, Tsan R, Huang WC, Wu Q, Chiu CH, Fidler IJ, et al. Survival of cancer cells is maintained by EGFR independent of its kinase activity. Cancer Cell. 2008;13(5):385–93.PubMedPubMedCentral Weihua Z, Tsan R, Huang WC, Wu Q, Chiu CH, Fidler IJ, et al. Survival of cancer cells is maintained by EGFR independent of its kinase activity. Cancer Cell. 2008;13(5):385–93.PubMedPubMedCentral
31.
Zurück zum Zitat Boerner JL, Demory ML, Silva C, Parsons SJ. Phosphorylation of Y845 on the epidermal growth factor receptor mediates binding to the mitochondrial protein cytochrome c oxidase subunit II. Mol Cell Biol. 2004;24(16):7059–71.PubMedPubMedCentral Boerner JL, Demory ML, Silva C, Parsons SJ. Phosphorylation of Y845 on the epidermal growth factor receptor mediates binding to the mitochondrial protein cytochrome c oxidase subunit II. Mol Cell Biol. 2004;24(16):7059–71.PubMedPubMedCentral
32.
Zurück zum Zitat Yao Y, Wang G, Li Z, Yan B, Guo Y, Jiang X, et al. Mitochondrially localized EGFR is independent of its endocytosis and associates with cell viability. Acta Biochim Biophys Sin (Shanghai). 2010;42(11):763–70. Yao Y, Wang G, Li Z, Yan B, Guo Y, Jiang X, et al. Mitochondrially localized EGFR is independent of its endocytosis and associates with cell viability. Acta Biochim Biophys Sin (Shanghai). 2010;42(11):763–70.
33.
Zurück zum Zitat Yue X, Song W, Zhang W, Chen L, Xi Z, Xin Z, et al. Mitochondrially localized EGFR is subjected to autophagic regulation and implicated in cell survival. Autophagy. 2008;4(5):641–9.PubMed Yue X, Song W, Zhang W, Chen L, Xi Z, Xin Z, et al. Mitochondrially localized EGFR is subjected to autophagic regulation and implicated in cell survival. Autophagy. 2008;4(5):641–9.PubMed
34.
Zurück zum Zitat Dreier A, Barth S, Goswami A, Weis J. Cetuximab induces mitochondrial translocalization of EGFRvIII, but not EGFR: involvement of mitochondria in tumor drug resistance? Tumour Biol. 2012;33(1):85–94.PubMed Dreier A, Barth S, Goswami A, Weis J. Cetuximab induces mitochondrial translocalization of EGFRvIII, but not EGFR: involvement of mitochondria in tumor drug resistance? Tumour Biol. 2012;33(1):85–94.PubMed
35.
Zurück zum Zitat Cao X, Zhu H, Ali-Osman F, Lo HW. EGFR and EGFRvIII undergo stress- and EGFR kinase inhibitor-induced mitochondrial translocalization: a potential mechanism of EGFR-driven antagonism of apoptosis. Mol Cancer. 2011;10:26.PubMedPubMedCentral Cao X, Zhu H, Ali-Osman F, Lo HW. EGFR and EGFRvIII undergo stress- and EGFR kinase inhibitor-induced mitochondrial translocalization: a potential mechanism of EGFR-driven antagonism of apoptosis. Mol Cancer. 2011;10:26.PubMedPubMedCentral
36.
Zurück zum Zitat Khalil MY, Grandis JR, Shin DM. Targeting epidermal growth factor receptor: novel therapeutics in the management of cancer. Expert Rev Anticancer Ther. 2003;3(3):367–80.PubMed Khalil MY, Grandis JR, Shin DM. Targeting epidermal growth factor receptor: novel therapeutics in the management of cancer. Expert Rev Anticancer Ther. 2003;3(3):367–80.PubMed
37.
Zurück zum Zitat Herbst RS, Sandler AB. Overview of the current status of human epidermal growth factor receptor inhibitors in lung cancer. Clin Lung Cancer. 2004;6 Suppl 1:S7–S19.PubMed Herbst RS, Sandler AB. Overview of the current status of human epidermal growth factor receptor inhibitors in lung cancer. Clin Lung Cancer. 2004;6 Suppl 1:S7–S19.PubMed
38.
Zurück zum Zitat Fukuoka M, Yano S, Giaccone G, Tamura T, Nakagawa K, Douillard JY, et al. Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small cell lung cancer (The IDEAL 1 Trial) [corrected]. J Clin Oncol. 2003;12:2237–46. Fukuoka M, Yano S, Giaccone G, Tamura T, Nakagawa K, Douillard JY, et al. Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small cell lung cancer (The IDEAL 1 Trial) [corrected]. J Clin Oncol. 2003;12:2237–46.
39.
Zurück zum Zitat Perez-Soler R, Chachoua A, Hammond LA, Rowinsky EK, Huberman M, Karp D, et al. Determinants of tumor response and survival with erlotinib in patients with non-small-cell lung cancer. J Clin Oncol. 2004;22(16):3238–47.PubMed Perez-Soler R, Chachoua A, Hammond LA, Rowinsky EK, Huberman M, Karp D, et al. Determinants of tumor response and survival with erlotinib in patients with non-small-cell lung cancer. J Clin Oncol. 2004;22(16):3238–47.PubMed
40.
Zurück zum Zitat Thatcher N, Chang A, Parikh P, Rodrigues Pereira J, Ciuleanu T, von Pawel J, et al. Gefitinib plus best supportive care in previously treated patients with refractory advanced non-small-cell lung cancer: results from a randomised, placebo-controlled, multicentre study (Iressa Survival Evaluation in Lung Cancer). Lancet. 2005;366(9496):1527–37.PubMed Thatcher N, Chang A, Parikh P, Rodrigues Pereira J, Ciuleanu T, von Pawel J, et al. Gefitinib plus best supportive care in previously treated patients with refractory advanced non-small-cell lung cancer: results from a randomised, placebo-controlled, multicentre study (Iressa Survival Evaluation in Lung Cancer). Lancet. 2005;366(9496):1527–37.PubMed
41.
Zurück zum Zitat Shepherd FA, Pereira RJ, Ciuleanu T, Tan EH, Hirsh V, et al. Erlotinib in previously treated non-small-cell lung cancer. N Engl J Med. 2005;353(2):123–32.PubMed Shepherd FA, Pereira RJ, Ciuleanu T, Tan EH, Hirsh V, et al. Erlotinib in previously treated non-small-cell lung cancer. N Engl J Med. 2005;353(2):123–32.PubMed
42.
Zurück zum Zitat Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med. 2004;350(21):2129–39.PubMed Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med. 2004;350(21):2129–39.PubMed
43.
Zurück zum Zitat Pao W, Chmielecki J. Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer. Nat Rev Cancer. 2010;10(11):760–74.PubMedPubMedCentral Pao W, Chmielecki J. Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer. Nat Rev Cancer. 2010;10(11):760–74.PubMedPubMedCentral
44.
Zurück zum Zitat Engelman JA, Zejnullahu K, Mitsudomi T, Song Y, Hyland C, Park JO, et al. MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science. 2007;316(5827):1039–43.PubMed Engelman JA, Zejnullahu K, Mitsudomi T, Song Y, Hyland C, Park JO, et al. MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science. 2007;316(5827):1039–43.PubMed
45.
Zurück zum Zitat Patel MR, Jay-Dixon J, Sadiq AA, Jacobson BA, Kratzke RA. Resistance to EGFR-TKI can be mediated through multiple signaling pathways converging upon cap-dependent translation in EGFR-wild type NSCLC. J Thorac Oncol. 2013;8(9):1142–7.PubMedPubMedCentral Patel MR, Jay-Dixon J, Sadiq AA, Jacobson BA, Kratzke RA. Resistance to EGFR-TKI can be mediated through multiple signaling pathways converging upon cap-dependent translation in EGFR-wild type NSCLC. J Thorac Oncol. 2013;8(9):1142–7.PubMedPubMedCentral
46.
Zurück zum Zitat Xu Y, Liu H, Chen J, Zhou Q. Acquired resistance of lung adenocarcinoma to EGFR-tyrosine kinase inhibitors gefitinib and erlotinib. Cancer Biol Ther. 2010;9(8):572–82.PubMed Xu Y, Liu H, Chen J, Zhou Q. Acquired resistance of lung adenocarcinoma to EGFR-tyrosine kinase inhibitors gefitinib and erlotinib. Cancer Biol Ther. 2010;9(8):572–82.PubMed
47.
Zurück zum Zitat Costanzo R, Piccirillo MC, Sandomenico C, Carillio G, Montanino A, Daniele G, et al. Gefitinib in non small cell lung cancer. J Biomed Biotechnol. 2011;2011:815269.PubMedPubMedCentral Costanzo R, Piccirillo MC, Sandomenico C, Carillio G, Montanino A, Daniele G, et al. Gefitinib in non small cell lung cancer. J Biomed Biotechnol. 2011;2011:815269.PubMedPubMedCentral
48.
Zurück zum Zitat Jiang Z, Li C, Li F, Wang X. EGFR gene copy number as a prognostic marker in colorectal cancer patients treated with cetuximab or panitumumab: a systematic review and meta analysis. PLoS One. 2013;8(2):e56205.PubMedPubMedCentral Jiang Z, Li C, Li F, Wang X. EGFR gene copy number as a prognostic marker in colorectal cancer patients treated with cetuximab or panitumumab: a systematic review and meta analysis. PLoS One. 2013;8(2):e56205.PubMedPubMedCentral
49.
Zurück zum Zitat Bourhis J, Lefebvre JL, Vermorken JB. Cetuximab in the management of locoregionally advanced head and neck cancer: expanding the treatment options? Eur J Cancer. 2010;46(11):1979–89.PubMed Bourhis J, Lefebvre JL, Vermorken JB. Cetuximab in the management of locoregionally advanced head and neck cancer: expanding the treatment options? Eur J Cancer. 2010;46(11):1979–89.PubMed
50.
Zurück zum Zitat Qiu LX, Mao C, Zhang J, Zhu XD, Liao RY, Xue K, et al. Predictive and prognostic value of KRAS mutations in metastatic colorectal cancer patients treated with cetuximab: a meta-analysis of 22 studies. Eur J Cancer. 2010;46(15):2781–7.PubMed Qiu LX, Mao C, Zhang J, Zhu XD, Liao RY, Xue K, et al. Predictive and prognostic value of KRAS mutations in metastatic colorectal cancer patients treated with cetuximab: a meta-analysis of 22 studies. Eur J Cancer. 2010;46(15):2781–7.PubMed
51.
Zurück zum Zitat Han W, Pan H, Chen Y, Sun J, Wang Y, Li J, et al. EGFR tyrosine kinase inhibitors activate autophagy as a cytoprotective response in human lung cancer cells. PLoS One. 2011;6(6):e18691.PubMedPubMedCentral Han W, Pan H, Chen Y, Sun J, Wang Y, Li J, et al. EGFR tyrosine kinase inhibitors activate autophagy as a cytoprotective response in human lung cancer cells. PLoS One. 2011;6(6):e18691.PubMedPubMedCentral
52.
Zurück zum Zitat Zou Y, Ling YH, Sironi J, Schwartz EL, Perez-Soler R, Piperdi B. The autophagy inhibitor chloroquine overcomes the innate resistance of wild-type EGFR non-small-cell lung cancer cells to erlotinib. J Thorac Oncol. 2013;8(6):693–702.PubMed Zou Y, Ling YH, Sironi J, Schwartz EL, Perez-Soler R, Piperdi B. The autophagy inhibitor chloroquine overcomes the innate resistance of wild-type EGFR non-small-cell lung cancer cells to erlotinib. J Thorac Oncol. 2013;8(6):693–702.PubMed
53.
Zurück zum Zitat Sakuma Y, Matsukuma S, Nakamura Y, Yoshihara M, Koizume S, Sekiguchi H, et al. Enhanced autophagy is required for survival in EGFR-independent EGFR-mutant lung adenocarcinoma cells. Lab Investig. 2013;93(10):1137–46.PubMed Sakuma Y, Matsukuma S, Nakamura Y, Yoshihara M, Koizume S, Sekiguchi H, et al. Enhanced autophagy is required for survival in EGFR-independent EGFR-mutant lung adenocarcinoma cells. Lab Investig. 2013;93(10):1137–46.PubMed
54.
Zurück zum Zitat Moreira-Leite FF, Harrison LR, Mironov A, Roberts RA, Dive C. Inducible EGFR T790M-mediated gefitinib resistance in non-small cell lung cancer cells does not modulate sensitivity to PI103 provoked autophagy. J Thorac Oncol. 2010;5(6):765–77.PubMed Moreira-Leite FF, Harrison LR, Mironov A, Roberts RA, Dive C. Inducible EGFR T790M-mediated gefitinib resistance in non-small cell lung cancer cells does not modulate sensitivity to PI103 provoked autophagy. J Thorac Oncol. 2010;5(6):765–77.PubMed
55.
Zurück zum Zitat Lee JG, Wu R. Combination erlotinib-cisplatin and Atg3-mediated autophagy in erlotinib resistant lung cancer. PLoS One. 2012;7(10):e48532.PubMedPubMedCentral Lee JG, Wu R. Combination erlotinib-cisplatin and Atg3-mediated autophagy in erlotinib resistant lung cancer. PLoS One. 2012;7(10):e48532.PubMedPubMedCentral
56.
Zurück zum Zitat Li YY, Lam SK, Mak JC, Zheng CY, Ho JC. Erlotinib-induced autophagy in epidermal growth factor receptor mutated non-small cell lung cancer. Lung Cancer. 2013;81(3):354–61.PubMed Li YY, Lam SK, Mak JC, Zheng CY, Ho JC. Erlotinib-induced autophagy in epidermal growth factor receptor mutated non-small cell lung cancer. Lung Cancer. 2013;81(3):354–61.PubMed
57.
Zurück zum Zitat Crighton D, Wilkinson S. O’Prey, Syed N, Smith P, Harrison PR, et al. DRAM, a p53-induced modulator of autophagy, is critical for apoptosis. Cell. 2006;126(1):121–34.PubMed Crighton D, Wilkinson S. O’Prey, Syed N, Smith P, Harrison PR, et al. DRAM, a p53-induced modulator of autophagy, is critical for apoptosis. Cell. 2006;126(1):121–34.PubMed
58.
Zurück zum Zitat Crighton D, Wilkinson S, Ryan KM. DRAM links autophagy to p53 and programmed cell death. Autophagy. 2007;3(1):72–4.PubMed Crighton D, Wilkinson S, Ryan KM. DRAM links autophagy to p53 and programmed cell death. Autophagy. 2007;3(1):72–4.PubMed
59.
Zurück zum Zitat O’Prey J, Skommer J, Wilkinson S, Ryan KM. Analysis of DRAM-related proteins reveals evolutionarily conserved and divergent roles in the control of autophagy. Cell Cycle. 2009;8(14):2260–5.PubMed O’Prey J, Skommer J, Wilkinson S, Ryan KM. Analysis of DRAM-related proteins reveals evolutionarily conserved and divergent roles in the control of autophagy. Cell Cycle. 2009;8(14):2260–5.PubMed
60.
Zurück zum Zitat Tasdemir E, Maiuri MC, Galluzzi L, Vitale I, Djavaheri-Mergny M, D’Amelio M, et al. Regulation of autophagy by cytoplasmic p53. Nat Cell Biol. 2008;10(6):676–87.PubMedPubMedCentral Tasdemir E, Maiuri MC, Galluzzi L, Vitale I, Djavaheri-Mergny M, D’Amelio M, et al. Regulation of autophagy by cytoplasmic p53. Nat Cell Biol. 2008;10(6):676–87.PubMedPubMedCentral
61.
Zurück zum Zitat Bokobza SM, Jiang Y, Weber AM, Devery AM, Ryan AJ. Combining AKT inhibition with chloroquine and gefitinib prevents compensatory autophagy and induces cell death in EGFR mutated NSCLC cells. Oncotarget. 2014;5(13):4765–78.PubMedPubMedCentral Bokobza SM, Jiang Y, Weber AM, Devery AM, Ryan AJ. Combining AKT inhibition with chloroquine and gefitinib prevents compensatory autophagy and induces cell death in EGFR mutated NSCLC cells. Oncotarget. 2014;5(13):4765–78.PubMedPubMedCentral
62.
Zurück zum Zitat Sobhakumari A, Schickling BM, Love-Homan L, Raeburn A, Fletcher EV, Case AJ, et al. NOX4 mediates cytoprotective autophagy induced by the EGFR inhibitor erlotinib in head and neck cancer cells. Toxicol Appl Pharmacol. 2013;272(3):736–45.PubMed Sobhakumari A, Schickling BM, Love-Homan L, Raeburn A, Fletcher EV, Case AJ, et al. NOX4 mediates cytoprotective autophagy induced by the EGFR inhibitor erlotinib in head and neck cancer cells. Toxicol Appl Pharmacol. 2013;272(3):736–45.PubMed
63.
Zurück zum Zitat Dragowska WH, Weppler SA, Wang JC, Wong LY, Kapanen AI, Rawji JS, et al. Induction of autophagy is an early response to gefitinib and a potential therapeutic target in breast cancer. PLoS One. 2013;8(10):e76503.PubMedPubMedCentral Dragowska WH, Weppler SA, Wang JC, Wong LY, Kapanen AI, Rawji JS, et al. Induction of autophagy is an early response to gefitinib and a potential therapeutic target in breast cancer. PLoS One. 2013;8(10):e76503.PubMedPubMedCentral
64.
Zurück zum Zitat Eimer S, Belaud-Rotureau MA, Airiau K, Jeanneteau M, Laharanne E, Véron N, et al. Autophagy inhibition cooperates with erlotinib to induce glioblastoma cell death. Cancer Biol Ther. 2011;11(12):1017–27.PubMed Eimer S, Belaud-Rotureau MA, Airiau K, Jeanneteau M, Laharanne E, Véron N, et al. Autophagy inhibition cooperates with erlotinib to induce glioblastoma cell death. Cancer Biol Ther. 2011;11(12):1017–27.PubMed
65.
Zurück zum Zitat Fung C, Chen X, Grandis JR, Duvvuri U. EGFR tyrosine kinase inhibition induces autophagy in cancer cells. Cancer Biol Ther. 2012;13(14):1417–24.PubMedPubMedCentral Fung C, Chen X, Grandis JR, Duvvuri U. EGFR tyrosine kinase inhibition induces autophagy in cancer cells. Cancer Biol Ther. 2012;13(14):1417–24.PubMedPubMedCentral
66.
Zurück zum Zitat Gorzalczany Y, Gilad Y, Amihai D, Hammel I, Sagi-Eisenberg R, Merimsky O. Combining an EGFR directed tyrosine kinase inhibitor with autophagy-inducing drugs: a beneficial strategy to combat non-small cell lung cancer. Cancer Lett. 2011;310(2):207–15.PubMed Gorzalczany Y, Gilad Y, Amihai D, Hammel I, Sagi-Eisenberg R, Merimsky O. Combining an EGFR directed tyrosine kinase inhibitor with autophagy-inducing drugs: a beneficial strategy to combat non-small cell lung cancer. Cancer Lett. 2011;310(2):207–15.PubMed
67.
Zurück zum Zitat Chang CY, Kuan YH, Ou YC, Li JR, Wu CC, Pan PH, et al. Autophagy contributes to gefitinib-induced glioma cell growth inhibition. Exp Cell Res. 2014;327(1):102–12.PubMed Chang CY, Kuan YH, Ou YC, Li JR, Wu CC, Pan PH, et al. Autophagy contributes to gefitinib-induced glioma cell growth inhibition. Exp Cell Res. 2014;327(1):102–12.PubMed
68.
Zurück zum Zitat Schmid K, Bago-Horvath Z, Berger W, Haitel A, Cejka D, Werzowa J, et al. Dual inhibition of EGFR and mTOR pathways in small cell lung cancer. Br J Cancer. 2010;103(5):622–62.PubMedPubMedCentral Schmid K, Bago-Horvath Z, Berger W, Haitel A, Cejka D, Werzowa J, et al. Dual inhibition of EGFR and mTOR pathways in small cell lung cancer. Br J Cancer. 2010;103(5):622–62.PubMedPubMedCentral
69.
Zurück zum Zitat Xu Z, Hang J, Hu J, Gao B. Gefitinib, an EGFR tyrosine kinase inhibitor, activates autophagy through AMPK in human lung cancer cells. J BUON. 2014;19(2):466–73.PubMed Xu Z, Hang J, Hu J, Gao B. Gefitinib, an EGFR tyrosine kinase inhibitor, activates autophagy through AMPK in human lung cancer cells. J BUON. 2014;19(2):466–73.PubMed
70.
Zurück zum Zitat La Monica S, Galetti M, Alfieri RR, Cavazzoni A, Ardizzoni A, Tiseo M, et al. Everolimus restores gefitinib sensitivity in resistant non-small cell lung cancer cell lines. Biochem Pharmacol. 2009;78(5):460–8.PubMed La Monica S, Galetti M, Alfieri RR, Cavazzoni A, Ardizzoni A, Tiseo M, et al. Everolimus restores gefitinib sensitivity in resistant non-small cell lung cancer cell lines. Biochem Pharmacol. 2009;78(5):460–8.PubMed
71.
Zurück zum Zitat Goldberg SB, Supko JG, Neal JW, Muzikansky A, Digumarthy S, Fidias P, et al. A phase I study of erlotinib and hydroxychloroquine in advanced non-small-cell lung cancer. J Thorac Oncol. 2012;7(10):1602–8.PubMedPubMedCentral Goldberg SB, Supko JG, Neal JW, Muzikansky A, Digumarthy S, Fidias P, et al. A phase I study of erlotinib and hydroxychloroquine in advanced non-small-cell lung cancer. J Thorac Oncol. 2012;7(10):1602–8.PubMedPubMedCentral
72.
Zurück zum Zitat Xinqun L, Zhen F. The epidermal growth factor receptor antibody cetuximab induces autophagy in cancer cells by downregulating HIF-1alpha and Bcl-2 and activating the beclin 1/Vps34 complex. Cancer Res. 2010;70(14):5942–52. Xinqun L, Zhen F. The epidermal growth factor receptor antibody cetuximab induces autophagy in cancer cells by downregulating HIF-1alpha and Bcl-2 and activating the beclin 1/Vps34 complex. Cancer Res. 2010;70(14):5942–52.
73.
Zurück zum Zitat Li X, Lu Y, Pan T, Fan Z. Roles of autophagy in cetuximab-mediated cancer therapy against EGFR. Autophagy. 2010;6(8):1066–77.PubMedPubMedCentral Li X, Lu Y, Pan T, Fan Z. Roles of autophagy in cetuximab-mediated cancer therapy against EGFR. Autophagy. 2010;6(8):1066–77.PubMedPubMedCentral
74.
Zurück zum Zitat Guo GF, Jiang WQ, Zhang B, Cai YC, Xu RH, Chen XX, et al. Autophagy-related proteins Beclin-1 and LC3 predict cetuximab efficacy in advanced colorectal cancer. World J Gastroenterol. 2011;17(43):4779–86.PubMedPubMedCentral Guo GF, Jiang WQ, Zhang B, Cai YC, Xu RH, Chen XX, et al. Autophagy-related proteins Beclin-1 and LC3 predict cetuximab efficacy in advanced colorectal cancer. World J Gastroenterol. 2011;17(43):4779–86.PubMedPubMedCentral
Metadaten
Titel
EGFR inhibitors and autophagy in cancer treatment
verfasst von
Jie Cui
Yun-Feng Hu
Xie-Min Feng
Tao Tian
Ya-Huan Guo
Jun-Wei Ma
Ke-Jun Nan
Hong-Yi Zhang
Publikationsdatum
01.12.2014
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 12/2014
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-014-2660-z

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