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Erschienen in: Tumor Biology 9/2016

23.06.2016 | Original Article

Epigenetic silencing of TPM2 contributes to colorectal cancer progression upon RhoA activation

verfasst von: Ji Cui, Yonghua Cai, Ying Hu, Zenghong Huang, Yanxin Luo, Andrew M. Kaz, Zihuan Yang, Dianke Chen, Xinjuan Fan, William M. Grady, Jianping Wang

Erschienen in: Tumor Biology | Ausgabe 9/2016

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Abstract

Beta-tropomyosin (β-tropomyosin, TPM2) has been found to be downregulated in colorectal cancer (CRC) in previous studies. In this study, we aimed to investigate the mechanisms and potential biological consequences of the downregulation of TPM2 in colorectal cancer. TPM2 expression in colorectal cancer was assessed by qRT-PCR and immunostaining. The biological functions of TPM2 were assessed in cell lines either overexpressing or underexpressingTPM2. Aberrant DNA methylation in the promoter region is associated with suppression of TPM2 expression in primary colorectal cancer tissue samples. Treatment with the demethylation agent 5-AZA can induceTPM2 expression in colorectal cancer cell lines. Reconstitution of TPM2 suppresses cell proliferation and migration in colorectal cancer cell lines, whereas the loss of TPM2 expression is associated with increased tumor proliferation and migration in vitro, which was accompanied by RhoA activation. In summary, our findings indicate that TPM2 appears to be commonly silenced by aberrant DNA methylation in colon cancer. TPM2 loss is associated with RhoA activation and tumor proliferation.
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Metadaten
Titel
Epigenetic silencing of TPM2 contributes to colorectal cancer progression upon RhoA activation
verfasst von
Ji Cui
Yonghua Cai
Ying Hu
Zenghong Huang
Yanxin Luo
Andrew M. Kaz
Zihuan Yang
Dianke Chen
Xinjuan Fan
William M. Grady
Jianping Wang
Publikationsdatum
23.06.2016
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 9/2016
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-016-5103-1

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