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Erschienen in: Tumor Biology 7/2015

01.07.2015 | Research Article

Elevated expression of immunity-related GTPase family M in gastric cancer

verfasst von: Zongchang Song, Chunliang Guo, Lu Zhu, Pinying Shen, Haitao Wang, Changsheng Guo, Jiahong Tang

Erschienen in: Tumor Biology | Ausgabe 7/2015

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Abstract

Recent researches have suggested that autophagy may play critical roles in tumorigenesis. Immunity-related GTPase family M (IRGM) is a human protein highlighted for its contribution to autophagy upon inflammation and infections. Studies have shown that IRGM is involved in the development of several cancers. In the current study, we investigated expression of IRGM and gastric cancer. Levels of messenger RNA (mRNA) and protein were examined by real-time reverse transcription PCR (RT-PCR) and Western blot, respectively. Data showed that mRNA level of IRGM was significantly increased in peripheral blood mononuclear cells (PBMCs) of gastric cancer patients than in PBMCs from healthy controls (p > 0.05). Moreover, both mRNA and protein levels were significantly higher in cancer tissues compared to adjacent noncancerous stomach tissues (1.28-fold, p < 0.001; 1.19-fold, p < 0.01, respectively). However, the level of IRGM seemed not to be affected by Helicobacter pylori infection. In addition, we investigated the correlation between IRGM expression and cancer stages and identified that stage IV patients had upregulated mRNA level and protein level of IRGM in cancer tissues than those stage I patients. Our findings suggest that expression of IRGM is dysregulated in gastric cancer and that the molecule may affect progression of the disease.
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Metadaten
Titel
Elevated expression of immunity-related GTPase family M in gastric cancer
verfasst von
Zongchang Song
Chunliang Guo
Lu Zhu
Pinying Shen
Haitao Wang
Changsheng Guo
Jiahong Tang
Publikationsdatum
01.07.2015
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 7/2015
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-3229-1

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