Tesc promotes tgf-ᾳ/egfr-foxm1-mediated tumor progression in cholangiocarcinoma

Cheng Han Hsieh, Cheng Ying Chu, Sey En Lin, Yu Chen S.H. Yang, Hung Shu Chang, Yun Yen

研究成果: 雜誌貢獻文章同行評審

摘要

Cholangiocarcinoma is a relatively uncommon but highly lethal malignancy. Improving outcomes in patients depends on earlier diagnosis and appropriate treatment; however, no satisfactory diagnostic biomarkers or targeted therapies are currently available. To address this shortcoming, we analyzed the transcriptomic datasets of cholangiocarcinoma from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases and found that TESC is highly expressed in cholangiocarcinoma. Elevated cellular levels of TESC are correlated with larger tumor size and predict a poor survival outcome for patients. Knockdown of TESC via RNA interference suppresses tumor growth. RNA-sequencing analysis showed that silencing of TESC decreases the level of FOXM1, leading to cell cycle arrest. Correlation analysis revealed that the cellular level of TESC is correlated with that of FOXM1 in cholangiocarcinoma patients. We further observed that upon TGF- ᾳ induction, TESC is upregulated through the EGFR-STAT3 pathway and mediates TGF- ᾳ -induced tumor cell proliferation. In vivo experiments revealed that knockdown of TESC significantly attenuates tumor cell growth. Therefore, our data provide novel insight into TESC-mediated oncogenesis and reveal that TESC is a potential biomarker or serves as a therapeutic target for cholangiocarcinoma.

原文英語
文章編號1105
期刊Cancers
12
發行號5
DOIs
出版狀態已發佈 - 五月 2020

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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