Knockdown of POLDIP2 suppresses tumor growth and invasion capacity and is linked to unfavorable transformation ability and metastatic feature in non-small cell lung cancer

Ying Chieh Chen, Chih Chi Kuo, Chih Feng Chian, Ching Tzao, Shan Yueh Chang, Yu Lueng Shih, Ya Wen Lin, Mu Hsien Yu, Her Young Su

研究成果: 雜誌貢獻文章

1 引文 斯高帕斯(Scopus)

摘要

The main problem in the treatment of non-small cell lung cancer (NSCLC) is metastasis. Epithelial–mesenchymal transition (EMT) is known as the critical signaling in tumor progression, metastasis, and also the drug resistance. In this study, we reported a novel gene Polymerase delta-interacting protein 2 (POLDIP2) was downregulated in NSCLC tissues and first demonstrated that overexpression of POLDIP2 increased the anchorage-independent growth (AIG) and invasiveness of H1299 cells. In addition, we examined that knockdown of POLDIP2 in H1299 and A549 cells reduced tumorigenicity and metastatic capacity in vitro and also in vivo. Moreover, downregulation of the cell proliferation marker cyclin D1 and EMT markers CDH2, Slug, and Twist was showed in H1299 cells by POLDIP2 knockdown, suggesting that the inhibition of malignancy was affected by modulating key genes for tumor growth and invasiveness. Taken together, our study is the first study that demonstrated that POLDIP2 gene was function as an oncogene in NSCLC and implied the oncogenic ability might be through promoting cell proliferation or EMT.
原文英語
頁(從 - 到)42-49
頁數8
期刊Experimental Cell Research
368
發行號1
DOIs
出版狀態已發佈 - 七月 1 2018

ASJC Scopus subject areas

  • Cell Biology

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