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논문 기본 정보

자료유형
학술저널
저자정보
Yi Bin (The First Affiliated Hospital of Soochow University People’s Republic of China) Hu You (The First Affiliated Hospital of Soochow University People’s Republic of China) Zhu Dongming (The First Affiliated Hospital of Soochow University People’s Republic of China) Yao Jun (The First Affiliated Hospital of Soochow University People’s Republic of China) Zhou Jian (The First Affiliated Hospital of Soochow University People’s Republic of China) Zhang Yi (The First Affiliated Hospital of Soochow University People’s Republic of China) He Zhilong (The First Affiliated Hospital of Soochow University People’s Republic of China) Zhang Lifeng (The First Affiliated Hospital of Soochow University People’s Republic of China) Zhang Zixiang (The First Affiliated Hospital of Soochow University People’s Republic of China) Yang Jian (The First Affiliated Hospital of Soochow University People’s Republic of China) Tang Yuchen (The First Affiliated Hospital of Soochow University People’s Republic of China) Huang Yujie (The First Affiliated Hospital of Soochow University People’s Republic of China) Li Dechun (The First Affiliated Hospital of Soochow University People’s Republic of China) Liu Qiuhua (The First People’s Hospital of Zhangjiagang City People’s Republic of China)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.44 No.5
발행연도
2022.5
수록면
561 - 569 (9page)
DOI
10.1007/s13258-022-01217-0

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Background Rho GDP dissociation inhibitor 2 (RhoGDI2) has been shown to contribute to the aggressive phenotypes of human cancers, such as tumor metastasis and chemoresistance. Objective This study aimed to assess the effects of RhoGDI2 on tumor progression and chemoresistance in pancreatic cancer cells. Methods The expression of RhoGDI2 in pancreatic cancer cells was detected by Western blot analysis. Gain-of-function and loss-of-function approaches were done to examine the malignant phenotypes of the RhoGDI2-expressing or RhoGDI2-depleting cells. The correlation between RhoGDI2 and Snail was also analyzed. Results Differential expression of RhoGDI2 protein in pancreatic cancer cell lines was identified. Gain-of-function and loss-of-function experiments showed that RhoGDI2 induced the malignant phenotypes of pancreatic cancer cells, including proliferation, migration, invasion, and gemcitabine (GEM) chemoresistance. The upregulation of RhoGDI2 stimulated the expression of Snail, resulting in the altered expression of epithelial marker E-cadherin and mesenchymal marker Vimentin, which were characteristics of the tumorigenic activity of epithelial?mesenchymal transition. The expression of RhoGDI2 and Snail was upregulated in clinical tumor samples, and higher expression of RhoGDI2 or Snail was significantly associated with poor patient survival in pancreatic ductal adenocarcinoma (PDAC). Conclusion The findings indicated that RhoGDI2 promoted GEM resistance and tumor progression in pancreatic cancer and that RhoGDI2 might be a potential therapeutic target in patients with PDAC.

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