A novel mechanism driving poor-prognostic gastric cancer: overexpression of the transcription factor Kruppel-like factor 16 promotes growth and metastasis of gastric cancer through regulating the Notch pathway

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標題:	A novel mechanism driving poor-prognostic gastric cancer: overexpression of the transcription factor Kruppel-like factor 16 promotes growth and metastasis of gastric cancer through regulating the Notch pathway
作者:	Sun, Ding-Ping Tian, Yu-Feng Lin, Chih-Chan Hung, Shih-Ting Uen, Yih-Huei Hseu, You-Cheng Chou, Chia-Lin Cheng, Li-Chin Wang, Wen-Ching Kuang, Yi-Yu Fang, Chia-Lang Lin, Kai-Yuan
貢獻者:	Chi Mei Med Ctr, Dept Surg Chia Nan Univ Pharm & Sci, Dept Food Sci & Technol Chi Mei Med Ctr, Dept Med Res Asia Univ Hosp, Dept Surg Asia Univ, Dept Biotechnol Tainan Municipal Nan Hosp, Dept Surg China Med Univ, Dept Cosmeceut Asia Univ, Dept Hlth & Nutr Biotechnol China Med Univ, Chinese Med Res Ctr Taipei Med Univ, Sch Med, Coll Med, Dept Pathol Taipei Med Univ Hosp, Taipei Med Univ, Dept Pathol Chia Nan Univ Pharm & Sci, Dept Biotechnol
關鍵字:	Gastric cancer KLF16 prognosis MFAP5 Notch pathway
日期:	2021
上傳時間:	2023-11-11 12:00:45 (UTC+8)
出版者:	E-CENTURY PUBLISHING CORP
摘要:	Gastric cancer (GC) is one of the most common malignant tumors worldwide and has high rates of morbidity and mortality. This study investigated the role of Kruppel-like factor 16 (KLF16) in GC. Real-time polymerase chain reaction, Western blotting, and immunohistochemistry were used to examine the expression of KLF16 in gastric cells and tissues. Gene overexpression and silencing were applied to study the involvement of KLF16 in GC cell growth and metastasis along with its underlying mechanism. The results indicate that KLF16 overexpression is significantly associated with nodal status, distant metastasis, staging, degree of differentiation, vascular invasion, and patient survival. Multivariate Cox proportional hazards regression model analysis revealed that the overexpression of KLF16 is an independent prognostic biomarker of GC. The in vitro study revealed that up-regulated KLF16 accelerates cell growth and metastasis, whereas the inhibition of KLF16 suppresses these cellular activities. The results of an animal study also indicated that the overexpression and silencing of KLF16 accelerate and repress xenograft proliferation and metastasis. Further studies of affected cell growth and metastasis revealed that KLF16 modulates the cell cycle and epithelial-mesenchymal transition through transcriptional regulation of microfibrillar-associated protein 5. Collectively, these results reveal that KLF16 overexpression is a potential prognostic biomarker and therapeutic target for the treatment of GC.
關聯:	AM J CANCER RES, v.11, n.6, pp.2717-2735
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