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TGIF1 组合式通过 AKT 信号通路抑制胃癌的增殖和侵袭
Authors Zhang J, Zhang F, Fan J, Feng B
Received 17 March 2020
Accepted for publication 19 December 2020
Published 18 March 2021 Volume 2021:13 Pages 2603—2612
DOI https://doi.org/10.2147/CMAR.S254348
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Ahmet Emre Eşkazan
Introduction: Gastric cancer is a kind of cancer with high mortality. TGIF1, as a transcription inhibitor, can inhibit the transcription of specific genes. The purpose of this study was to investigate the role of TGIF1 in gastric cancer by knocking down TGIF1.
Methods: The expression of TGIF1 was detected by qPCR and Western blotting; CCK8 assay, colony formation assay, transwell, and wound-healing assay were used to evaluate the proliferation, migration, and invasion of gastric cancer cells; cell apoptosis was analyzed by flow cytometry and Hoechst-PI double staining; cell cycle was detected by flow cytometry. Gelatinase experiment was performed to detect the expression level of MMP-2; apoptosis related proteins and AKT singling pathway were assessed by Western blotting.
Results: Knockdown of TGIF1 inhibited the proliferation, migration, and invasion of gastric cancer cells and promoted apoptosis. TGIF1 knockdown down-regulated the expression levels of MMP-2, Bcl2, CyclinD1, and p-Akt, and up-regulated the expression levels of Bax and Caspase3. These data suggested that knockdown of TGIF1 inhibited the development of gastric cancer via AKT signaling pathway.
Conclusion: TGIF1 knockdown inhibited the proliferation, migration, and invasion and promoted apoptosis of gastric cancer cells via the AKT signaling pathway, suggesting that TGIF1 is considered a potential inhibitor in gastric cancer.
Keywords: TGIF1, gastric cancer, AKT pathway, apoptosis, proliferation