TRIM11 Promotes Proliferation, Migration, Invasion and EMT of Gastric Cancer by Activating β-Catenin Signaling
Authors Lan Q, Tan X, He P, Li W, Tian S, Dong W
Received 16 November 2020
Accepted for publication 28 January 2021
Published 25 February 2021 Volume 2021:14 Pages 1429—1440
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Alberto Bongiovanni
Qingzhi Lan,1,2 Xiaoping Tan,3,* Pengzhan He,1,2,* Wei Li,1,2 Shan Tian,1,2 Weiguo Dong1
1Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, People’s Republic of China; 2Central Laboratory of Renmin Hospital, Wuhan, People’s Republic of China; 3Department of Gastroenterology, The First Affiliated Hospital of Yangtze University, Jingzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Weiguo Dong
Department of Gastroenterology, Renmin Hospital of Wuhan University, No. 238 Zhang Zhi-Dong Road, Wuhan, 430060, People’s Republic of China
Email [email protected]
Introduction: Gastric cancer (GC) is the sixth most common malignant tumor and the third leading cause of cancer-related death in the world. Studies have shown that TRIM protein can regulate transcription factor activity and is associated with many cancers. However, the role of TRIM11 in gastric cancer remains unclear.
Methods: TRIM11 protein levels were examined in 36 cases of GC tissues and 4 gastric cancer cell lines. TRIM11 overexpression and knockdown cells were constructed in MGC-803, HGC-27 and SGC-7901, respectively. The biological roles and mechanisms of TRIM11 were examined using CCK8, colony formation, transwell migration assay, invasion assay, Western blotting, Immunohistochemistry and in vivo nude mice experiments.
Results: We found that TRIM11 was upregulated in gastric cancer tissues and gastric cancer cell lines. Functionally, TRIM11 overexpression increased growth rate, colony formation, invasion and migration ability, EMT and β-catenin protein level and its downstream proteins such as CyclinD1 and C-myc, while TRIM11 knockdown shows the opposite effects.
Conclusion: In summary, our data show that TRIM11 is overexpressed in GC. TRIM11 promotes proliferation, migration, invasion and EMT of gastric cancer by activating β-catenin signaling.
Keywords: TRIM11, gastric cancer, proliferation, migration, invasion, EMT
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