Affiliations: [a] Department of Clinical Laboratory, The 89th Hospital of The People’s Liberation Army, Weifang, Shandong, China | [b] National Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy, Third Military Medical University, Chongqing, China | [c] Department of Clinical Laboratory, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, China | [d] Department of Pharmacy, Southwest Hospital, Third Military Medical University, Chongqing, China | [e] Department of Clinical Laboratory, The 904th Hospital of The People’s Liberation Army, Wuxi, Jiangsu, China | [f] College of Pharmacy, Chongqing Medical University, Chongqing, China
Correspondence:
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Corresponding authors: Jie Lin, Department of Clinical Laboratory, The 904th Hospital of The People’s Liberation Army, Wuxi, Jiangsu, China. E-mail: [email protected]. Bin Xiao, College of Pharmacy, Chongqing Medical University, Chongqing, China. E-mail: [email protected].
Note: [1] These authors contributed equally to this work.
Abstract: BACKGROUND: Gastric cancer is one of the leading causes of death worldwide. MicroRNA-30a (miR-30a) has been demonstrated to be involved in several types of cancer development. OBJECTIVE:We aimed to identify the molecular mechanism of miR-30a in gastric cancer. METHODS:We investigated the expression of miR-30a in gastric cancer tissues by qRT-PCR. The role of miR-30a on the metastasis and proliferation of gastric cancer was evaluated by cell migration assay, CCK-8 assay and tumor peritoneal dissemination model. The target of miR-30a in gastric cancer was identified. RESULTS:We discovered that miR-30a was significantly downregulated in gastric cancer tissues compared with adjacent nonmalignant tissues. The expression of miR-30a was inversely correlated with progression of gastric cancer. Gain- and loss-of function revealed that miR-30a acted as a potent tumor suppressor in gastric cancer. Re-expressed miR-30a inhibited gastric cancer cells migration, knock down miR-30a have the opposite effects. Furthermore, overexpression of miR-30a suppressed tumor peritoneal dissemination in vivo. We identified that fibroblast activation protein α (FAPα) was a direct target of miR-30a. The relative expression of FAPα was significantly higher in gastric cancer tissues compared with adjacent nonmalignant tissues. Inhibition of FAPα could recapitulate the effects of miR-30a, and overexpression of FAPα could abrogate the effect of miR-30a. CONCLUSION: MiR-30a inhibited gastric cancer metastasis by targeting FAPα, suggesting that miR-30a may function as a novel tumor suppressor in gastric cancer.
