Research Paper Volume 13, Issue 12 pp 16763—16772
Hsa-miR-30a-3p attenuates gastric adenocarcinoma proliferation and metastasis via APBB2
- 1 Department of Gastroenterology, Ninth People’s Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
Received: March 2, 2021 Accepted: May 19, 2021 Published: June 28, 2021https://doi.org/10.18632/aging.203197
How to Cite
Copyright: © 2021 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: There is a well-established relationship between cell cycle progression and the development of stomach adenocarcinoma. This study aimed to elucidate the molecular mechanism and biological function of APBB2 in gastric cancer.
Methods: Gastric adenocarcinoma (GA) data were downloaded from the TCGA-GA and GEO databases and analyzed to explore differentially expressed miRNAs and mRNAs. Moreover, potential target mRNAs were also predicted. The relative level of gene and protein expression in GA cell lines and gastric mucosa cells was detected by q-PCR and Western blot, respectively. Moreover, the influence of APBB2 on proliferation, metastasis, and cell cycle changes in SGC-7901 and BGC-823 cells was evaluated. The binding relationship between the target miRNA and mRNA was confirmed with a dual-luciferase reporter assay.
Results: High APBB2 expression was detected in GA patients, indicating that it may be represent a predictive biomarker for poor prognosis. Related experiments confirmed that APBB2 silencing inhibited GA cellular functions, including proliferation, cell cycle progression, migration, and invasion. In addition, to explore the molecular mechanism, our results indicated that the binding sites were located at hsa-mir-30a and the 3′-UTR of APBB2, suggesting that hsa-mir-30a can regulate the expression of APBB2. The biological functions of hsa-mir-30a were also evaluated. Hsa-mir-30a overexpression attenuated the proliferation and metastasis of cancer cells. In rescue experiments, hsa-mir-30a was confirmed to reverse the cell cycle promoting function associated with APBB2 overexpression.
Conclusion: Our findings show that hsa-mir-30a can attenuate the development of GA by down-regulating APBB2 expression.