J Cancer 2021; 12(11):3209-3221. doi:10.7150/jca.50403

Research Paper

Longnon-coding RNA BLACAT2 promotes gastric cancer progression via the miR-193b-5p/METTL3 pathway

Hao Hu1, Qi Kong1, Xiao-xu Huang1, Hao-ran Zhang1, Kai-feng Hu1, Yan Jing1, Yang-fan Jiang1,2, Yue Peng1,2, Long-chao Wu1,2, Qi-sheng Fu1, Li Xu1✉, Ya-bin Xia1✉

1. Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College, Wuhu, AnHui, 241001, P.R. China.
2. Wannan Medical College, Wuhu, AnHui, 241001, P.R. China.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Hu H, Kong Q, Huang Xx, Zhang Hr, Hu Kf, Jing Y, Jiang Yf, Peng Y, Wu Lc, Fu Qs, Xu L, Xia Yb. Longnon-coding RNA BLACAT2 promotes gastric cancer progression via the miR-193b-5p/METTL3 pathway. J Cancer 2021; 12(11):3209-3221. doi:10.7150/jca.50403. Available from https://www.jcancer.org/v12p3209.htm

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Gastric cancer is one of the leading prevalent and malignant cancers worldwide, especially in east Asia. However, the in-depth molecular mechanism underlying gastric cancer progression remains uncertain. Recently, studies have identified that long non-coding RNA (lncRNA) could play critical roles in the tumorigenesis of multiple types of cancer. Studies on long non-coding RNA BLACAT2 have proven that it participates in bladder cancer and colorectal cancer regulation and was identified as highly expressed using the cBioPortal for Cancer Genomics in gastric cancer. However, the precise function of lncRNA-BLACAT2 in the carcinogenesis and progression of gastric cancer remains largely unexplored. Our study discovered that lncRNA-BLACAT2 was significantly upregulated in gastric cancer. Different studies have illustrated that BLACAT2 promoted gastric cancer progression through regulating proliferation, migration, invasion, and apoptosis in terms of biological function.

Furthermore, BLACAT2 was verified to perform its function through interaction with miR-193b-5p using a luciferase reporter assay. On the other hand, MiR-193b-5p specific inhibitor treatment reversed the inhibitory effect of BLACAT2 on cell biological functions. Additional studies also discovered that Methyltransferase Like 3 (METTL3) was the downstream target of miR-193b-5p. Subsequently, restoration of METTL3 eliminated the suppressive effect of proliferation or the promotive effect of apoptosis caused by BLACAT2 knockdown. To sum up, these experimental results demonstrated that BLACAT2 acted as an oncogene in gastric cancer progression through the regulation of the miR-193b-5p/METTL3 pathway, hence providing new insights regarding the pathogenesis of gastric cancer.

Keywords: gastric cancer, lncRNA-BLACAT2 (BLACAT2), miR-193b-5p, METTL3, proliferation, apoptosis