Journal
JOURNAL OF CANCER
Volume 12, Issue 11, Pages 3209-3221Publisher
IVYSPRING INT PUBL
DOI: 10.7150/jca.50403
Keywords
gastric cancer; lncRNA-BLACAT2 (BLACAT2); miR-193b-5p; METTL3; proliferation; apoptosis
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Funding
- Natural Science Research Project of Colleges and Universities in Anhui Province [KJ2019A0412]
- Young and middle aged project of Wannan Medical College [WK2018F03]
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Research has shown that the long non-coding RNA BLACAT2 is significantly upregulated in gastric cancer and plays a promoting role in gastric cancer progression through interaction with miR-193b-5p. This interaction affects cell proliferation, migration, invasion, and apoptosis. Additionally, the downstream target of BLACAT2, METTL3, has been found to have a significant impact on the development of gastric cancer.
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.
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