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논문 기본 정보

자료유형
학술저널
저자정보
Tang Weiping (Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, Chaohu 238000, Anhui, P.R. China) Huang Can (Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, Chaohu 238000, Anhui, P.R. China) Jiang Bing (Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, Chaohu 238000, Anhui, P.R. China) Lin Junjun (Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, Chaohu 238000, Anhui, P.R. China) Lu Yecai (Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, Chaohu 238000, Anhui, P.R. China)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology Vol.34 No.7
발행연도
2024.7
수록면
1,433 - 1,442 (10page)
DOI
10.4014/jmb.2401.01027

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Gastric adenocarcinoma (GAC) is a common, malignant type of tumor in human, and is accompanied with higher mortality. Muscleblind-like 3 (MBNL3) was found to be a pivotal participator in aggravating this cancer’s progression. However, the regulatory effects of MBNL3 on GAC development have not been investigated. We therefore sought to study the functions of MBNL3 in GAC progression. In this study, it was demonstrated that MBNL3 exhibited higher expression, and GAC patients with higher MBNL3 expression had poor prognosis. Overexpression of MBNL3 facilitated, and knockdown of MBNL3 suppressed cell proliferation, invasion, and angiogenesis in GAC. Further experiments showed that miR-302e targets MBNL3. Rescue assays then uncovered that the miR-302e/MBNL3 axis aggravated GAC progression. In addition, MBNL3 activated the AKT/VEGFA pathway, and the suppressive regulatory impacts of MBNL3 knockdown on GAC cell proliferation, invasion, and angiogenesis could be rescued after 740 Y-P treatment. Through in vivo assay, it was proved that MBNL3 accelerated tumor growth in vivo. In conclusion, MBNL3 acted as a target of miR-302e to facilitate cell proliferation, invasion, and angiogenesis of gastric adenocarcinoma through the AKT/ VEGFA pathway. Our findings illustrate that MBNL3 may be an available bio-target for GAC treatment.

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