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MicroRNA-1269b 通过调控甲基转移酶样蛋白 3(METTL3)抑制胃癌发展。

MicroRNA-1269b inhibits gastric cancer development through regulating methyltransferase-like 3 (METTL3).

机构信息

Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan Hubei Province, China.

Department of General Practice, Renmin Hospital of Wuhan University, Wuhan Hubei Province, China.

出版信息

Bioengineered. 2021 Dec;12(1):1150-1160. doi: 10.1080/21655979.2021.1909951.

DOI:10.1080/21655979.2021.1909951
PMID:33818282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8806277/
Abstract

The dysregulation of microRNAs (miRNAs) expression is relevant to the progression of many tumors. As reported, the abnormal expression of miR-1269b is pivotal in certain cancers' progression. This work was designed to study the role and hidden mechanism of miR-1269b in gastric cancer (GC) progression. In this work, we proved that miR-1269b was lowly expressed in GC tissues and cell lines, which was associated with larger tumor size and lymph node metastasis. MiR-1269b overexpression repressed the multiplication, migration and invasion of GC cells while miR-1269b inhibition had the opposite effects. Methyltransferase-like 3 (METTL3) was identified as the direct target of miR-1269b in GC cells, and its overexpression reversed the inhibitory effect of transfection of miR-1269b mimics on GC cell viability, migration and invasion. On all accounts, these data indicated that miR-1269b inhibits GC progression via targeting METTL3.

摘要

miRNAs 表达失调与许多肿瘤的进展有关。据报道,miR-1269b 的异常表达在某些癌症的进展中起着关键作用。本研究旨在探讨 miR-1269b 在胃癌(GC)进展中的作用和潜在机制。本研究证明,miR-1269b 在 GC 组织和细胞系中低表达,与肿瘤体积较大和淋巴结转移有关。miR-1269b 过表达抑制 GC 细胞的增殖、迁移和侵袭,而 miR-1269b 抑制则产生相反的效果。甲基转移酶样 3(METTL3)被鉴定为 GC 细胞中 miR-1269b 的直接靶标,其过表达逆转了 miR-1269b 模拟物转染对 GC 细胞活力、迁移和侵袭的抑制作用。综上所述,这些数据表明 miR-1269b 通过靶向 METTL3 抑制 GC 进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/08f026bd56a3/KBIE_A_1909951_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/33f0308cf785/KBIE_A_1909951_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/832e84c181e5/KBIE_A_1909951_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/a2df793d6c76/KBIE_A_1909951_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/ea72fe69b08c/KBIE_A_1909951_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/08f026bd56a3/KBIE_A_1909951_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/33f0308cf785/KBIE_A_1909951_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/832e84c181e5/KBIE_A_1909951_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/a2df793d6c76/KBIE_A_1909951_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/ea72fe69b08c/KBIE_A_1909951_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f82/8806277/08f026bd56a3/KBIE_A_1909951_F0004_OC.jpg

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