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miR-29a-3p inhibits the malignant characteristics of non-small cell lung cancer cells by reducing the activity of the Wnt/beta-catenin signaling pathway  ( SCI-EXPANDED收录)   被引量:7

文献类型:期刊文献

英文题名:miR-29a-3p inhibits the malignant characteristics of non-small cell lung cancer cells by reducing the activity of the Wnt/beta-catenin signaling pathway

作者:Zhang, Kang[1];Han, Xiaoliang[1];Hu, Wenbin[1];Su, Chao[1];He, Binjun[1,2]

机构:[1]Shaoxing Univ, Affiliated Hosp, Shaoxing Municipal Hosp, Dept Cardiothorac Surg, Shaoxing 312000, Zhejiang, Peoples R China;[2]Shaoxing Univ, Affiliated Hosp, Shaoxing Municipal Hosp, Dept Cardiothorac Surg, 999 Zhongxing South Rd, Shaoxing 312000, Zhejiang, Peoples R China

年份:2022

卷号:24

期号:4

外文期刊名:ONCOLOGY LETTERS

收录:SCI-EXPANDED(收录号:WOS:000888225000001)、、Scopus(收录号:2-s2.0-85138591348)、WOS

语种:英文

外文关键词:non-small cell lung cancer; microRNA29a-3p; Wnt/beta-catenin pathway; proliferation; migration; invasion

外文摘要:MicroRNAs (miRNAs) can influence non-small cell lung cancer (NSCLC) in a tumor-suppressive and oncogenic manner. The present study aimed to investigate the effects and underlying mechanisms of miR-29a-3p in NSCLC. NSCLC cell lines (A549, H1299, and H460) and a normal lung epithelial cell line (BEAS-2B) were used. Additionally, a mouse lung tumor xenograft model was established using A549 cells and used to determine the effects of miR-29a-3p on NSCLC in vivo. Tumor volumes were measured every week. The expression of miR-29a-3p in cells and lung tissues were detected by RT-qPCR. Cell proliferation was detected using Cell Counting Kit-8 and EdU assays. Migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. Ki-67 expression was detected using immunohistochemical staining. The expression levels of Wnt3a and beta-catenin were determined using western blotting. miR-29a-3p expression was significantly downregulated in NSCLC cells and mice. In contrast to miR-29a-3p knockdown, miR-29a-3p overexpression decreased NSCLC cell proliferation, migration, and invasion as well as tumor growth in in the NSCLC mouse model. Moreover, miR-29a-3p overexpression decreased the protein expression levels of Wnt3a and beta-catenin. The inhibitory effects of miR-29a-3p on NSCLC cells were reversed by LiCl (an activator of the Wnt signaling pathway). In conclusion, miR-29a-3p prevented NSCLC tumor growth and cell proliferation, migration, and invasion by inhibiting the Wnt/beta-catenin signaling pathway. This finding offers novel insights into the prognosis and treatment of NSCLC.

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