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LINC01133 regulates MARCKS expression via sponging miR-30d-5p to promote the development of lung squamous cell carcinoma

细胞凋亡 细胞生长 马尔克斯 下调和上调 流式细胞术 癌症研究 细胞 细胞生物学 荧光素酶 细胞迁移 生物 分子生物学 细胞培养 转染 信号转导 基因 蛋白激酶C 生物化学 遗传学
作者
Yajun Zhang,Woda Shi,Rongjin Chen,Yan Gu,Mengjie Zhao,Jianxiang Song,Zhan Shi,Jixiang Wu,Hui‐Wen Chang,Ming Liu
出处
期刊:Translational Oncology [Elsevier]
卷期号:44: 101931-101931
标识
DOI:10.1016/j.tranon.2024.101931
摘要

LncRNAs are vital regulators for lung squamous cell carcinoma (LUSC). However, the detailed role that LINC01133 plays in LUSC is unclear. This work sought to explore the potential function of LINC01133.Levels of LINC01133, miR-30d-5p, and MARCKS were separately tested in both tissues and cells using qRT-PCR. Proliferation was assessed through MTT experiment and apoptosis was detected upon flow cytometry. Transwell experiments were implemented to evaluate migratory and invasive abilities. The interaction between two genes was affirmed through luciferase reporter assay and RNA pull-down experiment. Western blotting measured the protein level of MARCKS. Animal models were established and tissues were taken for IHC analysis of MARCKS and Ki67.LINC01133 was elevated in LUSC and its downregulation could suppress proliferation, migration and invasion but induced apoptosis. LINC01133 interacted with and regulated the binding of miR-30d-5p to MARCKS. LINC01133/miR-30d-5p axis mediated proliferation, apoptosis, migration and invasion in LUSC cells, as well as modulated tumor growth in animal models. LINC01133 interacted with miR-30d-5p to modulate MARCKS expression, contributes to promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. These findings could provide possible therapeutic targets in view of LUSC treatment in the future.
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