&lt;p&gt;Long Noncoding RNA KCNMB2-AS1 Increases ROCK1 Expression by Sponging microRNA-374a-3p to Facilitate the Progression of Non–Small-Cell Lung Cancer&lt;/p&gt;

Huang, Yang; Wang, Ziyi; Wang, Zhenyuan

doi:10.2147/cmar.s270646

Cited by 14 publications

(16 citation statements)

References 34 publications

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“…For example, long noncoding RNA KCNMB2-AS1 increased ROCK1 expression by Sponging microRNA-374a-3p to facilitate the progression of NSCLC. 17 LncRNA F630028O10Rik, a novel tumour suppressor, inhibited lung cancer angiogenesis by regulating miR-223-3p. 18 MT1DP loaded by folate-modified liposomes sensitizes erastin-induced ferroptosis via regulating miR-365a-3p/NRF2 axis in NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

Wang²,

Zhou

et al. 2021

CMAR

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Introduction NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development. Methods The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319. Results PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo. Conclusion In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC.

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Section: Discussionmentioning

confidence: 99%

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

Wang²,

Zhou

et al. 2021

CMAR

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“…KCNMB2-AS1 silencing hinders the proliferation, migration and invasion of NSCLC cells, promotes cell apoptosis, and inhibits tumor growth in vivo. KCNMB2-AS1 acts as a sponge for endogenous miR-374a-3p to increase ROCK1 expression ( 33 ). These results indicate that our constructed network was closely related to the metastasis and drug resistance of NSCLC.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1-miR-101-3p/miR-335-5p/miR-374a-3p/miR-628-5p-TRIM6 axis identified as the prognostic biomarker for lung adenocarcinoma via bioinformatics and meta-analysis

Ding¹,

Li²,

Shi³

et al. 2021

Transl Cancer Res TCR

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Background Overexpression of the tripartite motif containing 6 (TRIM6) is associated with dismal prognosis in cancer patients, but its exact roles in lung adenocarcinoma (LUAD) have not been reported. Methods The roles of TRIM6 are identified by using The Cancer Genome Atlas (TCGA), TIMER2, Gene Expression Omnibus (GEO), etc., and the regulatory networks and related-prognostic biomarkers of TRIM6 are identified via the ENCORI and LNCAR databases in the LUAD progression. Results TRIM6 expression level in LUAD tissues was significantly increased. TRIM6 over-expression level in LUAD patients was associated with smoking, clinical stage, histological type, lymph node metastasis, TP53 mutation and dismal prognosis, and related to prognosis-related age, race, sex, clinical stage and tumor purity of LUAD patients. TRIM6 overexpression was associated with the levels of CD8 + T cells, macrophages, neutrophils and myeloid dendritic cells, and correlated with the levels of LUAD immune cell markers CD8A, IRF5, CD163, VSIG4, MS4A4A, ITGAM, HLA-DPA1, NRP1, ITGAX, etc. TRIM6 might influence the progression of LUAD by regulating homologous recombination, oocyte meiosis, and ubiquitin-mediated proteolysis. LUAD patients with overexpression of miR-101-3p, miR-335-5p, miR-374a-3p, miR-628-5p, and NEAT1 had a poor prognosis. Conclusions NEAT1-miR-101-3p/335-5p/374a-3p/628-5p-TRIM6 network, which we constructed from our results, might be an important factor in the dismal prognosis of LUAD patients.

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“…KCNMB2-AS1 has been proved to be served as a ceRNA by sponging miR-130b-5p and miR-4294 in cervical cancer . Yang et al (2020) showed that KCNMB2-AS1/miR-374a-3p/ROCK1 axis promotes NSCLC progression. In the present study, we speculated that KCNMB2-AS1 might function as a ceRNA in BC.…”

Section: Discussionmentioning

confidence: 99%

KCNMB2-AS1 Promotes Bladder Cancer Progression Through Sponging miR-374a-3p to Upregulate S100A10

et al. 2021

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Long non-coding RNAs (lncRNAs) have been reported to play a crucial role in the pathogenesis of numerous cancers. However, the function of lncRNA KCNMB2-AS1 in bladder cancer (BC) remains unclear. In the present study, we aimed to explore the role and underlying mechanisms of KCNMB2-AS1 in bladder cancer progression. We found that lncRNA KCNMB2-AS1 was significantly upregulated both in BC tissues and cell lines, the expression level was highly correlated with pathological TNM stage. Functionally, knockdown of lncRNA KCNMB2-AS1 dramatically inhibited the proliferation, migration, and invasion and of BC cells in vitro, and suppressed tumor growth in vivo. Mechanistically, lncRNA KCNMB2-AS1 could function as a competitive endogenous RNA (ceRNA) through direct sponging miR-374a-3p, which regulated the expression of S100A10. In conclusion, our results demonstrated that lncRNA KCNMB2-AS1 can promote the progression of bladder cancer through regulation of miR-374a-3p/S100A10.

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<p>Long Noncoding RNA KCNMB2-AS1 Increases ROCK1 Expression by Sponging microRNA-374a-3p to Facilitate the Progression of Non–Small-Cell Lung Cancer</p>

Cited by 14 publications

References 34 publications

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

LncRNA NEAT1-miR-101-3p/miR-335-5p/miR-374a-3p/miR-628-5p-TRIM6 axis identified as the prognostic biomarker for lung adenocarcinoma via bioinformatics and meta-analysis

KCNMB2-AS1 Promotes Bladder Cancer Progression Through Sponging miR-374a-3p to Upregulate S100A10

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