ArticleOncoTargets and therapy2016
miR-32 inhibits proliferation, epithelial-mesenchymal transition, and metastasis by targeting TWIST1 in non-small-cell lung cancer cells.
Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed.
- Trial
- Upregulation of miR-32 in tissue and plasma and its association with PTEN expression in colorectal cancer.BMC cancer · 2026Article
- Overexpression of miR-32 in Chinese hamster ovary cells increases production of Fc-fusion protein.AMB Express · 2023Article
- Exosomal miRNA Expression Profiling and the Roles of Exosomal miR-4741, miR-32, miR-3149, and miR-6727 on Gastric Cancer Progression.BioMed research international · 2022Article
- Magic and mystery of microRNA-32.Journal of cellular and molecular medicine · 2021Review
- LincRNA-ROR is activated by H3K27 acetylation and induces EMT in retinoblastoma by acting as a sponge of miR-32 to activate the Notch signaling pathway.Cancer gene therapy · 2021Article
- MicroRNA-32 and MicroRNA-548a Promote the Drug Sensitivity of Non-Small Cell Lung Cancer Cells to Cisplatin by Targeting ROBO1 and Inhibiting the Activation of Wnt/β-Catenin Axis.Cancer management and research · 2021Article
- MicroRNA 495 Inhibits Proliferation and Metastasis and Promotes Apoptosis by Targeting Twist1 in Gastric Cancer Cells.Oncology research · 2019Article
- miR-516a-3p promotes proliferation, migration, and invasion and inhibits apoptosis in lung adenocarcinoma by targeting PTPRD.International journal of clinical and experimental pathology · 2019Article
- Exploration of the diagnostic value and molecular mechanism of miR‑1 in prostate cancer: A study based on meta‑analyses and bioinformatics.Molecular medicine reports · 2018Article
- MicroRNA-32 Regulates Development and Progression of Hepatocellular Carcinoma by Targeting ADAMTS9 and Affects Its Prognosis.Medical science monitor basic research · 2018Article
- Role of MicroRNAs in Treatment Response in Prostate Cancer.Current cancer drug targets · 2018Review
- Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.Oncology reports · 2017Article
- Non-coding RNAs as emerging regulators of epithelial to mesenchymal transition in non-small cell lung cancer.Oncotarget · 2017Review
- Vasculogenic mimicry and expression of Twist1 and KAI1 correlate with metastasis and prognosis in lung squamous cell carcinoma.International journal of clinical and experimental pathology · 2017Article
- Recent progress on the effects of microRNAs and natural products on tumor epithelial-mesenchymal transition.OncoTargets and therapy · 2017Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBy analyzing published microRNA microarray studies, miR-32 was found to be markedly reduced in non-small-cell lung cancer (NSCLC) tissues compared with that in nontumor tissues. However, little is known about its role and molecular mechanism involved in NSCLC development and progression. Here, we report the effect of miR-32 on NSCLC cell proliferation, epithelial-mesenchymal transition (EMT), and metastasis.
methodsQuantitative real-time PCR was performed to detect the expression level of miR-32 in primary NSCLC cases and cell lines. miR-32-overexpressing H1299 and A549 cells were constructed by lipofection transfection. MTT, transwell chamber, and Western blot assays were used to assess the effect of miR-32 on proliferation, EMT, and metastasis of NSCLC cells, respectively. Target prediction and luciferase reporter assays were performed to investigate the targets of miR-32. Tumor formation assay in vivo was performed to investigate the antitumor effect of miR-32.
resultsAn inverse correlation existed between miR-32 expression level and NSCLC cell proliferation, EMT, and metastasis, and upregulation of miR-32 repressed NSCLC cell proliferation, EMT, and metastasis. Moreover, we identified and validated that TWIST1 was a direct target of miR-32, and miR-32 regulated NSCLC cell proliferation, EMT, and metastasis, at least in part via modulation of TWIST1. The animal experiments showed that overexpression of miR-32 inhibited the growth of NSCLC tumors in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.