ArticleOncotarget2016
Decreased expression of microRNA-320a promotes proliferation and invasion of non-small cell lung cancer cells by increasing VDAC1 expression.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
- The AGO2 adaptor LIMD1 expands the functional and evolutionary reach of microRNA targeting.Science advances · 2026Article
- Combined single-cell transcriptome and Mendelian randomization to identify and validate prognostic genes associated with endoplasmic reticulum stress and butyrate metabolism in lung adenocarcinoma.Frontiers in genetics · 2026Article
- CircZNF609/miR-324-5p/voltage-dependent anion channel 1 axis promotes malignant progression of ovarian cancer cells.iScience · 2024Article
- Gene signatures of endoplasmic reticulum stress and mitophagy for prognostic risk prediction in lung adenocarcinoma.IET systems biology · 2024Article
- The expression ofFrontiers in endocrinology · 2024Article
- The Growth of A549 Cell Line is Inhibited by Pemetrexed Through Up-regulation of hsa-MiR-320a Expression.Advanced biomedical research · 2024Article
- The Effect of MiR320a on Lung Cancer.MicroRNA (Shariqah, United Arab Emirates) · 2024Review
- A novel necroptosis related gene signature and regulatory network for overall survival prediction in lung adenocarcinoma.Scientific reports · 2023Article
- Integrative analysis of the prognostic value and immune microenvironment of mitophagy-related signature for multiple myeloma.BMC cancer · 2023Article
- Voltage-Dependent Anion Channel 1 Expression in Oral Malignant and Premalignant Lesions.Diagnostics (Basel, Switzerland) · 2023Article
- MicroRNAs as Regulators of Cancer Cell Energy Metabolism.Journal of personalized medicine · 2022Review
- Development and validation of endoplasmic reticulum stress-related eight-gene signature for predicting the overall survival of lung adenocarcinoma.Translational cancer research · 2022Article
- Overexpressed VDAC1 in breast cancer as a novel prognostic biomarker and correlates with immune infiltrates.World journal of surgical oncology · 2022Article
- Pan-Cancer Analysis of Voltage-Dependent Anion Channel (VDAC1) as a Cancer Therapeutic Target or Diagnostic Biomarker.Disease markers · 2022Article
- VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases.Biomolecules · 2020Review
- P53-regulated miR-320a targets PDL1 and is downregulated in malignant mesothelioma.Cell death & disease · 2020Article
- Decreased serum exosomal miR-320a expression is an unfavorable prognostic factor in patients with hepatocellular carcinoma.The Journal of international medical research · 2020Article
- MicroRNA-320a suppresses tumor progression by targeting PBX3 in gastric cancer and is downregulated by DNA methylation.World journal of gastrointestinal oncology · 2019Article
- VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer.Oncology letters · 2019Article
- Circulating mir-320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk.International journal of cancer · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates that Voltage Dependent Anion Channel 1 (VDAC1) correlates with the initiation and progression of non-small cell lung cancer (NSCLC). However, the regulatory mechanism of VDAC1 in NSCLC remains unclear. Previous studies have reported that expression of miR-320a was decreased in human primary squamous cell lung carcinoma, which prompted us to investigate whether there is a functional link between decreased miR-320a and a high expression of VDAC1. In the present report, using computational analysis, we first show that miR-320a has a potential binding site on VDAC1 mRNA, and expression of miR-320a was decreased in NSCLC cell lines. Using gain-of-function and rescue experiments, we demonstrate that VDAC1 is a direct target of miR-320a in NSCLC cells, and miR-320a inhibits VDAC1 expression in NSCLC cells. Further we show that MiR-320a was significantly decreased in NSCLC tissues compared with adjacent non-tumor tissues, and MiR-320a level is negatively correlated with VDAC1 in NSCLC tissues by Pearson's correlation coefficient analysis. Moreover, using cellular ATP assay, we found that suppression of VDAC1 expression may inhibit cell proliferation and invasion of NSCLC by decreasing cell energy and metabolism. Importantly, we showed that ectopic overexpression of miR-320a blocked tumor cell proliferation and invasion, both in vitro and in vivo, through inhibiting VDAC1. Our results suggest that reduced expression of miR-320a facilitates the development of NSCLCs by increasing VDAC1 expression. We identified a novel regulatory mechanism between miR-320a and VDAC1, and miR-320a may serve as a tumor suppressor gene and a promising therapeutic target of NSCLCs.
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