ArticleOncoTargets and therapy2019
MiR-34c acts as a tumor suppressor in non-small cell lung cancer by inducing endoplasmic reticulum stress through targeting HMGB1.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Endoplasmic reticulum stress-related genes play a role in the prognosis of lung adenocarcinoma.Discover oncology · 2025Article
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- Decoding contextual crosstalk: revealing distinct interactions between non-coding RNAs and unfolded protein response in breast cancer.Cancer cell international · 2024Review
- Starvation insult induces the translocation of high mobility group box 1 to cytosolic compartments in glioma.Oncology reports · 2023Article
- Downregulation of circ-YES1 suppresses NSCLC migration and proliferation through the miR-142-3p-HMGB1 axis.Respiratory research · 2023Article
- Identification of Potential microRNA Panels for Male Non-Small Cell Lung Cancer Identification Using Microarray Datasets and Bioinformatics Methods.Journal of personalized medicine · 2022Article
- MicroRNA-34c-5p provokes isoprenaline-induced cardiac hypertrophy by modulating autophagyActa pharmaceutica Sinica. B · 2022Article
- High Mobility Group Box 1: Biological Functions and Relevance in Oxidative Stress Related Chronic Diseases.Cells · 2022Review
- Up-regulation of LINC00665 contributes to the progression of glioma and correlates with its MRI characteristics.American journal of translational research · 2022Article
- HMGB1 as a therapeutic target in disease.Journal of cellular physiology · 2021Review
- MicroRNA-212-5p and its target PAFAH1B2 suppress vascular proliferation and contraction via the downregulation of RhoA.PloS one · 2021Article
- Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer.Journal of hematology & oncology · 2020Review
- Crosstalk between noncoding RNAs and ferroptosis: new dawn for overcoming cancer progression.Cell death & disease · 2020Review
- MicroRNA-129-5p represses the growth and aggressiveness of oral squamous cell carcinoma via suppressing HMGB1.The Kaohsiung journal of medical sciences · 2020Article
- MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Upregulation of miR-34c after silencing E2F transcription factor 1 inhibits paclitaxel combined with cisplatin resistance in gastric cancer cells.World journal of gastroenterology · 2020Article
- Circ_002117 binds to microRNA-370 and promotes endoplasmic reticulum stress-induced apoptosis in gastric cancer.Cancer cell international · 2020Article
- circGFRA1 Enhances NSCLC Progression by Sponging miR-188-3p.OncoTargets and therapy · 2020Article
- The Expression of miR-34c-5p Induces G0/G1 Cell Cycle Arrest and Apoptosis in SW480 Colon Cancer Cell.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of miR-34c in lung cancer.
methodsThe levels of microRNA-34c (miR-34c) expression in non-small cell lung cancer (NSCLC) tissue and cell lines were examined by the qRT-PCR assay. High mobility group box 1 (HMGB1) expression in NSCLC was assessed by immunohistochemical analysis (IHC), qRT-PCR, and Western blot assays. The effects of miR-34c overexpression or HMGB1 knockdown on cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Cellular reactive oxygen species (ROS) production in NSCLC cells was detected using a ROS kit. The levels of Bax, p-ERK, eIF2α, GADD153, and IRE1α expression in treated NSCLC cells were measured by Western blot assays. In addition, the interaction between miR-34c and HMGB1 was verified by the dual-luciferase reporter assay.
resultsmiR-34c was only slightly expressed, while HMGB1 was highly expressed in NSCLC tissues and cell lines. Overexpression of miR-34c or knockdown of HMGB1 inhibited cell proliferation, promoted cell apoptosis, and induced ER stress in NSCLC cells. In terms of mechanism, miR-34c negatively regulated HMGB1 expression by directly targeting the 3'-untranslated region (UTR) of HMGB1 mRNA. In addition, we proved that HMGB1 overexpression could block the effects of miR-34c on NSCLC cell proliferation, apoptosis, and ER stress.
conclusionmiR-34c may suppress NSCLC tumors by targeting HMGB1 mRNA, promoting endoplasmic reticulum stress, and increasing ROS levels. Our findings suggest that miR-34c has a role in NSCLC.
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