ArticleOncology reports2020
Long noncoding RNA OSER1‑AS1 promotes the malignant properties of non‑small cell lung cancer by sponging microRNA‑433‑3p and thereby increasing Smad2 expression.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Fuelling the Fight from the Gut: Short-Chain Fatty Acids and Dexamethasone Synergise to Suppress Gastric Cancer Cells.Cancers · 2025Article
- Exosome therapeutics for non-small cell lung cancer tumorigenesis.Cancer cell international · 2024Review
- SMAD Proteins in TGF-β Signalling Pathway in Cancer: Regulatory Mechanisms and Clinical Applications.Diagnostics (Basel, Switzerland) · 2023Review
- MALAT1-miRNAs network regulate thymidylate synthase and affect 5FU-based chemotherapy.Molecular medicine (Cambridge, Mass.) · 2022Review
- LncRNA-m18as1 competitively binds with miR-18a-5p to regulate follicle-stimulating hormone secretion through the Smad2/3 pathway in rat primary pituitary cells.Journal of Zhejiang University. Science. B · 2022Article
- CTBP1-AS2 promoted non-small cell lung cancer progression via sponging the miR-623/MMP3 axis.Environmental science and pollution research international · 2022Article
- Regulation of apoptosis, autophagy and ferroptosis by non-coding RNAs in metastatic non-small cell lung cancer (Review).Experimental and therapeutic medicine · 2022Review
- LncRNA OSER1-AS1 regulates the inflammation and apoptosis of rheumatoid arthritis fibroblast like synoviocytes via regulating miR-1298-5p/E2F1 axis.Bioengineered · 2022Article
- CircRNA circ_0008037 facilitates tumor growth and the Warburg effect via upregulating NUCKS1 by binding to miR-433-3p in non-small cell lung cancer.Thoracic cancer · 2022Article
- Circ-MBOAT2 knockdown represses tumor progression and glutamine catabolism by miR-433-3p/GOT1 axis in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2021Article
- Identification of Prognostic Factors Related to Super Enhancer-Regulated ceRNA Network in Metastatic Lung Adenocarcinoma.International journal of general medicine · 2021Article
- Comprehensive analysis of lncRNA biomarkers in kidney renal clear cell carcinoma by lncRNA-mediated ceRNA network.PloS one · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OSER1 antisense RNA 1 (OSER1‑AS1), a long noncoding RNA, has been well studied in the context of hepatocellular carcinoma. However, its expression status, specific functions, and tumorigenic mechanism in non‑small cell lung cancer (NSCLC) remain uninvestigated. Hence, this study aimed to assess OSER1‑AS1 expression, test the malignancy‑related biological functions of OSER1‑AS1, and illustrate how they affect NSCLC progression. OSER1‑AS1 expression in NSCLC was measured by reverse transcription‑quantitative polymerase chain reaction. Cell Counting Kit‑8 assay, flow cytometry, cell migration and invasion assay, and tumor xenograft assay were performed to analyze the effects of OSER1‑AS1 on the malignant phenotypes of NSCLC cells. Bioinformatics prediction with luciferase reporter and RNA immunoprecipitation assays were performed to determine the interaction between OSER1‑AS1 and microRNA‑433‑3p (miR‑433‑3p). OSER1‑AS1 was strongly expressed in NSCLC tissues and cell lines. Enhanced OSER1‑AS1 expression was significantly correlated with tumor size, TNM stage, and lymph node metastasis in patients with NSCLC. Patients with NSCLC exhibiting high OSER1‑AS1 expression had shorter overall survival than those exhibiting low OSER1‑AS1 expression. Functionally, a reduction in OSER1‑AS1 expression led to significant decreases in NSCLC cell proliferation, migration, and invasion as well as an increase in cell apoptosis in vivo. OSER1‑AS1 knockdown suppressed the tumorigenic ability of NSCLC cells in vivo. Mechanistically, OSER1‑AS1 acts as a competing endogenous RNA (ceRNA) in NSCLC cells by sponging miR‑433‑3p and thereby increasing the expression of mothers against decapentaplegic homolog 2 (Smad2). Finally, restoration experiments revealed that the suppression of miR‑433‑3p and restoration of Smad2 both counteracted the suppressive effects of OSER1‑AS1 depletion in NSCLC cells. Our findings illustrate the biological importance of the OSER1‑AS1/miR‑433‑3p/Smad2 pathway in NSCLC progression and offer a novel perspective regarding the identification of effective therapeutic and diagnostic targets.
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