ArticleCell death discovery2021
LncRNA LINC00667 aggravates the progression of hepatocellular carcinoma by regulating androgen receptor expression as a miRNA-130a-3p sponge.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Pharmacological targeting of HDAC/BET pathway enhances 5-FU efficacy in esophageal squamous cancer cells.Archives of pharmacal research · 2025Article
- LincRNA-miR interactions in hepatocellular carcinoma: comprehensive review and in silico analysis: a step toward ncRNA precision.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hepatocellular Carcinoma: A Comprehensive Review.Diseases (Basel, Switzerland) · 2025Review
- A novel miRNA-based model for predicting the 3-year recurrence risk of hepatocellular carcinoma following liver transplantation.Journal of gastrointestinal oncology · 2025Article
- Mechanism and implications of advanced glycation end products (AGE) and its receptor RAGE axis as crucial mediators linking inflammation and obesity.Molecular biology reports · 2025Review
- LINC00667: A Novel Vital Oncogenic LincRNA.Current medicinal chemistry · 2025Review
- Crosstalk between RNA-binding proteins and non-coding RNAs in tumors: molecular mechanisms, and clinical significance.International journal of biological sciences · 2025Review
- MicroRNAs in Hepatocellular Carcinoma Pathogenesis: Insights into Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Prognostic significance of CHCHD2P9 and ZNF204P in breast cancer: exploring their expression patterns and associations with malignancy-related genes.Molecular biology reports · 2024Article
- Long Intergenic Non-Coding RNAs of Human Chromosome 18: Focus on Cancers.Biomedicines · 2024Review
- ZMIZ2 facilitates hepatocellular carcinoma progression via LEF1 mediated activation of Wnt/β-catenin pathway.Experimental hematology & oncology · 2024Article
- Article
- Endocrine nuclear receptors and long non‑coding RNAs reciprocal regulation in cancer (Review).International journal of oncology · 2024Review
- LINC01133 can induce acquired ferroptosis resistance by enhancing the FSP1 mRNA stability through forming the LINC01133-FUS-FSP1 complex.Cell death & disease · 2023Article
- MiRNAs in Alcohol-Related Liver Diseases and Hepatocellular Carcinoma: A Step toward New Therapeutic Approaches?Cancers · 2023Review
- Article
- Integrative Analysis Revealed LINC00847 as a Potential Target of Tumor Immunotherapy.Applied biochemistry and biotechnology · 2023Article
- MicroRNA based combinatorial therapy against TKIs resistant CML by inactivating the PI3K/Akt/mTOR pathway: a review.Medical oncology (Northwood, London, England) · 2023Review
- Docetaxel-resistant triple-negative breast cancer cell-derived exosomal lncRNA LINC00667 reduces the chemosensitivity of breast cancer cells to docetaxel <em>via</em> targeting miR-200b-3p/Bcl-2 axis.European journal of histochemistry : EJH · 2022Article
- Article
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10 authors.
Funding
Abstract
Emerging studies have found long noncoding RNAs, widely expressed in eukaryotes, crucial regulators in the progression of human cancers, including hepatocellular carcinoma (HCC). Although the long intergenic noncoding RNA 667 (LINC00667) can promote the progression of a variety of cancer types, the expression pattern, the role in cancer progression, and the molecular mechanism involved in HCC remain unclear. This study aims to investigate the function and mechanism of LINC00667 in HCC progression. The effects of LINC00667 silencing in cell proliferation, cell migration, and cell invasion, and androgen receptor (AR) expression were determined with loss-of-function phenotypic analysis in Huh-7 and HCCLM3 cells, and subsequently testified in vivo in tumor growth. We found that the expression of LINC00667 was upregulated in HCC tissues and cell lines. Upregulation of LINC00667 was significantly associated with the unfavorable prognosis of HCC in our study patients. On the other hand, low expression of LINC00667 significantly inhibited the cell proliferation, cell migration and cell invasion of HCC in vitro and tumor growth in vivo. This inhibitory effect could be counteracted by miR-130a-3p inhibitor. LINC00667 reduced the inhibition of AR expression by miR-130a-3p, which correlated with the progression of HCC. Our finding suggests LINC00667 is a molecular sponge in the miR-130s-3p/AR signal pathway in the progression of HCC, in which it relieves the repressive function of miR-130a-3p on the AR expression. This indicates LINC00667 functions as a tumor promotor in promoting HCC progression through targeting miR-130a-3p/AR axis, making a novel biomarker and potential therapeutic target for HCC.
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