ArticleApplied biochemistry and biotechnology2022
LncRNA LINC00665 Promotes Ovarian Cancer Cell Proliferation and Inhibits Apoptosis via Targeting miR-181a-5p/FHDC.
Article in Applied biochemistry and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- miR-423-5p mediates LINC00886 regulation of ovarian cancer aggressiveness and immune evasion via the TLR4/Myd88/NF-κB/PD-L1 pathway.Hereditas · 2025Article
- Article
- Pathologic and genomic characteristics of myoepithelioma-like tumor of the vulvar region: three case reports.Diagnostic pathology · 2025Article
- Mechanisms of apoptosis-related non-coding RNAs in ovarian cancer: a narrative review.Apoptosis : an international journal on programmed cell death · 2025Review
- Long Non-Coding RNAs in Ovarian Cancer: Mechanistic Insights and Clinical Applications.Cancers · 2025Review
- Article
- TRPM2-AS promotes ovarian cancer cell proliferation and inhibits cell apoptosis by upregulating the nearby gene TRPM2 via miR-6764-5p.Cell division · 2024Article
- STAU1-mediated CNBP mRNA degradation by LINC00665 alters stem cell characteristics in ovarian cancer.Biology direct · 2024Article
- Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.Non-coding RNA research · 2024Review
- ncRNA-mediated low expression of P2RY14 correlates with poor prognosis and tumor immune infiltration in ovarian carcinoma.Annals of translational medicine · 2023Article
- Long noncoding RNA LINC00665 is a diagnostic biomarker that enhances cell proliferation and migration in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous reports indicate that long intergenic non-coding RNA LINC00665 naturally occurred vital effects in various cancers. Herein, the role of LINC00665 in ovarian cancer progress was explored. We found that LINC00665 was upregulated in ovarian cancer cell lines. Besides, a series of assays including flow cytometry, wound-healing, transwell, cell counting Kit-8 (CCK-8), and EdU assay confirmed that the knockdown of LINC00665 could reduce the viability, proliferation, and migration of SKOV-3 and OVCAR-3 cells. Accumulating evidence indicates that many lncRNAs can function as endogenous miRNA sponges by competitively binding common miRNAs. In this study, the bioinformatics analysis suggests that LNC00665 specifically binds to miR-181a-5p. LINC00665 downregulated the miR-181a-5p in SKOV-3 and OVCAR-3 cells. The knockdown of miR-181a-5p evidently reverses the inhibitory effect of sh-LINC00662. Besides, FH2 domain containing 1 (FHDC1) has been proved to deed as an effective target of miR-181a-5p. The results reveal the knockdown of LINC00665 facilitates ovarian cancer via development by sponging miR-181a-5p and up-regulating FHDC1 expression. These may contribute to ovarian cancer therapy.
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