ArticleCancer cell international2020
LINC00689 promotes prostate cancer progression via regulating miR-496/CTNNB1 to activate Wnt pathway.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Investigating the expression of CTLA-4 and CD28 genes as immune regulators in patients with colorectal polyps.BMC cancer · 2026Article
- Iroquois homeobox 4 (IRX4) derived micropeptide promotes prostate cancer progression and chemoresistance through Wnt signalling dysregulation.Communications medicine · 2024Article
- Long noncoding RNA mediates enzalutamide resistance and transformation in neuroendocrine prostate cancer.Frontiers in oncology · 2024Review
- SNHG1 functions as a ceRNA in hypertrophic scar fibroblast proliferation and apoptosis through miR-320b/CTNNB1 axis.Archives of dermatological research · 2023Article
- Importance of long non-coding RNAs in the pathogenesis, diagnosis, and treatment of prostate cancer.Frontiers in oncology · 2023Review
- Unlocking the role of non-coding RNAs in prostate cancer progression: exploring the interplay with the Wnt signaling pathway.Frontiers in pharmacology · 2023Review
- Sequence complementarity between human noncoding RNAs and SARS-CoV-2 genes: What are the implications for human health?Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Prognostic Value of miR-1826 in Prostate Cancer and Its Regulatory Effect on Tumor Progression.OncoTargets and therapy · 2021Article
- NNT-AS1 modulates prostate cancer cell proliferation, apoptosis and migration through miR-496/DDIT4 axis.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulating evidence has proved the significant influence of long non-coding RNAs (lncRNAs) in cancer formation and development, including PCa.
methodsThe role of LINC00689 in PCa was confirmed by RT-qPCR, MTT, colony formation, flow cytometry, western blot and transwell assays. Besides, the binding ability between LINC00689 and miR-496 was validated by using luciferase reporter assay. Then RT-qPCR, RIP and luciferase reporter and western blot assays were employed to verify the interactions among LINC00689, miR-496 and CTNNB1. Furthermore, the rescuing role of CTNNB1 in Wnt pathway was proved by RT-qPCR, TOP/FOP Flash and western blot assays.
resultsLINC00689 was upregulated in PCa tissues and cells as well as at the terminal stage. Further, knock down of LINC00689 repressed PCa cell proliferation, migration and invasion, and initiated PCa cell apoptosis. Additionally, miR-496 inhibitor and pcDNA3.1/CTNNB1 could neutralize the prohibitive effects of LINC00689 silencing on cell proliferation, migration and invasion, meanwhile, could offset the encouraging role of knocking down LINC00689 in cell apoptosis. Moreover, CTNNB1 upregulation exerted redemptive function in Wnt pathway inhibited by LINC00689 depletion.
conclusionsTo sum up, LINC00689 promotes PCa progression via regulating miR-496/CTNNB1 to activate Wnt pathway, which may contribute to research about new targets for PCa treatment.
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