ArticleCancer cell international2020
LncRNA HOTAIR induces sunitinib resistance in renal cancer by acting as a competing endogenous RNA to regulate autophagy of renal cells.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Long Non-Coding RNAs in Pathogenesis of Renal Cell Carcinoma: Epigenetic Regulation, Signaling Pathways, and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Short and Long Non-Coding RNAs in Renal Cell Carcinoma.Non-coding RNA · 2026Review
- Plasma exosomal lncRNA SLC16A1-AS1 as an early diagnostic biomarker for renal cell carcinoma.Frontiers in oncology · 2026Article
- The Biological Role and Clinical Significance of BECLIN-1 in Cancer.International journal of molecular sciences · 2025Review
- Crosstalk between noncoding RNAs and autophagy in renal cell carcinoma: Deciphering molecular pathways and therapeutic prospects.Cancer cell international · 2025Review
- POGZ targeted by LINC01355/miR-27b-3p retards thyroid cancer progression via interplaying with MAD2L2.3 Biotech · 2025Article
- Long non‑coding RNA signatures in breast cancer: Properties as biomarkers?Experimental and therapeutic medicine · 2025Article
- MATN1-AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma.Journal of cellular and molecular medicine · 2025Article
- Long noncoding RNAs involved in therapeutic response: implications for cervical cancer drug resistance.Frontiers in oncology · 2025Review
- HOTAIR in cancer: diagnostic, prognostic, and therapeutic perspectives.Cancer cell international · 2024Review
- Review
- The Estrogen-Autophagy Axis: Insights into Cytoprotection and Therapeutic Potential in Cancer and Infection.International journal of molecular sciences · 2024Review
- An oncogenic role of lncRNA SNHG1 promotes ATG7 expression and autophagy involving tumor progression and sunitinib resistance of Renal Cell Carcinoma.Cell death discovery · 2024Article
- A Study on Associations of Long Noncoding RNA HOTAIR Polymorphisms With Genetic Susceptibility to Chronic Kidney Disease.Journal of clinical laboratory analysis · 2024Article
- Long noncoding RNATranslational andrology and urology · 2024Article
- Long non-coding RNAs: regulators of autophagy and potential biomarkers in therapy resistance and urological cancers.Frontiers in pharmacology · 2024Review
- The role of HOTAIR in the modulation of resistance to anticancer therapy.Frontiers in molecular biosciences · 2024Review
- Autophagy-related lncRNAs in tumor progression and drug resistance: A double-edged sword.Genes & diseases · 2024Review
- Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
- Long non-coding RNAs: controversial roles in drug resistance of solid tumors mediated by autophagy.Cancer chemotherapy and pharmacology · 2023Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCell autophagy has been proposed to be involved in drug resistance therapy. However, how the long non-coding RNA (lncRNA) reduces risks of drug resistance in renal cancer (RC) cells needs a thorough inquiry. This study was assigned to probe the effect and mechanism of HOTAIR on sunitinib resistance of RC.
methodsClinical RC tissues and para-carcinoma tissues were obtained to detect the expressions of miR-17-5p, HOTAIR and Beclin1. Sunitinib-resistant cells (786-O-R and ACHN-R) were constructed using parental RC cells (786-O and ACHN). The resistance of 786-O-R and ACHN-R cells to sunitinib was examined. Western blot and qRT-PCR were assayed to obtain the expressions of miR-17-5p, HOTAIR and Beclin1. The effects of HOTAIR knockdown or miR-17-5p overexpression/knockdown on cell autophagy and sunitinib resistance were measured by MDC staining, immunofluorescence and Western blot. The sensitivity of RC cells to sunitinib and change in cell clone formation after sunitinib treatment were assessed by CCK-8 assay and colony formation assay, respectively. The relationships among HOTAIR, miR-17-5p and Beclin1 were verified by dual-luciferase reporter gene and RIP assay. The role of HOTAIR knockdown in sunitinib resistance was verified in nude mice.
resultsHOTAIR expression in sunitinib-resistant cells is higher than that in parental cells. Knockdown of HOTAIR in sunitinib-resistant cells lead to refrained sunitinib resistance and cell autophagy both in vivo and in vitro. Activation of autophagy could raise resistance to sunitinib in RC cells, while inhibition of autophagy could improve the sensitivity of sunitinib-resistant cells to sunitinib. HOTAIR could compete with miR-17-5p to regulate Beclin1 expression. Knockdown of miR-17-5p in parental cells increases cell resistant to sunitinib, and overexpression of miR-17-5p in sunitinib-resistant cells increases cell sensitive to sunitinib.
conclusionHOTAIR negatively targets miR-17-5p to activate Beclin1-mediated cell autophagy, thereby enhancing sunitinib resistance in RC cells.
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