ArticleAging2023
LncRNA LINC00667 gets involved in clear cell renal cell carcinoma development and chemoresistance by regulating the miR-143-3p/ZEB1 axis.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Long non-coding RNA (lncRNA) XIST drives TGF-β-induced renal cancer progression via miR-141-3p/ZEB1 signaling.Translational andrology and urology · 2026Article
- Long Non-Coding RNAs in Pathogenesis of Renal Cell Carcinoma: Epigenetic Regulation, Signaling Pathways, and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- FOXP3-activated KCNMB2-AS1 promotes clear cell renal cell carcinoma through the miR-744-3p/CD1D axis.Cell division · 2025Article
- LINC00332 as a potential diagnostic marker for the low-grade tumors in renal cell carcinoma patients.BMC urology · 2025Article
- Mitochondrial ribosomal protein L12 mediates metabolic reorganization in clear cell renal cell carcinoma by regulating mitochondrial biosynthesis.Cell communication and signaling : CCS · 2025Article
- Review
- Biological functions and potential mechanisms of miR‑143‑3p in cancers (Review).Oncology reports · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundClear cell renal cell carcinoma (ccRCC) is identified as a malignant tumor in the urinary tract. The research was an attempt to probe the biological function and molecular mechanism of lncRNA LINC00667 in ccRCC development.
methodsqRT-PCR monitored LINC00667, miR-143-3p, and ZEB1 levels. The models of LINC00667, miR-143-3p, and ZEB1 overexpression or knockdown were constructed in ccRCC cells. Cell proliferation, apoptosis, migration, and invasion of the cells were detected. The levels of apoptosis-associated proteins and epithelial-mesenchymal transition (EMT)-related proteins, and ZEB1 were detected by WB. Dual-luciferase reporter assay and RNA pull-down assay identified the binding association between LINC00667 and miR-143-3p, miR-143-3p and ZEB1. Moreover, a xenograft tumor model in nude mice was used for evaluating tumor growth
resultsLINC00667 and ZEB1 displayed high expression in ccRCC tissues and cells. miR-143-3p was lowly expressed in ccRCC tissues and cells. LINC00667 targeted and repressed miR-143-3p, which inhibited ZEB1 expression in a targeted manner. Overexpression of LINC00667 facilitated ccRCC cell proliferation, migration, invasion and EMT and retarded apoptosis, whereas LINC00667 knockdown or miR-143-3p overexpression exerted reverse effects. The rescue experiments indicated that overexpressing miR-143-3p dampened LINC00667-mediated oncogenic effects. Overexpressing ZEB1 diminished miR-143-3p-mediated tumor-suppressive effects.
conclusionsLINC00667 is up-regulated in ccRCC and enhances the ZEB1 expression by targeting miR-143-3p, which in turn accelerates ccRCC progression and induces chemoresistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.