ArticleMolecular medicine reports2021
LncRNA LINC00963 promotes colorectal cancer cell proliferation and metastasis by regulating miR‑1281 and TRIM65.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025Review
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Dysregulated miRNA Expression and Androgen Receptor Loss in Racially Distinct Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- lncRNA TRPM2-AS Promotes Colorectal Cancer Progression by Regulating miR-22-3p and FSTL1.Journal of oncology · 2022Article
- Depletion of Fibroblast Growth Factor 12 Restrains the Viability, Stemness, and Motility of Colorectal Cancer.BioMed research international · 2022Article
- Multidimension Analysis of the Prognostic Value, Immune Regulatory Function, and ceRNA Network of LY6E in Individuals with Colorectal Cancer.Journal of immunology research · 2022Article
- Insights into the Role of Matrix Metalloproteinases in Precancerous Conditions and in Colorectal Cancer.Cancers · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reportedly, long‑chain non‑coding RNA LINC00963 features prominently in cancer biology. However, functional details of LINC00963 in colorectal cancer (CRC) remain to be elucidated. Reverse transcription‑quantitative (RT‑q)PCR was performed to examine LINC00963 and microRNA (miR)‑1281 expression levels in 53 matched pairs of cancerous and non‑cancerous tissues from patients with CRC. Tripartite motif‑containing 65 (TRIM65) protein expression in CRC cells was detected via western blot analysis. Furthermore, LINC00963 overexpression plasmid, LINC00963 small interfering RNA, miR‑1281 mimics or miR‑1281 inhibitors were transfected into CRC cells, and Cell Counting Kit‑8, colony formation and Transwell assays were adopted to study the effects of LINC00963 and miR‑1281 on the malignant phenotypes of CRC cells. Bioinformatics analysis, dual‑luciferase, RNA pull‑down and immunoprecipitation assays, RT‑qPCR and western blot analysis were performed to investigate the regulatory relationship between LINC00963, miR‑1281 and TRIM65. LINC00963 was highly expressed in CRC tissues and cells, while miR‑1281 was downregulated. Functionally, LINC00963 facilitated the proliferation, colony formation, migration and invasion of CRC cells, and increased the expression levels of Ki67, matrix metalloproteinase (MMP)2 and MMP9, while miR‑1281 had the opposite biological functions. Mechanistically, LINC00963 sponged miR‑1281 and repressed its expression in CRC cells, resulting in the upregulation of TRIM65. LINC00963 positively regulates TRIM65 in CRC progression by repressing miR‑1281 expression, showing potential as a therapeutic target for treating CRC.
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