ArticleCancer cell international2022
LINC00665 up-regulates SIN3A expression to modulate the progression of colorectal cancer via sponging miR-138-5p.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Prognostic and clinicopathological values of LINC00665 in cancers: a systematic review and China population-based meta-analysis.Clinical and experimental medicine · 2023Pooled it
- Article
- Transcriptome-proteome integration analysis identifies elevated expression of LARP7 promoting the tumorigenesis and development of gastrointestinal stromal tumors.Translational oncology · 2025Article
- Prognostic markers and molecular pathways in primary colorectal cancer with a high potential of liver metastases: a systems biology approach.Research in pharmaceutical sciences · 2025Article
- Identification of miR-20a as a Diagnostic and Prognostic Biomarker in Colorectal Cancer: MicroRNA Sequencing and Machine Learning Analysis.MicroRNA (Shariqah, United Arab Emirates) · 2025Article
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
- 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 2 institutions in 1 country.
Funding
Abstract
backgroundColorectal cancer (CRC) is a malignant tumor affecting people worldwide. Long noncoding RNAs (lncRNAs) is a crucial factor modulating various cancer progression, including CRC. Long intergenic non-protein coding RNA 665 (LINC00665) has been proven as an oncogene in several cancers, but its function in CRC is still unclear.
methodsQRT-PCR was performed for RNA quantification. Functional assays were designed and carried to test cell phenotype while mechanism experiments were adopted for detecting the interaction of LINC00665, microRNA-138-5p (miR-138-5p) and SIN3 transcription regulator family member A (SIN3A). In vivo experiments were conducted to test LINC00665 function on modulating CRC tumor progression.
resultsLINC00665 displayed high expression in CRC tissues and cells, and promoted tumor progression in vivo. MiR-138-5p displayed abnormally low expression in CRC, and was verified to be sponged by LINC00665. Furthermore, SIN3A, as the downstream mRNA of miR-138-5p, exerted promoting impacts on CRC cells. Rescue experiments certified that overexpressed SIN3A or silenced miR-138-5p could offset the repressed function of LINC00665 knockdown on CRC progression.
conclusionsLINC00665 could sponge miR-138-5p to up-regulate SIN3A expression, thus accelerating CRC progression.
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