ArticleCell cycle (Georgetown, Tex.)2022
LINC01615 activates ZEB2 through competitively binding with miR-3653-3p to promote the carcinogenesis of colon cancer cells.
Article in Cell cycle (Georgetown, Tex.), 2022. 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, 14 citations in OpenAlex.
- YY1-mediated transcriptional regulation of LINC01615 inhibits WNT2 mRNA degradation to promote gastric cancer progression.Scientific reports · 2025Article
- Identification of progression related LncRNAs in colorectal cancer aggressiveness.Scientific reports · 2025Article
- Cancer-Derived Exosomal LINC01615 Induces M2 Polarization of Tumor-Associated Macrophages via RBMX-EZH2 Axis to Promote Colorectal Cancer Progression.International journal of nanomedicine · 2025Article
- Precision Nanomedicine: Lapatinib-Loaded Chitosan-Gold Nanoparticles Targeting LINC01615 for Lung Cancer Therapy.The AAPS journal · 2024Article
- Functional identification of cis-regulatory long noncoding RNAs at controlled false discovery rates.Nucleic acids research · 2024Article
- Construction of an EMT-related lncRNA prognostic signature for lung adenocarcinoma and functional verification of its hub gene LINC01615.Journal of cancer research and clinical oncology · 2023Article
- Hsa_circ_0017956 Acts as miR-758-3p Sponge to Facilitate the Progression of Non-small-Cell Lung Cancer by Regulating FOXP4 Expression.Molecular biotechnology · 2023Article
- Article
- Comprehensive Analysis of LINC01615 in Head and Neck Squamous Cell Carcinoma: A Hub Biomarker Identified by Machine Learning and Experimental Validation.Journal of oncology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a newly discovered cancer-related molecule, we explored the unreported mechanism of LINC01615 intervention in colon cancer.LINC01615 expression in clinical samples and cells were detected. Effects of LINC01615 silencing/overexpression on the malignant development of colon cancer cells were analyzed through cell function experiments. Changes at the level of molecular biology were detected by quantitative real-time polymerase chain reaction and Western blot. Bioinformatics analysis and dual luciferase reporter assay were involved in the display and verification of targeted binding sequences. The rescue tests and correlation analysis examined the relationship among LINC01615, miR-3653-3p and zinc finger E-box binding homeobox 2 (ZEB2) in colon cancer cells. The xenograft experiment and immunohistochemistry were performed to verify these results.TCGA suggested that LINC01615 was high-expressed in colon cancer, as verified in clinical and cell samples, and patients with LINC01615 overexpression suffered from a poor prognosis. Silent LINC01615 blocked the malignant development of colon cancer cells through regulating related genes expressions, while overexpressed LINC01615 had the opposite effect. LINC01615, which was targeted by miR-3653-3p, partially offset the inhibitory effect of miR-3653-3p on colon cancer cells. The downstream target gene ZEB2 of miR-3653-3p was high-expressed in colon cancer. MiR-3653-3p was negatively correlated with LINC01615 or ZEB2, while LINC01615 was positively correlated with ZEB2. Therefore, LINC01615 induced ZEB2 up-regulation, while miR-3653-3p reduced ZEB2 level. The results of
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