ArticleInternational journal of molecular sciences2024
LINC00662 Promotes Aggressive Traits by Modulating OCT4 Expression through miR-335-5p in Gallbladder Cancer Cells.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- LINC01770 Is Associated with Stem-like Features and Aggressive Traits in Breast Cancer Cells Through a Putative miR-335-5p/OCT4 Axis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Prognostic value of Linc00662/miR-16-5p/FASN in cervical cancer and regulation of tumor progression.Hereditas · 2025Article
- Molecular Mechanisms of Lymph Node Metastasis in Gallbladder Cancer: Insights into the Tumor Microenvironment.Biomedicines · 2025Review
- Connexin46 in the nucleus of cancer cells: a possible role as transcription modulator.Cell communication and signaling : CCS · 2025Article
- Molecular Interplay Between Non-Coding RNAs and Connexins and Its Possible Role in Cancer.International journal of molecular sciences · 2025Review
- Development of a senescence-related lncRNA signature in endometrial cancer based on multiple machine learning models.Frontiers in genetics · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Long non-coding RNAs (lncRNAs) are nucleotide sequences that participate in different biological processes and are associated with different pathologies, including cancer. Long intergenic non-protein-coding RNA 662 (LINC00662) has been reported to be involved in different cancers, including colorectal, prostate, and breast cancer. However, its role in gallbladder cancer has not yet been described. In this article, we hypothesize that LINC00662 has an important role in the acquisition of aggressiveness traits such as a stem-like phenotype, invasion, and chemoresistance in gallbladder cancer. Here, we show that LINC00662 is associated with larger tumor size and lymph node metastasis in patients with gallbladder cancer. Furthermore, we show that the overexpression of LINC00662 promotes an increase in CD133
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