ArticleCommunications biology2024
KLF15 transcriptionally activates LINC00689 to inhibit colorectal cancer development.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Targeting WWP1 ameliorates osteoarthritis by suppressing KLF15 ubiquitination to restore mtDNA and mitochondrial function.Molecular genetics and genomics : MGG · 2026Article
- Retraction Note: circGIGYF1 inhibits stemness and metastasis in colorectal cancer by promoting WWP2-HOXD13 interaction to regulate β-catenin signalling.Communications biology · 2026Article
- The current and future landscape of RNA-based therapies and diagnostics.Communications medicine · 2025Article
- KLF1 Promotes Non-Small Cell Lung Cancer Cell Proliferation and Invasion by Upregulating the LINC02159/DYNC1H1 Pathway.The Kaohsiung journal of medical sciences · 2025Article
- From Transcription Factors Dysregulation to Malignancy: In Silico Reconstruction of Cancer's Foundational Drivers-The Eternity Triangle.International journal of molecular sciences · 2025Article
- reDA: differential abundance testing on scATAC-seq data using random walk with restart.Bioinformatics (Oxford, England) · 2025Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer is a grievous health concern, we have proved long non-coding RNA LINC00689 is considered as a potential diagnosis biomarker for colorectal cancer, and it is necessary to further investigate its upstream and downstream mechanisms. Here, we show that KLF15, a transcription factor, exhibits the reduced expression in colorectal cancer. KLF15 suppresses the proliferative and metastatic capacities of colorectal cancer cells both in vitro and in vivo by transcriptionally activating LINC00689. Subsequently, LINC00689 recruits PTBP1 protein to enhance the stability of LATS2 mRNA in the cytoplasm. This stabilization causes the suppression of the YAP1/β-catenin pathway and its target downstream genes. Our findings highlight a regulatory network involving KLF15, LINC00689, PTBP1, LATS2, and the YAP1/β-catenin pathway in colorectal cancer, shedding light on potential therapeutic targets for colorectal cancer therapy.
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Registered trials
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