Détail du document
Identifiant
doi:10.1038/s42003-023-05757-3...
Auteur
Cao, Yan Li, Jian Zhang, Gang Fang, Hao Du, Yongliang Liang, YanLangue
enEditeur
Nature
Catégorie
Life Sciences
Année
2024
Date de référencement
31/01/2024
Mots clés
colorectal ptbp1 cancer klf15Résumé
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.
KLF15 transcriptionally activates LINC00689 , leading to the stabilization of LATS2 mRNA by recruiting PTBP1, which in turn suppresses colorectal tumorigenesis by inhibiting oncogenes like YAP1 and β-catenin.
Cao, Yan,Li, Jian,Zhang, Gang,Fang, Hao,Du, Yongliang,Liang, Yan, 2024, KLF15 transcriptionally activates LINC00689 to inhibit colorectal cancer development, Nature
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