KLF15 transcriptionally activates LINC00689 to inhibit colorectal cancer development

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.