Cell Death Dis:FXR plays a carcinogenic role in colorectal tumors by antagoning the Wnt/beta-catenin signal.

Colorectal cancer (CRC) is the second leading cause of cancer-related deaths, with approximately 1,800,000 new cases diagnosed with CRC each year worldwide.
although great progress has been made in the treatment of CRC, the prognostication of the disease is not satisfactory due to the metastasis and recurrence of tumors in patients with advanced CRC.
more and more studies have shown that the molecular pathogenesis of CRC is a multi-step and continuous process, it is important to explore the precise mechanisms of the development of colorectal cancer to develop better treatment strategies.
previous studies have found that bile acid is widely involved in the pathogenesis of malignant tumors, including liver cell carcinoma, stomach cancer, esophageal cancer and pancreatic cancer.
levels of bile acid in the feces were associated with the development of colorectal cancer.
FXR (Faniol X-perceptor, encoded by NR1H4) as a nucleic subject of bile acid, is a key regulatory factor for the steady state of bile acid, and there is growing evidence that FXR plays a key role in the development of human tumors.
the function and exact molecular mechanism of FXR in CRC still need to be further studied.
study, we looked at the correlation between FXR and Wnt/beta-catenin signal transductivity paths during the development of colorectal cancer.
researchers found that FXR expression levels were lowered in colorectal cancer tissue, corresponding to poor prognostication in patients.
in-body inhibition of FXR expression level can promote the growth and invasion of colorectal cancer cells, while endogenous inhibition of expression can promote the formation and metastasis of transplant tumors, while FXR's heterogeneous expression presents the opposite esophysic.
the study showed that FXR was able to act as a tumor suppressor by antagoning the Wnt/beta-catenin signal transducting path.
in addition, the researchers confirmed the interaction of FXR/beta-catenin in colorectal cancer cells, which weakens the formation of the beta-catenin/TCF4 complex.
, the researchers found that the absence of beta-catenin increased FXR's transcriptional activation of SHP.
, the above results show that in colorectal cancer FXR can play its tumor suppression role through an antagonists of the Wnt/beta-catenin signal transduction path.
.