Br J Cancer: CDX2 regulates the expression of Snail and the stability β-catenin to inhibit the invasion and metastasis of colorectal cancer

Colorectal cancer (CRC) is the second most common cause of cancer-related deaths, with approximately 1,800,000 new cases diagnosed with CRC each year worldwide.
that although significant progress has been made in early detection and comprehensive treatment of CRC, the prognostication of most patients with late CRC is still poor.
metastasis and recurrence of cancer remain the main causes of death in CRC patients.
more and more emerging studies have confirmed that multiple genes and cell paths are involved in the development and metastasis of CRC tumors.
therefore, clarifying potential molecular mechanisms may provide CRC patients with effective treatment strategies to improve prognostication.
Previous studies have shown that CDX2 is involved in the development of various cancers and plays a vital role in the invasion and metastasis of cancer, but the role of CDX2 in the CRC endosthast-interstital transformation (EMT) process is still unknown.
mechanism diagram The study aims to reveal the role of CDX2 in CRC invasion and metastasis through immunosociative chemical analysis and a series of internal and external source experiments.
researchers found that the level of CDX2 expression in CRC tissue decreased, while the decrease in CDX2 corresponded to a patient's poor prognostic.
low CDX2 can promote the invasion of colon cancer cells and promote liver metastasis of cancer by inducing the EMT process.
further studies of the expression of CDX2 in CRC tissues and normal tissues have shown that CDX2 reduces Snail expression, β-catenin stabilization, and nuclear transport by inhibiting phosphorylation of Akt and GSK-3 beta.
knock β-catenin is able to medium and knock down the regulatory effect of CDX2 on Slug and ZEB1.
mechanism studies have shown that CDX2 can bind directly to the promoter of PTEN and activate its expression by regulating the expression of PTEN to antagonate the PI3K/Akt activity in CRC.
, the study found for the first time that CDX2 can regulate the stability of β-catenin by regulating the expression of Snail and by activating the expression of PTEN in reverse, ultimately inhibiting the transfer of EMT processes and CRC.
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