Knockdown of PYCR1 inhibits proliferation, drug resistance and EMT in colorectal cancer cells by regulating STAT3-Mediated p38 MAPK and NF-κB signalling pathway

PYCR1 exerts an important role in various cancers, but its effect on colorectal cancer (CRC) and the potential mechanism remain to be clarified. In this study, we aimed to explore the effect of PYCR1 on CRC and further explore the special molecular mechanism. The expression of PYCR1 in CRC tissues and cells was analysed by RT-PCR assay. Cell proliferation was explored using an MTT assay. A CoIP assay was performed to determine the binding activity of PYCR1 and STAT3. Western blot was used to measure the protein expression of P-gp, MRP1, E-cadherin and vimentin. The results revealed that PYCR1 is highly expressed in CRC tissues and cells. PYCR1-siRNA inhibited the proliferation, drug resistance and epithelial–mesenchymal transition (EMT) of CRC cells. The CoIP assay result demonstrated that PYCR1 interacts directly with STAT3, and STAT3 overexpression partly reverses the effect of PYCR1 on proliferation, drug resistance and EMT of CRC cells. What is more, si-PYCR1 inhibited STAT3-mediated p38 MAPK and NF-κB signalling pathways. Collectively, it suggests that knockdown of PYCR1 inhibits proliferation, drug resistance and EMT potentially by regulating STAT3-mediated p38 MAPK and NF-κB signalling pathways in CRC cells.