Conclusion
Our research not only indicated the potential signaling pathway of FKBP14 in colon carcinoma cells but also provided novel insight into the treatment for colon carcinoma.
Methods
In the present study, FKBP14 induced silencing and overexpression in colon carcinoma cells by using RNA interference (RNAi) and lentiviral vector, respectively. A specific JAK/STAT inhibitor AG490 was used to explore the relationship between FKBP14 and STAT3 in colon carcinoma cells. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to examine the level of FKBP14 in colon carcinoma cells. Cell counting kit-8 (CCK-8) assay was used to determine the proliferation rate of colon carcinoma cells. Further, the migration rate of colon carcinoma cells was analyzed by performing a migration assay.
Purpose
FK506-binding proteins 14 (FKBP14), a highly conserved protein, is identified as an oncogene in certain human tumors. However, the detailed biological function of FKBP14 in colon carcinoma remains unclear. The purpose of the present research is to examine the role of FKBP14 in human colon carcinoma cells.
Results
Our results demonstrated that FKBP14 was upregulated in human colon carcinoma tissues. Moreover, high level of FKBP14 was associated with poor prognosis of colon carcinoma patients. Further, our findings firstly elucidated that FKBP14 was a pro-proliferation and migration factor in colon carcinoma cells. More importantly, FKBP14 might be a novel component in IL-6/JAK/STAT3 pathway and targeted STAT3 in colon carcinoma cells.