The Promotion Of TF10 On Glucose Metabolism And Proliferation Of Breastcancer Cells

Objective:Glycolysis metabolism reorganization is of great significance to tumorigenesis. The overexpression of TF10 can cause a wide variety of tumorigenesis and promote the transference and metastasis, resulting in poor prognosis. Until now, little is known about the function of TF10 in glucose metabolism. We try to explore the function of TF10 in glucose metabolism and investigate the mechanism of TF10 in regulating glucose metabolism. Then we investigate whether TF10 promotes proliferation of breast cancer cells through glucose metabolism and observe the expression of TF10 in breast cancer patients.Method:1?Explore the function of TF10 in glucose metabolism by the gene chip technology; 2?Investigate the mechanism of TF10 in regulating glucose metabolism through reporter assay?chromatin immunoprecipitation?glycolysis metabolites analysis; 3?Investigate the mechanism of TF10 in promoting breast cancer cell proliferation by cell growth curve; 4?Detect the expression of TF10 in breast cancer patients by immunohistochemistry.Result:1?Gene chip analysis showed that TF10 could promote the glucose metabolism in breast cancer cells; The Real-Time PCR result showed that TF10 promoted transcriptional expression of PFKL?PK10? LDHA; 2?TF10 could promote the activities of PFKL?PKM2? LDHA promoter. CHIP further showed that TF10 could be directly recruited to PFKL?PKM2? LDHA promoter. Besides, TF10 could enhance glucose consumption, pyruvate and lactate production; 3?TF10 overexpression promoted proliferation of breast cancer cells through glucose metabolism, which LDHA is necessary; 4?Immunohistochemistry showed that TF10 was expressed in breast cancer tissues. The expression of TF10 was positively correlated with PKM2 and LDHA in breast cancer patients.Conclusion:Our findings demonstrate a novel function of TF10 in breast cancer glucose metabolism, and a new mechanism of how TF10 promotes breast cancer cell proliferation.