Tubulin alpha 1c promotes aerobic glycolysis and cell growth through upregulation of yes association protein expression in breast cancer.

Abstract

Tubulin alpha 1c (TUBA1C) as a member of α-tubulin was identified to take part in the occurrence and development of hepatocellular carcinoma and pancreatic cancer. Using the bioinformatics, we noticed that TUBA1C level was also increased in breast cancer was also demonstrated. Here, we explored TUBA1 role in modulation of breast cancer cell aerobic glycolysis, growth and migration and explored whether yes association protein (YAP) was involved. Fifty-five matched breast cancer tissues and the para-carcinoma normal tissues were included in this study and used to verify TUBA1C expression using quantitative reverse transcription-PCR and western blotting. ATP level, lactate secretion and glucose consumption were used to assess aerobic glycolysis. Cell growth, invasion, migration and tumorigenesis were detected using cell count kit-8, transwell, wound healing and animal assays. TUBA1 was upregulated in breast cancer, which associated with advanced primary tumor, lymph node, metastasis stage and tumor size. Silencing of TUBA1C with sh-TUBA1C infection led to significant inhibitions in ATP level, lactate secretion, glucose consumption, cell growth, migration, invasion and tumorigenesis, as well as declined YAP expression, while TUBA1C overexpression induced a opposite result. And, the above tendencies induced by TUBA1C downregulation were reversed by YAP overexpression. This study revealed that TUBA1C was overexpressed in breast cancer and promoted aerobic glycolysis and cell growth through upregulation of YAP expression.