HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway.

Abstract

Cervical cancer (CC) is one of the most common malignancy and is the second leading cause of death in gynecologic malignancies worldwide. The homeobox transcription factor homeobox C13 (HOXC13) has been demonstrated to play crucial roles in various cancers. However, its function in CC remains to be addressed. In the present study, upregulation of HOXC13 expression in human CC tissues was found in The Cancer Genome Atlas (TCGA) dataset and clinical samples and was associated with tumor size, FIGO stage and lymph node metastasis. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays suggested that the expression of HOXC13 was up-regulated in CC cells. Cell Counting Kit (CCK)-8, colony formation and cell cycle analysis assays indicated that HOXC13 promoted the proliferation and cycle progression of CC cells in vitro. Of note, knockdown of HOXC13 hinders tumor growth of xenograft tumor mice in vivo. Moreover, transwell and glycolysis measurement assays demonstrated that HOXC13 enhanced the migration, invasion and glycolysis of CC cells in vitro. Further mechanism analysis suggested that HOXC13 participated in CC progression through regulation of the β-catenin/c-Myc signaling pathway. Collectively, HOXC13 facilitated cell proliferation, migration, invasion and glycolysis through modulating β-catenin/c-Myc signaling pathway in CC, indicating that HOXC13 may provide a promising therapeutic target for the therapy of CC.