Transcriptional factor FOXS1 promotes colorectal cancer cell proliferation and invasion in vitro and tumor growth in vivo

Abstract

Abstract Colorectal cancer (CRC) has emerged as a major public health concern due to its high incidence and mortality worldwide and a series of transcription factors have been proven by a number of studies to play crucial roles in the development of CRC. In this study, integrative bioinformatics analyses were performed to analyze differentially expressed transcription factors in CRC. FOXS1 was shown to be considerably up-regulated in CRC and linked to patients’ survival according to online data. Furthermore, the expression level of FOXS1 showed to be increased within clinical CRC tissues and cell lines. Concerning cellular functions, FOXS1 knockdown significantly suppressed colony formation and cell invasion of CRC cells; regarding epithelial-mesenchymal transition (EMT) markers, FOXS1 knockdown dramatically elevated E-cadherin proteins but reduced N-cadherin, vimentin, and β-catenin proteins than normal control and sh-NC groups. Conversely, FOXS1 facilitated CRC cell aggressiveness. In the subcutaneous xenograft tumor model, FOXS1 knockdown inhibited, whereas FOXS1 overexpression facilitated tumor growth and EMT. In conclusion, FOXS1 is significantly up-regulated in CRC. Functionally, FOXS1 knockdown repressed the capacity of cancer cells to proliferate and invade in vitro and inhibited tumor growth in the subcutaneous xenograft tumor model in vivo. FOXS1 exerts the oncogenic role in CRC through facilitating the EMT process in CRC.