Kaposi's sarcoma(KS) originates from vascular endothelial cells, with KS-associated herpesvirus(KSHV) as the etiological agent. SRY-box transcription factor 5(SOX5) plays different roles in various types of cancer...Kaposi's sarcoma(KS) originates from vascular endothelial cells, with KS-associated herpesvirus(KSHV) as the etiological agent. SRY-box transcription factor 5(SOX5) plays different roles in various types of cancer, although its role in KS remains poorly understood. In this study, we identified the role of SOX5 in KS tissues and KSHV-infected cells and elucidated the molecular mechanism. Thirty-two KS patients were enrolled in this study. Measurement of SOX5 m RNA and protein levels in human KS tissues and adjacent control tissues revealed lower levels in KS tissues, with KS patients having higher SOX5 level in the early stages of the disease compared to the later stages. And SOX5 m RNA and protein was also lower in KSHV-infected cells(iSLK-219 and iSLK-BAC) than normal cells(iSLK-Puro). Additionally, SOX5 overexpression inhibited cell proliferation and promoted apoptosis and decreased KSHV-infected cell migration and invasion. Moreover, we found that SOX5 overexpression suppressed the epithelial-to-mesenchymal transition of KSHV-infected cells. These results suggest SOX5 is a suppressor factor during KS development and a potential target for KS treatment.展开更多
基金supported by the National Natural Science Foundation of China (U160311781560473)+1 种基金Xinjiang Production and Construction Corps Key Areas Innovation Team Project (2018CB002)Shihezi University International Cooperation Project (GJHZ201901)。
文摘Kaposi's sarcoma(KS) originates from vascular endothelial cells, with KS-associated herpesvirus(KSHV) as the etiological agent. SRY-box transcription factor 5(SOX5) plays different roles in various types of cancer, although its role in KS remains poorly understood. In this study, we identified the role of SOX5 in KS tissues and KSHV-infected cells and elucidated the molecular mechanism. Thirty-two KS patients were enrolled in this study. Measurement of SOX5 m RNA and protein levels in human KS tissues and adjacent control tissues revealed lower levels in KS tissues, with KS patients having higher SOX5 level in the early stages of the disease compared to the later stages. And SOX5 m RNA and protein was also lower in KSHV-infected cells(iSLK-219 and iSLK-BAC) than normal cells(iSLK-Puro). Additionally, SOX5 overexpression inhibited cell proliferation and promoted apoptosis and decreased KSHV-infected cell migration and invasion. Moreover, we found that SOX5 overexpression suppressed the epithelial-to-mesenchymal transition of KSHV-infected cells. These results suggest SOX5 is a suppressor factor during KS development and a potential target for KS treatment.
