SOX5 promotes epithelial–mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma

Wang, Dong; Han, Song; Wang, Xing; Peng, Rui; Li, Xiangcheng

doi:10.1007/s12032-014-0461-2

Cited by 34 publications

(36 citation statements)

References 34 publications

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“…In search of EMT markers that could be more specifically modulated by NK cells, we reevaluated the proteomic data and noticed that MeDeBO cells exposed to either NK cells or cytokines showed upregulation of SOX5, a transcription factor involved in the negative regulation of MITF and in the induction of EMT (see Supplementary Table S1; refs. 38,39). We analyzed this molecule in the melanoma lesions and found a clear statistical correlation between the rich NK-cell infiltrate and the high expression of SOX5 ( Supplementary Fig.…”

Section: Discussionmentioning

confidence: 94%

NK-cell Editing Mediates Epithelial-to-Mesenchymal Transition via Phenotypic and Proteomic Changes in Melanoma Cell Lines

et al. 2018

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Tumor cell plasticity is a major obstacle for the cure of malignancies as it makes tumor cells highly adaptable to microenvironmental changes, enables their phenotype switching among different forms, and favors the generation of prometastatic tumor cell subsets. Phenotype switching toward more aggressive forms involves different functional, phenotypic, and morphologic changes, which are often related to the process known as epithelial-mesenchymal transition (EMT). In this study, we report natural killer (NK) cells may increase the malignancy of melanoma cells by inducing changes relevant to EMT and, more broadly, to phenotype switching from proliferative to invasive forms. In coculture, NK cells induced effects on tumor cells similar to those induced by EMT-promoting cytokines, including upregulation of stemness and EMT markers, morphologic transition, inhibition of proliferation, and increased capacity for Matrigel invasion. Most changes were dependent on the engagement of NKp30 or NKG2D and the release of cytokines including IFNγ and TNFα. Moreover, EMT induction also favored escape from NK-cell attack. Melanoma cells undergoing EMT either increased NK-protective HLA-I expression on their surface or downregulated several tumor-recognizing activating receptors on NK cells. Mass spectrometry-based proteomic analysis revealed in two different melanoma cell lines a partial overlap between proteomic profiles induced by NK cells or by EMT cytokines, indicating that various processes or pathways related to tumor progression are induced by exposure to NK cells. NK cells can induce prometastatic properties on melanoma cells that escape from killing, providing important clues to improve the efficacy of NK cells in innovative antitumor therapies. .

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Section: Discussionmentioning

confidence: 94%

NK-cell Editing Mediates Epithelial-to-Mesenchymal Transition via Phenotypic and Proteomic Changes in Melanoma Cell Lines

et al. 2018

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“…Previous reports have demonstrated that EMT promotes cancer development via migration and invasion (24); SOX5, in addition to SOX9, has been reported to regulate EMT (25,26). To determine whether SOX6 suppressed the migration and invasion of U2OS cells via EMT regulation, markers of EMT were detected following the overexpression or downregulation of SOX6 in U2OS cells.…”

Section: Sox6 Suppresses Emt Of Os Cells Via the Regulation Of Twist1mentioning

confidence: 99%

SOX6 is downregulated in osteosarcoma and suppresses the migration, invasion and epithelial-mesenchymal transition via TWIST1 regulation

Wang

et al. 2018

Mol Med Report

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Transcription factor SOX6 (SOX6) has been reported to serve essential roles in numerous types of cancers. However, the expression and functions of SOX6 in osteosarcoma (OS) have not been analyzed. In the present study, the patterns of SOX6 expression in OS cell lines and tissues were investigated by reverse transcription‑quantitative polymerase chain reaction and western blotting. The results of the present study revealed that SOX6 was notably downregulated in OS tissues and cell lines. Subsequently, gain‑ and loss‑of‑function studies demonstrated that SOX6 inhibited OS cell migration and invasion. In addition, SOX6 may have suppressed epithelial‑mesenchymal transition via twist‑related protein 1 (TWIST1) modulation. Chromatin immunoprecipitation (ChIP), quantitative ChIP and dual luciferase activity assays were used to confirm the binding of SOX6 to the promoter region of TWIST1. Additionally, colony formation assays and Cell Counting Kit‑8 assays demonstrated that SOX6 suppressed cell proliferation. The findings of the present study indicated that SOX6 serves as a tumor suppressor in OS and may be a potential therapeutic target for OS.

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“…SOX5 functions as transcription factors and primarily plays important roles in the regulation of embryonic development, cell fate, and chondrogenesis13. Elevated SOX5 transcripts have been related to invasive growth and reduced apoptosis in tumors and have been associated with progression of certain cancers141516. Recent studies have suggested the involvement of SOX5 in B-cell development9 and Th17 differentiation17, suggesting a role of SOX5 in immune responses.…”

mentioning

confidence: 99%

Modulation of IL-6 induced RANKL expression in arthritic synovium by a transcription factor SOX5

Feng

Shi

et al. 2016

Sci Rep

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Receptor activator of nuclear factor κB ligand (RANKL) is critically involved in bone erosion of rheumatoid arthritis (RA). We previously reported association between younger age at onset of RA and a RANKL promoter SNP that conferred an elevated promoter activity via binding to a transcription factor SOX5. Here we study the regulation of SOX5 levels in relation to RANKL expression in RA synovial fibroblasts (SF) and the development of bone erosion in the collagen-induced arthritis (CIA) mouse. Our data indicated SOX5 levels were higher in synovium and synovial fluid from RA compared to osteoarthritis patients. Pro-inflammatory cytokines upregulated SOX5 and RANKL expression in both primary RA SF and the rheumatoid synovial fibroblast cell line, MH7A. Overexpression of SOX5 resulted in significantly increased RANKL levels, while knockdown of SOX5 resulted in diminished IL-6 mediated RANKL upregulation in MH7A cells. Chromatin immunoprecipitation (ChIP) showed approximately 3-fold enrichment of RANKL-specific DNA in anti-SOX5 immunoprecipitate in IL-6 treated MH7A cells as compared to untreated cells. Locally silencing SOX5 gene significantly diminished RANKL positive cells and bone erosion in CIA mice. These findings suggest SOX5 is an important regulator of IL-6-induced RANKL expression in RA SF.

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SOX5 promotes epithelial–mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma

Cited by 34 publications

References 34 publications

NK-cell Editing Mediates Epithelial-to-Mesenchymal Transition via Phenotypic and Proteomic Changes in Melanoma Cell Lines

NK-cell Editing Mediates Epithelial-to-Mesenchymal Transition via Phenotypic and Proteomic Changes in Melanoma Cell Lines

SOX6 is downregulated in osteosarcoma and suppresses the migration, invasion and epithelial-mesenchymal transition via TWIST1 regulation

Modulation of IL-6 induced RANKL expression in arthritic synovium by a transcription factor SOX5

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