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Tex10 is upregulated and promotes cancer stem cell properties and chemoresistance in hepatocellular carcinoma.

ABSTRACT: Testis expressed 10 (Tex10), a new core component of the pluripotency circuitry, has been reported to positively regulate embryonic stem cell (ESC) super-enhancers to promote ESC self-renewal; however, the expression and function of Tex10 in hepatocellular carcinoma (HCC) and liver cancer stem cells remains unclear. The present study was designed to investigate the expression patterns of Tex10 with immunohistochemistry, western blotting and RT-qPCR in samples from HCC patients and HCC cell lines. The results obtained show that Tex10 was highly expressed in HCC tissues, and elevated Tex10 protein levels positively correlate with the poorly differentiated carcinoma. Likewise, we found that Tex10 expression in the high-metastasis HCCLM3 potential cell line was higher than that in the low-metastasis HepG2 potential cell line, and Tex10 expression in liver cancer stem cells was also higher than that in adhered HCC cells. In addition, Tex10 knockdown decreased stem cell marker expression and drug resistance. Tex10 promoted cancer stemness through activation of the STAT3 signaling pathway. Taken together, our study demonstrates that Tex10 plays a potent carcinogenic role in HCC tumorigenesis by maintaining cancer stem cell properties through activation of the STAT3 signaling pathway and promoting chemo-resistance. Thus, targeting Tex10 may provide a novel and effective therapeutic strategy to suppress the tumorigenicity of advanced HCC.

SUBMITTER: Xiang X

PROVIDER: S-EPMC6110582 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Tex10 is upregulated and promotes cancer stem cell properties and chemoresistance in hepatocellular carcinoma.

Xiang Xiaocong X Deng Li L Xiong Rong R Xiao Dongqin D Chen Zhu Z Yang Fei F Liu Kang K Feng Gang G

Cell cycle (Georgetown, Tex.) 20180725 11

Testis expressed 10 (Tex10), a new core component of the pluripotency circuitry, has been reported to positively regulate embryonic stem cell (ESC) super-enhancers to promote ESC self-renewal; however, the expression and function of Tex10 in hepatocellular carcinoma (HCC) and liver cancer stem cells remains unclear. The present study was designed to investigate the expression patterns of Tex10 with immunohistochemistry, western blotting and RT-qPCR in samples from HCC patients and HCC cell lines ...[more]

PMID: 30045663

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Project description:BackgroundmiR-500a-3p has been demonstrated to be involved in the development, progression and metastasis in several human cancers. Constitutive activation of JAK/STAT3 signaling pathway has been reported to play an important role in the development and progression of hepatocellular carcinoma (HCC).The purpose of this study was to determine the biological roles and clinical significance of miR-500a-3p in HCC and to identify whether miR-500a-3p has an effect on the activity of JAK/STAT3 signaling in HCC.MethodsmiR-500a-3p expression was examined by real-time PCR in 8 paired HCC tissues and individual 120 HCC tissues respectively. Statistical analysis was performed to explore the clinical correlation between miR-500a-3p expression and clinicopathological features and overall and relapse-free survival in HCC patients. In vitro and in vivo assays were performed to investigate the biological roles of miR-500a-3p in HCC. The bioinformatics analysis, real-time PCR, western blot and luciferase reporter assay were performed to discern and examine the relationship between miR-500a-3p and its potential targets. Clinical correlation of miR-500a-3p with its targets was examined in HCC tissues.ResultsmiR-500a-3p is dramatically elevated in HCC tissues and cells and high expression of miR-500a-3p correlates with poor overall and relapse-free survival in HCC patients. Upregulating miR-500a-3p enhances, while silencing miR-500a-3p suppresses, the spheroid formation ability, fraction of side population and expression of cancer stem cell factors in vitro and tumorigenicity in vivo in HCC cells. Our findings further reveal miR-500a-3p promotes the cancer stem cell characteristics via targeting multiple negative regulators of JAK/STAT3 signaling pathway, including SOCS2, SOCS4 and PTPN11, leading to constitutive activation of STAT3 signaling. Moreover, the inhibitory effects of anti-miR-500a-3p on cancer stem cell phenotypes and activity of STAT3 signaling were reversed by silencing SOCS2, SOCS4 and PTPN11 in miR-500a-3p-downexpressing cells, respectively. Clinical correlation of miR-500a-3p with the targets was examined in human HCC tissues.Conclusionour results uncover a novel mechanism by which miR-500a-3p promotes the stemness maintenance of cancer stem cell in HCC, suggesting that silencing miR-500a-3p may serve as a new therapeutic strategy in the treatment of hepatocellular carcinoma.

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Tex10 is upregulated and promotes cancer stem cell properties and chemoresistance in hepatocellular carcinoma.

Publications

Tex10 is upregulated and promotes cancer stem cell properties and chemoresistance in hepatocellular carcinoma.

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