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The suppressive role of SOX7 in hepatocarcinogenesis.

Wang C, Guo Y, Wang J, Min Z - PLoS ONE (2014)

Bottom Line: We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor samples, and the expression of SOX7 was negatively correlated with tumor size.SOX7 expression was also reduced in four HCC cell lines (SMMC-7721, Hep3B, HepG2 and Huh 7).The expression of Ki-67, a proliferation marker, was also reduced in SOX7-overexpression tumors.

View Article: PubMed Central - PubMed

Affiliation: Department of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China.

ABSTRACT
SOX7 is a transcription factor mediating various developmental processes. However, its role in hepatocellular carcinoma (HCC) remains unclear. Here, we assessed the role of SOX7 in hepatocarcinogenesis. We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor samples, and the expression of SOX7 was negatively correlated with tumor size. SOX7 expression was also reduced in four HCC cell lines (SMMC-7721, Hep3B, HepG2 and Huh 7). Overexpression of SOX7 could inhibit HCC cell growth, with G1to S phase arrest. In SOX7-overexpression cells, cyclin D1 and c-myc, two cell cycle promoters, were down-regulated. Moreover, ectopic expression of cyclin D1 or c-myc could override G1 to S pahse arrest induced by SOX7. Furthermore, overexpression of SOX7 suppressed tumor formation with down-regulation of cyclin D1 and c-myc in vivo. The expression of Ki-67, a proliferation marker, was also reduced in SOX7-overexpression tumors. Taken together, our study suggests that SOX7 plays an important inhibitory role in hepatocarcinogenesis, and might be a novel target for HCC therapy.

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Overexpression of SOX7 suppressed tumor formation.(A) A representative picture of tumor growth in nude mice subcutaneously inoculated with vector or SOX7 transfected HCC cells. The tumors were outlined by red circle. (B) Subcutaneous tumor growth curve of nude mice with different treatment. (C) A representative picture of the isolated tumors. (D) The mean tumor weights in nude mice with different treatment. (E) Western blotting analysis of SOX7, cyclin D1, c-myc and GAPDH levels in the subcutaneous tumor samples. (F) Representative pictures (left panel) and quantification (right panel) of immunohistochemistry-detected Ki-67 expression in the subcutaneous tumor samples. The data were means ± SD of three separate experiments. * indicates p<0.05.
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pone-0097433-g005: Overexpression of SOX7 suppressed tumor formation.(A) A representative picture of tumor growth in nude mice subcutaneously inoculated with vector or SOX7 transfected HCC cells. The tumors were outlined by red circle. (B) Subcutaneous tumor growth curve of nude mice with different treatment. (C) A representative picture of the isolated tumors. (D) The mean tumor weights in nude mice with different treatment. (E) Western blotting analysis of SOX7, cyclin D1, c-myc and GAPDH levels in the subcutaneous tumor samples. (F) Representative pictures (left panel) and quantification (right panel) of immunohistochemistry-detected Ki-67 expression in the subcutaneous tumor samples. The data were means ± SD of three separate experiments. * indicates p<0.05.

Mentions: To investigate the effects of SOX7 on tumorgenesis in vivo, HCC cells transfected with vector or SOX7 were injected subcutaneously into nude mice to initiate tumor formation. Four weeks later, large tumors were seen in the vector groups, while the tumor volume was still minimal in those mice transplanted with the SOX7-expression cells (Fig. 5A, 5B). At the end of experiments tumors were isolated (Fig. 5C) and weighed. Tumors from SOX7-transfected nude mice weighed significantly less than the control mice (Fig. 5D). These results were consistent with the anti-proliferation function of SOX7 and indicated that SOX7 overexpression elicited a strong anti-tumor effect on HCC in vivo. We also analyzed the cyclin D1 and c-myc expression in these tumors. SOX7 was overexpressed successfully, and the expression of cyclin D1 and c-myc was reduced in SOX7-overexpression tumors (Fig. 5E), similar to the results in vitro. To confirm the anti-proliferation role of SOX7 in vivo, we detected the expression of Ki-67, a proliferation marker, in above tumors. Ki-67 expression was significantly decreased after SOX7 overexpression (Fig. 5F), indicating that SOX7 could inhibit proliferation in vivo. Taken together, we found that overexpression of SOX7 suppressed tumor formation by proliferation inhibition via down-regulation of cyclin D1 and c-myc.


The suppressive role of SOX7 in hepatocarcinogenesis.

Wang C, Guo Y, Wang J, Min Z - PLoS ONE (2014)

Overexpression of SOX7 suppressed tumor formation.(A) A representative picture of tumor growth in nude mice subcutaneously inoculated with vector or SOX7 transfected HCC cells. The tumors were outlined by red circle. (B) Subcutaneous tumor growth curve of nude mice with different treatment. (C) A representative picture of the isolated tumors. (D) The mean tumor weights in nude mice with different treatment. (E) Western blotting analysis of SOX7, cyclin D1, c-myc and GAPDH levels in the subcutaneous tumor samples. (F) Representative pictures (left panel) and quantification (right panel) of immunohistochemistry-detected Ki-67 expression in the subcutaneous tumor samples. The data were means ± SD of three separate experiments. * indicates p<0.05.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4016311&req=5

pone-0097433-g005: Overexpression of SOX7 suppressed tumor formation.(A) A representative picture of tumor growth in nude mice subcutaneously inoculated with vector or SOX7 transfected HCC cells. The tumors were outlined by red circle. (B) Subcutaneous tumor growth curve of nude mice with different treatment. (C) A representative picture of the isolated tumors. (D) The mean tumor weights in nude mice with different treatment. (E) Western blotting analysis of SOX7, cyclin D1, c-myc and GAPDH levels in the subcutaneous tumor samples. (F) Representative pictures (left panel) and quantification (right panel) of immunohistochemistry-detected Ki-67 expression in the subcutaneous tumor samples. The data were means ± SD of three separate experiments. * indicates p<0.05.
Mentions: To investigate the effects of SOX7 on tumorgenesis in vivo, HCC cells transfected with vector or SOX7 were injected subcutaneously into nude mice to initiate tumor formation. Four weeks later, large tumors were seen in the vector groups, while the tumor volume was still minimal in those mice transplanted with the SOX7-expression cells (Fig. 5A, 5B). At the end of experiments tumors were isolated (Fig. 5C) and weighed. Tumors from SOX7-transfected nude mice weighed significantly less than the control mice (Fig. 5D). These results were consistent with the anti-proliferation function of SOX7 and indicated that SOX7 overexpression elicited a strong anti-tumor effect on HCC in vivo. We also analyzed the cyclin D1 and c-myc expression in these tumors. SOX7 was overexpressed successfully, and the expression of cyclin D1 and c-myc was reduced in SOX7-overexpression tumors (Fig. 5E), similar to the results in vitro. To confirm the anti-proliferation role of SOX7 in vivo, we detected the expression of Ki-67, a proliferation marker, in above tumors. Ki-67 expression was significantly decreased after SOX7 overexpression (Fig. 5F), indicating that SOX7 could inhibit proliferation in vivo. Taken together, we found that overexpression of SOX7 suppressed tumor formation by proliferation inhibition via down-regulation of cyclin D1 and c-myc.

Bottom Line: We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor samples, and the expression of SOX7 was negatively correlated with tumor size.SOX7 expression was also reduced in four HCC cell lines (SMMC-7721, Hep3B, HepG2 and Huh 7).The expression of Ki-67, a proliferation marker, was also reduced in SOX7-overexpression tumors.

View Article: PubMed Central - PubMed

Affiliation: Department of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China.

ABSTRACT
SOX7 is a transcription factor mediating various developmental processes. However, its role in hepatocellular carcinoma (HCC) remains unclear. Here, we assessed the role of SOX7 in hepatocarcinogenesis. We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor samples, and the expression of SOX7 was negatively correlated with tumor size. SOX7 expression was also reduced in four HCC cell lines (SMMC-7721, Hep3B, HepG2 and Huh 7). Overexpression of SOX7 could inhibit HCC cell growth, with G1to S phase arrest. In SOX7-overexpression cells, cyclin D1 and c-myc, two cell cycle promoters, were down-regulated. Moreover, ectopic expression of cyclin D1 or c-myc could override G1 to S pahse arrest induced by SOX7. Furthermore, overexpression of SOX7 suppressed tumor formation with down-regulation of cyclin D1 and c-myc in vivo. The expression of Ki-67, a proliferation marker, was also reduced in SOX7-overexpression tumors. Taken together, our study suggests that SOX7 plays an important inhibitory role in hepatocarcinogenesis, and might be a novel target for HCC therapy.

Show MeSH
Related in: MedlinePlus