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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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SOX7 overexpression inhibited HCC cell growth.Overexpression of SOX7 inhibited cell growth as determined by MTT assay and colony formation assay. Viability of SOX7-transfected or vector-transfected SMMC-7721(A) and Hep3B (B) cells were determined on days 1 to 5. (C) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained SOX7-transfected or vector-transfected SMMC-7721 and Hep3B cells. (D) Both SOX7-specific siRNAs (siSOX7a and siSOX7b) silenced SOX7 in L02 cells successfully. SOX7 expression was detected by western blotting. (E) Viability of L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC were determined on days 1 to 5. (F) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC. Each bar represents the average ± SD of three independent experiments. * indicates p<0.05.
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pone-0097433-g002: SOX7 overexpression inhibited HCC cell growth.Overexpression of SOX7 inhibited cell growth as determined by MTT assay and colony formation assay. Viability of SOX7-transfected or vector-transfected SMMC-7721(A) and Hep3B (B) cells were determined on days 1 to 5. (C) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained SOX7-transfected or vector-transfected SMMC-7721 and Hep3B cells. (D) Both SOX7-specific siRNAs (siSOX7a and siSOX7b) silenced SOX7 in L02 cells successfully. SOX7 expression was detected by western blotting. (E) Viability of L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC were determined on days 1 to 5. (F) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC. Each bar represents the average ± SD of three independent experiments. * indicates p<0.05.

Mentions: To address the function of SOX7 down-regulation in HCC, we examined the effects of SOX7 on cell growth by MTT assay and colony formation assay. Hep3B and SMMC-7721 cells were transfected with either empty vector or SOX7 expression vector. Reduction of viability was observed in SOX7-overexpressed cells compared with cells transfected with empty vector (Fig. 2A, 2B). Moreover, SOX7-overexpressed cells formed fewer colonies than the control cells (Fig. 2C). Similar results were observed in both two types of HCC cells. Because of low expression of SOX7 in HCC cells, we examined the effects of SOX7 knockdown on cell growth in nontumorigenic L02 cells. It was confirmed that SOX7 was knockdown effectively by both siRNAs (Fig. 2D). Both MTT assay and colony formation assay indicated that SOX7 knockdown promoted proliferation of L02 cells (Fig. 2E, 2F). Collectively, these data suggested that SOX7 had an anti-proliferation roleHCC.


The suppressive role of SOX7 in hepatocarcinogenesis.

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

SOX7 overexpression inhibited HCC cell growth.Overexpression of SOX7 inhibited cell growth as determined by MTT assay and colony formation assay. Viability of SOX7-transfected or vector-transfected SMMC-7721(A) and Hep3B (B) cells were determined on days 1 to 5. (C) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained SOX7-transfected or vector-transfected SMMC-7721 and Hep3B cells. (D) Both SOX7-specific siRNAs (siSOX7a and siSOX7b) silenced SOX7 in L02 cells successfully. SOX7 expression was detected by western blotting. (E) Viability of L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC were determined on days 1 to 5. (F) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC. Each bar represents the average ± SD of three independent 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-g002: SOX7 overexpression inhibited HCC cell growth.Overexpression of SOX7 inhibited cell growth as determined by MTT assay and colony formation assay. Viability of SOX7-transfected or vector-transfected SMMC-7721(A) and Hep3B (B) cells were determined on days 1 to 5. (C) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained SOX7-transfected or vector-transfected SMMC-7721 and Hep3B cells. (D) Both SOX7-specific siRNAs (siSOX7a and siSOX7b) silenced SOX7 in L02 cells successfully. SOX7 expression was detected by western blotting. (E) Viability of L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC were determined on days 1 to 5. (F) Representative pictures (left panel) and quantification (right panel) of crystal violet-stained L02 cells transfected with siRNAs (siSOX7a and siSOX7b) or siNC. Each bar represents the average ± SD of three independent experiments. * indicates p<0.05.
Mentions: To address the function of SOX7 down-regulation in HCC, we examined the effects of SOX7 on cell growth by MTT assay and colony formation assay. Hep3B and SMMC-7721 cells were transfected with either empty vector or SOX7 expression vector. Reduction of viability was observed in SOX7-overexpressed cells compared with cells transfected with empty vector (Fig. 2A, 2B). Moreover, SOX7-overexpressed cells formed fewer colonies than the control cells (Fig. 2C). Similar results were observed in both two types of HCC cells. Because of low expression of SOX7 in HCC cells, we examined the effects of SOX7 knockdown on cell growth in nontumorigenic L02 cells. It was confirmed that SOX7 was knockdown effectively by both siRNAs (Fig. 2D). Both MTT assay and colony formation assay indicated that SOX7 knockdown promoted proliferation of L02 cells (Fig. 2E, 2F). Collectively, these data suggested that SOX7 had an anti-proliferation roleHCC.

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