Wen-Song Cai

Guangzhou Medical University, Shengcheng, Guangdong, China

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Publications (11)17 Total impact

  • Wen-Song Cai · Fei Shen · Zhe Feng · Ji-Wei Chen · Qi-Cai Liu · Er-Mao Li · Bo Xu · Jie Cao
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    ABSTRACT: Liver metastasis is a major cause of mortality from colon cancer. To investigate the role of cyclin-dependent kinase 8 (CDK8) in the progression of colon cancer hepatic metastasis. In this present study, human colon cancer HCT116 or HCT116-LUC-GFP cells were transfected with Lentiviral vector-mediated knockdown of CDK-8. After transfection, metastasis and invasion potential of colon cancer cell was investigated by wound healing and transwell invasion assays, respectively. A mice model of colon cancer liver metastases was established and observed with bioluminescence imaging. The protein expression of CDK-8, β-catenin, E2F1, MMP-7 and E-cadherin in liver tissues were detected by Western Blot. Our results revealed that lentiviral vector-mediated knockdown of CDK-8 inhibited metastasis and invasion of colon cancer cells in vitro and in vivo, respectively. Protein expression of CDK-8, β-catenin, MMP-7 and E-cadherin were inhibited, but protein expression of E2F1 was enhanced. In sum, our data provided compelling evidence that CDK-8 played a significant role in colon cancer hepatic metastasis by regulating the Wnt/β-catenin signal pathway and might sever as a potential therapeutic target for colon cancer patients.
    No preview · Article · Sep 2015 · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
  • Fei Shen · Wen-Song Cai · Jiang-Lin Li · Zhe Feng · Jie Cao · Bo Xu
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    ABSTRACT: There are conflicting reports on the correlation between manganese (Mn) levels and breast cancer. The purpose of the present study is to clarify the association between Mn levels and breast cancer using a meta-analysis approach. We searched articles indexed in Pubmed and the Chinese Journal Full-text Database (CJFD) published as of August 2014 that met our predefined criteria. Eleven eligible studies involving 1302 subjects were identified. Overall, pooled analysis indicated that subjects with breast cancer had lower Mn levels than the healthy controls (SMD = -1.51, 95% CI = [-2.47, -0.56]). Further subgroup analysis found a similar pattern in China (SMD = -1.32, 95% CI = [-2.33, -0.32]) and Korea (SMD = -4.08, 95% CI = [-4.63, -3.54]), but not in Turkey (SMD = -0.96, 95% CI = [-3.19, 1.27]). Further subgroup analysis also found a similar pattern in different sample specimens (serum: SMD = -1.24, 95% CI = [-2.31, -0.16]; hair: SMD = -1.99, 95% CI = [-3.91, -0.06]) and different types of Mn measurement (inductively coupled plasma-atomic absorption spectrometry (ICP-AAS): SMD = -1.14, 95% CI = [-2.24, -0.04]; graphite furnace atomic absorption spectroscopy (GFAAS): SMD = -1.94, 95% CI = [-2.38, -1.49]; inductively coupled plasma-atomic emission spectrometry (ICP-AES): SMD = -3.77, 95% CI = [-4.70, -2.85]). No evidence of publication bias was observed. In conclusion, this meta-analysis supports a significant association between deficient Mn levels and breast cancer. However, the subgroup analysis found that there was contradiction regarding races and geography, like China and Turkey. Thus this finding needs further confirmation by trans-regional multicenter, long-term observation in a cohort design to obtain better understanding of causal relationships between Mn levels and breast cancer, through measuring Mn at baseline to investigate whether the highest Mn category versus lowest was associated with breast cancer risk.
    No preview · Article · Jun 2015 · International Journal of Clinical and Experimental Medicine
  • Fei Shen · Wen-Song Cai · Jiang-Lin Li · Zhe Feng · Jie Cao · Bo Xu
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    ABSTRACT: There are conflicting reports on the correlation between serum levels of selenium (Se), copper (Cu), and magnesium (Mg) with thyroid cancer. The purpose of the present study is to clarify the association between Se, Cu, and Mg levels with thyroid cancer using a meta-analysis approach. We searched articles indexed in PubMed published as of January 2015 that met our predefined criteria. Eight eligible articles involving 1291 subjects were identified. Overall, pooled analysis indicated that subjects with thyroid cancer had lower serum levels of Se and Mg, but higher levels of Cu than the healthy controls [Se: standardized mean difference (SMD) = -0.485, 95% confidence interval (95%CI) = (-0.878, -0.092), p = 0.016; Cu: SMD = 2.372, 95%CI = (0.945, 3.799), p = 0.001; Mg: SMD = -0.795, 95%CI = (-1.092, -0.498), p < 0.001]. Further subgroup analysis found lower serum levels of Se in thyroid cancer in Norway [SMD = -0.410, 95%CI = (-0.758, -0.062), p = 0.021] and Austria [SMD = -0.549, 95%CI = (-0.743, -0.355), p < 0.001], but not in Poland (SMD = -0.417, 95%CI = (-1.724, 0.891), p = 0.532]. Further subgroup analysis also found that patients with thyroid cancer had higher serum levels of Cu in China [SMD = 1.571, 95%CI = (1.121, 2.020), p < 0.001] and Turkey [SMD = 0.977, 95%CI = (0.521, 1.432), p < 0.001], but not in Poland [SMD = 3.471, 95%CI = (-0.056, 6.997], p = 0.054]. In conclusion, this meta-analysis supports a significant association between serum levels of Se, Cu, and Mg with thyroid cancer. However, the subgroup analysis found that there was significant effect modification of Se, Cu levels by ethnic, like China and Poland. Thus, this finding needs further confirmation by a trans-regional multicenter study to obtain better understanding of causal relationship between Se, Cu, and Mg with thyroid cancer of different human races or regions.
    No preview · Article · Mar 2015 · Biological trace element research
  • Fei Shen · Wen-Song Cai · Zhe Feng · Jiang-Lin Li · Ji-Wei Chen · Jie Cao · Bo Xu
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    ABSTRACT: MicroRNAs (miRNAs) have emerged as important regulators that potentially play critical roles in cancer cell biological processes. Previous studies have shown that miR-492 plays an important role in cell tumorigenesis in multiple kinds of human cancer cells. However, the underlying mechanisms of this microRNA in breast cancer remain largely unknown. In the present study, we investigated miR-492's role in cell proliferation of breast cancer. MiR-492 expression was markedly upregulated in breast cancer tissues and breast cancer cells. Overexpression of miR-492 promoted the proliferation and anchorage-independent growth of breast cancer cells. Bioinformatics analysis further revealed sex-determining region Y-box 7 (SOX7), a putative tumor suppressor, as a potential target of miR-492. Data from luciferase reporter assays showed that miR-492 directly binds to the 3'-untranslated region (3'-UTR) of SOX7 messenger RNA (mRNA) and repressed expression at both transcriptional and translational levels. Ectopic expression of miR-492 led to downregulation of SOX7 protein, which resulted in the upregulation of cyclin D1 and c-Myc. In functional assays, SOX7 silenced in miR-492-in-transfected ZR-75-30 cells has positive effect to promote cell proliferation, suggesting that direct SOX7 downregulation is required for miR-492-induced cell proliferation and cell cycle of breast cancer. In sum, these results suggest that miR-492 represents a potential onco-miR and participates in breast cancer carcinogenesis by suppressing SOX7 expression.
    No preview · Article · Nov 2014 · Tumor Biology
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    ABSTRACT: Background and aims: The resistance to irradiation is common and a great drawback in the treatment of cancer with radiotherapy; the underlying mechanism is unclear. GATA binding protein 6 (GATA6) is associated with the pathogenesis of cancer. This study aims to investigate the role of GATA6 on compromising irradiation effect on HT55 and HT29 cells, 2 colorectal cancer cell lines. Methods: Human colon cancer cell lines, HT55 and HT29 cells, were treated with irradiation in the culture. Apoptosis of HT55 and HT29 cells was determined by flow cytometry. The expression of PAR2 and GATA6 in HT55 and HT29 cells was analyzed by real time RT-PCR and Western blotting. The gene silence and gene over expression were employed to observe the effect of GATA6 on p53 expression in HT55 and HT29 cells. Results: The results showed that HT55 and HT29 cells expressed protease-activated receptor-2 (PAR2). Irradiation induced 38.6% HT55 cell and 33.8% HT29 cell apoptosis, which reduced to 4.2% and 5.6%, respectively after activation of PAR2. Exposure to irradiation increased the expression of GATA6; the latter played a critical role in suppression of p53 expression in HT55 and HT29 cells. Inhibition of GATA6 significantly increased the effect of irradiation on HT55 and HT29 cells. Conclusions: Activation of PAR2 compromises the effect of irradiation on inducing colorectal cancer cell apoptosis, which can be prevented by inhibition of GATA6 expression.
    No preview · Article · May 2014 · Archives of Biochemistry and Biophysics
  • Jiang-lin Li · Wen-song Cai · Fei Shen · Zhe Feng · Guang-hui Zhu · Jie Cao · Bo Xu
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    ABSTRACT: The pathogenesis of hepatic fibrosis is to be further investigated. Protease-activated receptor-2 (PAR2) plays a role in hepatic fibrosis. This study aims to elucidate the role of activation of PAR2 in the regulation of hepatic stellate cell activities. In this study, the expression of PAR2, Fas and caveolin-1 in human hepatic stellate cell line, HHStec cell (HHStecs) was assessed by real time RT-PCR and Western blot. The levels of collagen were determined by enzyme-linked immunosorbent assay. The PAR2 gene was silenced in HHStecs using RNA interference. Apoptosis of HHStecs was assessed by flow cytometry. The results showed that HHStecs expressed PAR2, which was up regulated by activation with phorbol myristate acetate (PMA). Activation of PAR2 increased the release of collagen from HHStecs. Exposure to PMA induced HHStec apoptosis, which was significantly inhibited by activation of PAR2. The PAR2 activation also suppressed the expression of caveolin-1 and Fas in HHStecs. Over expression of caveolin-1 in HHStecs blocked PAR2-reduced apoptosis. We conclude that HHStecs express PAR2. Activation of PAR2 increases HHStecs to release collagen and reduces the activation-induced HHStec apoptosis, which can be inhibited by the over expression of caveolin-1.
    No preview · Article · Mar 2014 · Archives of Biochemistry and Biophysics
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    ABSTRACT: Liver metastasis is a major cause of mortality in colorectal cancer (CRC). The current study was to investigate the ability of ulinastatin (UTI) and curcumin (CUR) to inhibit CRC liver metastases via modulating matrix metalloproteinase-9 (MMP-9) and E-cadherin expression. Human CRC HCT-116 cells were treated with compounds individually and in combination in order to understand the effect on cell migration and invasion. The HCT-116 cell line was established to stably express luciferase and green fluorescent protein (GFP) by lentiviral transduction (HCT-116-Luc-GFP). We identified an anti-metastasis effect of UTI and CUR on a CRC liver metastasis mouse model. Tumor development and therapeutic responses were dynamically tracked by bioluminescence imaging. Expression of MMP-9 and E-cadherin in metastatic tumors was detected by immunohistochemical assay. Results of wound healing and cell invasion assays suggest that treatment with UTI, CUR, and UTI plus CUR, respectively, significantly inhibit HCT-116 cell migration and invasion. Furthermore, results of CRC hepatic metastasis on a nude mouse model showed that treatment with UTI, CUR alone, and a combination notably inhibited hepatic metastases from CRC and prolonged survival of tumor-bearing mice, especially in the UTI plus CUR group. These results suggest that the combination of UTI and CUR together may offer greater inhibition against metastasis of CRC.
    Preview · Article · Feb 2014 · OncoTargets and Therapy
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    ABSTRACT: High recurrence of colon cancer liver metastasis is observed in patients after hepatic surgery, and the cause is believed to be mostly due to the growth of residual microscopic metastatic lesions within the residual liver. Therefore, triggering the progression of occult metastatic foci may be a novel strategy for improving survival from colon cancer liver metastases. In the present study, we identified an anti-recurrence effect of ulinastatin on colon cancer liver metastasis in mice after hepatectomy. Transwell cell invasion assays demonstrated that ulinastatin significantly inhibited the in vitro invasive ability of colon cancer HCT116 cells. Moreover, gelatin zymography and ELISA analysis showed that MMP-9 activity and plasmin activity of colon cancer HCT116 cells were inhibited by ulinastatin, respectively. Furthermore, in vivo BALB/C nu/nu mice model indicated that ulinastatin effectively reduced recurrence after resection of hepatic metastases from colon cancer. The optimum timing for ulinastatin administration was one week after hepatectomy. Taken together, our findings point to the potential of ulinastatin as an effective approach in controlling recurrence of hepatic metastases from colon cancer after hepatectomy via its anti-plasmin activity.
    Preview · Article · Apr 2013
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    ABSTRACT: To investigate the effect of osteopontin (OPN) on the invasion and metastasis of human hapatocellular carcinoma (HCC). HCC cell lines (HCC-LM3) were transfected with the chemically synthesized small interfering RNA (siRNA). Real-time PCR and Western blot were used to quantify the mRNA and OPN protein levels. The malignant phenotypes including cellular growth, colony formation and invasion capability of the HCC cells were analyzed. The OPN mRNA and proteins levels were decreased by 75% and 80% in OPN siRNA treated cells. Colony formation and migratory capability were reduced in OPN siRNA treated cells (P < 0.05). The specific siRNA is able to reduce the OPN expression at both the mRNA and protein levels and significantly inhibits the invasiveness of HCC cells.
    No preview · Article · Jul 2009 · Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology
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    ABSTRACT: To investigate the stimulated effect of liver regeneration on colon cancer cells in remnant liver in rats. Rat models with liver metastases or retro-peritoneal metastases of colon cancer were established: animals underwent 37% or 70% liver resection and were compared with a sham laparotomy (15, 25, 15 cases, respectively). Metastases were performed two weeks before resection. Rats were killed 3 weeks after the resection. Total body weight, liver and tumor weights were recorded. The human colon adenocarcinoma cell line Lovo was cultured in the presence of portal serum withdrawn 24 hours and 14 days after partial hepatectomy (PH). DNA synthesis was assessed by flow cytometry analysis for 5-Bromodeoxyuridine (5-BrdU) incorporation. The tumor growth was accelerated in the remnant liver in 70% PH group, but the tumors in 37% PH group and retro-peritoneal site were not influenced by PH. Compared with the control group, after cultured 72 hours with portal serum withdrawn 24 h after PH, a higher 5-BrdU incorporation was found in the Lovo cell lines (P < 0.05), and it reached the peak after 120 hours of culture (P < 0.05). No difference was found between the groups when cultured with the portal serum withdrawn 14 d after PH (P > 0.05). PH may accelerate the growth of residual microscopic tumor in the liver which contributes to local recurrence. It has no systemic effect and effects on the cancer cell lines in extrahepatic sites. The excision extension is related to the stimulating effects on the cancer cell line, and subtotal hepatectomy is presumably a major determinant.
    No preview · Article · Mar 2009 · Zhonghua wai ke za zhi [Chinese journal of surgery]
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    ABSTRACT: To study the relationship between the dynamic changes of caveolin-1 with the degrees of liver fibrosis and portal venous pressure (PVP) in the process of rat liver cirrhosis formation induced by dimethylnitrosamine (DMN); also to investigate the mechanisms of caveolin-1 in the regulation of endothelial nitric oxide synthase (eNOS). Liver cirrhosis was induced in rats by DMN. The degrees of liver fibrosis and PVP were measured. NOS activity was assessed by citrulline generation. Protein expressions of caveolin-1, eNOS and caveolin-1-eNOS interactions were examined by Western blot and immunoprecipitation, respectively. Four weeks after DMN administration, liver fibrosis was at its peak and then decreased gradually. Immunoprecipitation and Western blot demonstrated that there was enhanced binding of caveolin-1 with eNOS in the process of rat liver cirrhosis. An increase in caveolin-1 expression was detected but the expression of eNOS was lower in cirrhotic tissues than in normal liver tissues. Caveolin-1 protein levels were positively correlated with the degrees of liver fibrosis and the levels of PVP (r=0.967, P < 0.01; r=0.922, P < 0.01, respectively), while NOS catalytic activity was negatively correlated with the degrees of liver fibrosis and levels of PVP (r= 0.973, P < 0.01; r=-0.947, P < 0.01) respectively. Caveolin-1 upregulation is associated with the development of portal hypertension in liver cirrhosis. Over-expression of caveolin-1 in perisinusoidal cells may promote caveolin-1-eNOS binding and reduce the activity of eNOS.
    No preview · Article · Mar 2008 · Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology