Jun Jin

Publications (3)27.57 Total impact

• Article: A chimeric SM5-1 antibody inhibits hepatocellular carcinoma cell growth and induces caspase-dependent apoptosis.

  Jianxin Dai, Jun Jin, Bohua Li, Hao Wang, Sheng Hou, Weizhu Qian, Geng Kou, Dapeng Zhang, Jing Li, Min Tan, Jing Ma, Yajun Guo
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  ABSTRACT: cSM5-1 is a mouse-human chimeric antibody which has a high specificity for hepatocellular carcinoma, melanoma and breast cancer. In this study, cSM5-1 was found to be able to inhibit cell growth and induce apoptosis in hepatocellular carcinoma cells. The antitumor activity of cSM5-1 was closely correlated with the expression level of the SM5-1 binding protein in the cancer cells. The role of caspases in cSM5-1-induced apoptosis was also investigated, indicating that cSM5-1-induced apoptosis was partially caspase-dependent and caspase-10 played a critical role. These in vitro data indicate that cSM5-1 has the potential to be a promising candidate for cancer treatment.
  Cancer Letters 01/2008; 258(2):208-14. · 4.24 Impact Factor
• Source

  Available from: pubget.com

  Article: TIP30 inhibits growth of HCC cell lines and inhibits HCC xenografts in mice in combination with 5-FU.

  Jian Zhao, Xia Zhang, Mei Shi, Hao Xu, Jun Jin, Haidong Ni, Silei Yang, Jianxin Dai, Mengchao Wu, Yajun Guo
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  ABSTRACT: Hepatocellular carcinoma (HCC) is an aggressive cancer with a poor prognosis. The specific cellular gene alterations responsible for hepatocarcinogenesis are not well known. Previous works showed that loss of TIP30, also called CC3, a putative tumor suppressor, increased the incidence of hepatocellular carcinoma in mice, and some clinical samples of human HCC tissues had aberrant expression of TIP30. Here, we report that the introduction of TIP30 by an adenovirus vector into HCC cell lines that had decreased expressions of TIP30 inhibited cell proliferation, decreased anchorage-dependent growth, suppressed invasion through the extracellular matrix, and inhibited tumorigenesis in nude mice. Moreover, exogenous expression of Tip30 sensitized HCC cells to cytotoxic drugs and to apoptosis induced by tumor necrosis factor-related ligands in vitro. Ectopic expression of TIP30 in HCC cells enhanced p53 expression and decreased Bcl-2/Bcl-xL expression. Treatment of nude mice bearing subcutaneously established HCC tumors with a combination of an adenovirus expressing TIP30 and the cytotoxic drug 5-fluorouracil completely suppressed tumor growth and prolonged survival. In conclusion, TIP30 may play an important role in the suppression of hepatocarcinogenesis by acting as a tumor suppressor. Overexpression of TIP30 might be a promising candidate as a treatment for HCC that would increase sensitivity to chemotherapeutic drugs.
  Hepatology 08/2006; 44(1):205-15. · 11.66 Impact Factor
• Article: TIP30 inhibits growth of HCC cell lines and inhibits HCC xenografts in mice in combination with 5‐FU

  Jian Zhao, Xia Zhang, Mei Shi, Hao Xu, Jun Jin, Haidong Ni, Silei Yang, Jianxin Dai, Mengchao Wu, Yajun Guo
  [show abstract] [hide abstract]
  ABSTRACT: Hepatocellular carcinoma (HCC) is an aggressive cancer with a poor prognosis. The specific cellular gene alterations responsible for hepatocarcinogenesis are not well known. Previous works showed that loss of TIP30, also called CC3, a putative tumor suppressor, increased the incidence of hepatocellular carcinoma in mice, and some clinical samples of human HCC tissues had aberrant expression of TIP30. Here, we report that the introduction of TIP30 by an adenovirus vector into HCC cell lines that had decreased expressions of TIP30 inhibited cell proliferation, decreased anchorage-dependent growth, suppressed invasion through the extracellular matrix, and inhibited tumorigenesis in nude mice. Moreover, exogenous expression of Tip30 sensitized HCC cells to cytotoxic drugs and to apoptosis induced by tumor necrosis factor–related ligands in vitro. Ectopic expression of TIP30 in HCC cells enhanced p53 expression and decreased Bcl-2/Bcl-xL expression. Treatment of nude mice bearing subcutaneously established HCC tumors with a combination of an adenovirus expressing TIP30 and the cytotoxic drug 5-fluorouracil completely suppressed tumor growth and prolonged survival. In conclusion, TIP30 may play an important role in the suppression of hepatocarcinogenesis by acting as a tumor suppressor. Overexpression of TIP30 might be a promising candidate as a treatment for HCC that would increase sensitivity to chemotherapeutic drugs. (HEPATOLOGY 2006;44:205–215.)
  Hepatology 06/2006; 44(1):205 - 215. · 11.66 Impact Factor