The expression of TRAIL and its receptors in gastric cancer and the apoptotic effect of rh-TRAIL on SGC7901 cells.

نویسندگان

  • Jian-Kun Hu
  • Kun Yang
  • Chun-Mei Li
  • Bo Zhang
  • Zhi-Xin Chen
  • Xin-Zu Chen
  • Jia-Ping Chen
چکیده

This study investigated the expression of TRAIL and its receptors in human gastric cancer and normal gastric tissues, the effects of rh-TRAIL with or without chemotherapeutic drugs in apoptosis of the gastric cancer cell line SGC7901 and the expression changes of DR4 and DR5 in SGC7901 cells influenced by chemotherapeutic drugs. The expression of TRAIL, DR4 and DcR1 were studied in 34 cases of human gastric cancer tissues and 15 cases of adjacent normal mucosa tissues, as well as 21 cases of distant normal mucosa tissues by means of immunohistochemistry. In addition, the expression of FasL were studied in gastric cancer tissues by immunohistochemistry. The effects of treatment with rh-TRAIL alone and/or chemotherapeutic drugs on SGC7901 cell growth inhibition were measured by MTT assay and the mRNA changes of DR4 and DR5 were detected by RT-PCR technique. The expression of TRAIL, DR4 and DcR1 in gastric cancer were lower than those of normal tissues (P<0.05). There was significant relationship between the expression of TRAIL and Borrmann type of gastric cancer (P=0.039), and so was the expression of DcR1 and tumor location (P=0.01). The correlation coefficient between the expression of TRAIL and FasL was 0.354 (P=0.04). Rh-TRAIL protein had inhibiting effect on the growth of SGC7901 cells. DDP and 5-FU increased the growth-inhibiting ability of rh-TRAIL to SGC7901 cells. DDP facilitated the induction of expression of DR4 and DR5 significantly in cell line (P<0.05), but 5-FU influenced only the expression of DR5 significantly. From the results, we concluded that the expression of TRAIL and its receptors were lower in gastric cancer than those of normal tissue, and the apoptosis-inducing effect of rh-TRAIL was enhanced when concomitant with chemotherapeutic drugs.

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عنوان ژورنال:
  • Oncology reports

دوره 21 3  شماره 

صفحات  -

تاریخ انتشار 2009