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目的探讨中介素(IMD)在肝细胞癌中的作用及其相关分子机制。方法以重组人IMD1-53及其受体拮抗剂IMD17-47处理肝癌细胞系Hep G2细胞,CCK-8法检测细胞增殖,TOPFlash/FOPFlash荧光素酶活性比值检测经典Wnt信号通路转录活性,实时定量PCR法检测Wnt信号通路下游c-myc、cyclin D1表达。结果 IMD可以呈剂量依赖性关系诱导肝癌Hep G2细胞增殖,并可被IMD受体竞争性拮抗剂IMD17-47阻断;IMD可激活经典Wnt信号转录活性及下游靶基因m RNA水平,阻断Wnt信号途径可在一定程度上抑制由IMD导致的Hep G2细胞增殖。结论 IMD通过与受体结合,激活Wnt信号通路发挥其促肝癌细胞增殖作用,为肝癌的治疗提出新的思路。
Objective To investigate the role of interleukin (IMD) in hepatocellular carcinoma and its related molecular mechanisms. Methods The Hep G2 cells were treated with recombinant human IMD1-53 and its receptor antagonist IMD17-47. The proliferation of Hep G2 cells was detected by CCK-8 assay. The transcriptional activity of the classic Wnt signaling pathway was detected by TOPFlash / FOPFlash luciferase assay. PCR to detect the expression of c-myc and cyclin D1 downstream of Wnt signaling pathway. Results IMD could induce Hep G2 cell proliferation in a dose-dependent manner and could be blocked by IMD17-47, an IMD receptor antagonist. IMD could activate the canonical Wnt signaling activity and downstream target gene m RNA levels, blocking Wnt The signaling pathway can inhibit the proliferation of Hep G2 cells induced by IMD to a certain extent. Conclusion IMD can activate Wnt signaling pathway to promote the proliferation of hepatocellular carcinoma cells by binding to receptor and provide new ideas for the treatment of hepatocellular carcinoma.