| Hepatocellular carcinoma (HCC), one of the most frequent tumor world-wide, was well-known for its highly invasive, rapid guowth, metastatic activity and poor prognosis. The emergence, devolepment and metastasis of HCC was a complex process. The TGF B -Smad signaling pathway was an important pathway to induce emergence, devolpment and metastasis of HCC. In this pathway, TGF P i first binded to the type II receptor, which occurs in the cell membrane as a digmeric form, then the TGF B RI which also occurs in anoligorneric form is recruited into the complex. TGF0 RII phosphorylates TGFB RI in the GS domain to activate it. This activated the type I kinase and transiently associate with and phosphory lation of R-Smads (receptor-regulated Smads, such as Smad2 and Smads). The phosphorylation of R-Smads resucts in formation of a heteromeric complex with another commin Smad (smad4) and translocates into the cell nucleus. The activated Smad compex bind to target promoters in association with DNA-binding cofactors, activate specifical target genes. It can inhibit cell prolferation through triggered GI periods interruption, promote cell to differentite, induce cell to apoptosis, and so on. The TGF B -Smad signaling pathway will interrupt if one of factor inactive. So that it would led to emergence of HCC, and Smad4 is the easiest change in this pathway. It had tested that the interruption of TGF B -Smad enhance the emergence of HCC. It was helpful in learning the relationship between TGF B signaling pathway and emergencedevolepment and metastasis of HCC through study the TGFB1. TGF B R II and Smadt in HCC. It also would provide the oretic basis for diagnosis, judgeing to stage of HCC's invasion and predicting the prognosis, finding new methods of therapy. There was no report about the relationship among TGF B1, TGF B RII , Smad4 and HCC in our country. In the present study, we detected the expression of TGF B 1, TGF B R II and Smad4 by immuohistochemistry method in 45 samples of HCC, which were obtained from 45 patients who underwent surgery, to investigate the relationship between the Smad, TGFB 1, TGF B R II and HCC and the relationship among the three factors.Materials and MethodsTissue of HCC were obtained from 45 patients who underwent surgery, including 36 specimens of adjacent noncancer liver tissues (ANLT). There are 33 males and 12 females.The age of patients ranged from 27 to 69 years old (mean: 51.5years old).34 patients' AFP level exceed 400ng/ml (76.5%), 32 patients HBsAg was positive (71.1%). The diameter (d) of tumor (d^5cm,ll samples; 5cm10cm 9samples) ranged from 2.0cm to 13.0cm (mean:7.6cm). Tumors were graded according to the criteria described by Edmondson and Steiner, Grade 1,4samples; GradeII,15 samples; Grade III, 20 smples; Grade IV, 6 samples. 14 samples were well encapsulated, 16 samples have portal vein thrombosis. According to clinicopathological feature of HCC, all cases were divided into two groups: higher invasive HCC(27 samples) and lower invasive(19 sample). No patients had received radiotherapy, chemotherapy, immunotherapy or TECA before the surgery.A total of three cases of laceration injury of liver were used as normal controls.Using the monoclone antibodies of anti-Smad4 and poyclone antibodies of TGF B1 and TGF B R II . Immunohistochemical stainings (SABC methods).were proformedThe immunohistochemical stainings of Smad4, TGF B 1 and TGF B RII were assessed according to both the distribution (the percentage of positive cells) and the instensity of staining. Those having positive staining in less than 3 score wereregarded as "-" , greater than 3 score as "+" .Statistical analysis was executed by SPSS 10.0 Software,P valus less than 0.05 were considered significant. Results1.The expressions of Smad4 TGF B RII in normal control were all positive, While, TGF B1 are all negative.2.The positive rate of Smad4, TGF B 1 and TGF & R II in HCC were respectively 51.5%(23/45), 62.2%(28/45) and 42.2%(19/45).3.There were no obvious relations...
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