ABSTRACT
JNK is a key protein in the third stages of MAPK pro-tein kinase activation cascade,and is located in the key node of multiple signal transduction network.It plays a pivotal role in the cell proliferation,differentiation,apoptosis and some other important cell biological processes.Therefore it acts as an im-portant factor in regulating the development of some major human diseases,such as cancer.But the functional diversity and com-plexity of three JNK isoforms in different cell types make it diffi- cult to develop anticancer drugs with JNK as a treatment target. In this review,we summarized the apoptotic signaling network of JNK and the regulation functions of JNK in cell apoptosis and proliferation.We also discuss the different functions of 3 JNK isoforms in human cancer.
ABSTRACT
Objective:To study the mechanism of apoptosis in laryngeal carcinoma cell induced by Stat3 antisense oligodeoxynucleotide (ASODN).Method:The designed Stat3 ASODN was transferred into laryngeal cacinoma Hep-2 cell by lipofection. Expression of Bcl-2, Bax and C-Myc were detected by Western blot and PCR.Result:Western blot and PCR results demonstrated that Stat3 ASODN could significantly increased the expression of Bax and decreased the expression of Bcl-2 and C-Myc when the concentration of antisense oligodeoxynucleotide were heightened.Conclusion:Stat3 ASODN participate in apoptosis by enhancing the expression of Bax and reducing the expression of Bcl-2 and C-Myc.
ABSTRACT
Objective:To explore the role of excessive iodide in inducing apoptosis in thyroid cells and its mechanism.Methods:Normal primary thyroid cells were cultured in NaI of different concentrations with or without IL-1? and methimazole.The morphological changes in thyroid cells were observed by light microscopy and apotosis rate was determined by flow cytometry techique.In the meantime Fas,FasL,p53 level were determined by histochemistry.Results:Thyroid cells treated with iodide excess underwent the morphological changes and apoptosis. There was a gradually increased apotosis rate and Fas/FasL protein expression accompanying increase in iodide concentrations.No changes in p53 protein expression was shown. IL-1? enhanced the effect of iodide cytotoxicity,whereas methimazole inhibited the role of iodide inducing apotosis.Conclusion:These data indicate that excess molecular iodide induces apoptosis in thyroid cell through Fas/FasL channel, but independent of p53.