Objective To investigate the potential roles of 14 -3 -3 in the pathogenesis of the cervical cancer.Methods Tissues from 107 patients with cervical cancer(cervical cancer group),50 cases of cervical intra-epithelial neoplasia (cervical intraepithelial neoplasia group)and 50 cases of chronic cervicitis (chronic cervicitis group)were obtained.Immunohistochemistry was performed to determine the expression of 14 -3 -3 protein in tissues of the three groups.Results The positive rate of 14 -3 -3 in cervical cancer group(75.70%)was signifi-cantly higher than that in cervical intraepithelial neoplasia group and chronic cervicitis group(42.00%,30.00%, respectively)(χ2 =17.00,29.96,all P <0.01),while there was no significant difference of 14 -3 -3 level between the cervical intraepithelial neoplasia group and chronic cervicitis group(χ2 =1.56,P >0.05).Moreover,in the cervi-cal cancer group,the positive rate of 14 -3 -3 in lymph node metastasis group was 88.89%,which was higher than that in negative lymph node metastasis group (63.16%)(χ2 =5.15,P <0.05).Conclusion The expression level of 14 -3 -3 protein in cervical cancer is increased,it may be correlated with cervical cancer cell malignant differenti-ation and metastasis.Perhaps,14 -3 -3 will play a key role as a novel target for tumor therapy.

AIM:To study the effects of transforming growth factor-β_1 (TGF-β_1) on cell apoptosis,cell cycle,production of endogenous TGF-β_1,expressions of P27~(Kip1),cyclin E and bcl-2 mRNA levels in NB4 cells. METHODS:Apoptotic morphological changes were observed by Wright-Giemsa staining. Cell cycle and apoptosis were detected with flow cytometry. Semiquantitative RT-PCR was used to examine the mRNA levels of endogenous TGF-β_1,P27~(Kip1),cyclin E and bcl-2. RESULTS:TGF-β_1 significantly restrained the growth and promoted the apoptosis of NB4 cells. The blockage of NB4 cells treated by TGF-β_1 at concentration of 5 μg/L was in G1 phase. Endogenous TGF-β_1 mRNA expression in NB4 cells was up-regulated when the concentration of exogenous TGF-β_1 was <5 μg/L. Meanwhile,the expression of endogenous TGF-β_1 mRNA was down-regulated when the concentration of exogenous TGF-β_1 was 10 μg/L. After treated with TGF-β_1 at concentration of 5 μg/L,P27~(Kip1) mRNA expression in NB4 cells was up-regulated,cyclin E and bcl-2 were reduced. CONCLUSION:TGF-β_1 is able to induce apoptosis and cell cycle distribution abnormally in NB4 cells by (1) Up-regulation of endogenous TGF-β_1,so that NB4 cells was induced into apoptosis through consequently high expression of P27~(Kip1). (2) TGF-β_1 may lead to cell cycle arrest by inhibiting the expression of cyclin E directly,or by inhibiting the activity of cyclin E through the increased expression of P27~(Kip1). (3) Down-regulation of bcl-2 induces apoptosis of NB4 cells.

OBJECTIVETo study the change of WT1 gene expression during human leukemic K562 cell differentiation and apoptosis induced by bufalin.

METHODSCell viability was determined by trypan blue exclusion, cell differentiation and apoptosis by nitro blue tetrazolium (NBT) reduction test, morphology and flow cytometry, expression of WT1 protein by Western blot analysis, and expression of WT1 mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTS(1) The cell proliferation was inhibited by bufalin and the IC(50) at 24, 48, 72 h were 0.026, 0.032 and 0.006 micro mol/L, respectively. (2) Bufalin induced K562 cell differentiation towards macrophage/monocyte within concentration from 0.01 to 0.05 micro mol/L and apoptosis at higher than 0.026 micro mol/L. (3) The expression of WT1 protein and mRNA were downregulated by bufalin in the initial stage of differentiation and apoptosis induced by bufalin.

CONCLUSIONK562 cell differentiation and apoptosis induced by bufalin might relate to the downregulation of WT1 expression.

Apoptosis ; Cell Differentiation ; Cell Proliferation ; Down-Regulation ; Humans ; WT1 Proteins ; genetics