Anti-Sonic hedgehog blocking antibody enhances killing effect of PBMCs on cervical carcinoma HeLa cells

AIM: To investigate the effect of anti-Sonic hedgehog(Shh) blocking antibody on the killing effect of peripheral blood mononuclear cells(PBMCs) on cervical carcinoma HeLa cells. METHODS: The expression levels of Shh and Shh signaling molecules in HeLa cells were detected by immunocytochemistry and RT-PCR. PBMCs from health peoples were isolated by the method of Ficoll density gradient centrifugation, and then co-cultured with HeLa cells in vitro. The expression of CD3, CD69 and CD71 was assayed by flew cytometry. The concentrations of IFN-γ, IL-10 and IL-4 in culture supernatants were detected by ELISA. The killing effect of PBMCs on HeLa cells was observed under microscope. RESULTS: Shh and Shh signaling molecules were expressed in HeLa cells. The level of Shh expression didn't change significantly in the 6th passage of HeLa cells. CD3⁺ cells were increased in the co-culture system. The expression of CD69 and CD 71, and the secretion of IFN-γ were increased, while the secretion of IL-10 was decreased in the co-culture system treated with anti-Shh blocking antibody. Anti-Shh blocking antibody has no effect on the secretion of IL-4. The killing effect of PBMCs on HeLa cells was strengthened by anti-Shh blocking antibody. CONCLUSION: Anti-Shh blocking antibody promotes the activation of PBMCs and enhances the killing effect of PBMCs on cervical carcinoma HeLa cells.     

Expression and significance of miR-193b in cervical cancer

AIM: To investigate the expression of microRNA-193b(miR-193b) in the cervical tissues, and further to explore the effect of silencing miR-193b on diamminedichloroplatinum(DDP)-treated HeLa cell viability. METHODS: The expression levels of miR-193b in different cervical tissues were examined by qPCR. After transfection of miR-193b-inhibitor, the cell migration was determined by Transwell assay, the sensitivity of HeLa cells to DDP was measured by MTT assay, the protein levels of phosphate and tension homology deleted on chromsome ten(PTEN), protein kinase B(Akt), p-Akt and p-glycoprotein(P-gp) were determined by Western blot. RESULTS: The mRNA level of miR-193b was significantly increased in the cervical cancer tissues compared with normal cervical tissues(P<0.05). Knockdown of miR-193b obviously inhibited migration and enhanced sensitivity to DDP of HeLa cells(P<0.05). Additionally, after transfection of miR-193b-inhibitor, the expression of PTEN was increased, whereas the protein levels of p-Akt and P-gp were decreased(P<0.05). CONCLUSION: miR-193b is highly expressed in the cervical cancer tissues. Inhibition of miR-193b augments the sensitivity to DDP of HeLa cells, at least in part, through PTEN-PI3K/Akt signaling pathway.     

Effects of Smo gene silencing on cell activity and apoptosis of human cervical carcinoma HeLa cells

AIM: To investigate the effect of Hedgehog (Hh) signaling pathway on the viability and apoptosis of cervical carcinoma cells by shRNA technique to knock down Smoothened (Smo) gene. METHODS: Smo shRNA was used to transfect the cervical carcinoma HeLa cells. The expression of Smo and Gli1 at mRNA and protein levels in the HeLa cells was determined by RT-PCR and Western blot, respectively. The effect of Smo gene silencing on the growth of the cells was measured by MTT assay. The apoptosis and cell cycle were determined by flow cytometry. RESULTS: Compared with control group, the mRNA and protein expression of Smo and Gli1 were evenly reduced obviously after transfected with Smo shRNA for 72 h (P<0.05). The viability of HeLa cells transfected with Smo shRNA was significantly inhibited. The percentages of the cells in G₀/G₁ phase and early apoptosis rate were obviously higher in Smo shRNA transfection group than those in control group. CONCLUSION: Smo gene silencing effectively inhibits the cell growth and induces the apoptosis of human cervical carcinoma cells.     

Effects of down-regulation of AEG-1 expression on cell cycle and invasion of human cervical carcinoma cells

AIM: To investigate the effects of down-regulation of astrocyte elevated gene-1 (AEG-1) expression on cell cycle and invasion of human cervical carcinoma SiHa cells.METHODS: The protein expression of AEG-1 was detected by Western blotting in normal cervical tissues, cervical squamous cell carcinoma tissues, HeLa cells, SiHa cells and CaSki cells. Control siRNA or AEG-1 siRNA was transfected into SiHa cells, and the protein expression of AEG-1 in SiHa cells was detected by Western blotting. The changes of cell cycle distribution and cell invasion were determined by flow cytometry and Boyden chamber, respectively. The protein levels of cyclin D1, cyclin-dependent kinase 2(CDK2) and matrix metalloproteinase-9 (MMP-9) were analyzed by Western blotting.RESULTS: The protein expression of AEG-1 in cervical squamous cell carcinoma tissues was significantly higher than that in normal cervical tissues (P<0.05). Meanwhile, the protein expression of AEG-1 in the 3 cervical carcinoma cell lines was obviously higher than that in normal cervical tissues, in which SiHa cells displayed the highest AEG-1 protein level (P<0.05). In addition, AEG-1 siRNA effectively down-regulated the protein expression of AEG-1 in SiHa cells, which led to increase the percentage at G0/G1 phase and reduced the invasion of SiHa cells. Furthermore, the protein levels of cyclin D1, CDK2 and MMP-9 in AEG-1 siRNA group were markedly lower than those in non-treatment group and control siRNA group (P<0.05).CONCLUSION: Over-expression of AEG-1 may be closely associated with the occurrence and development of cervical carcinoma, and the AEG-1 down-regulation-mediated cell cycle arrest and attenuation of invasion may be tightly related to the down-regulations of cyclin D1, CDK2 and MMP-9 at protein levels.     

Influence of GPIF on the expression of costimulatory molecules lineaged T cells in mice with immunodeficiency in vivo

AIM:To investigate the effects of goat placenta immunoregulating factor (GPIF) on the expression of costimulatory molecules lineaged T cells in BALB/c mice. METHODS:Animal model for immunodeficiency made from BALB/c mice with whole-body irradiation by 5 Gy 60Coγ-ray was applied for research. The immunosuppressive mice were injected with GPIF for seven days continuously. FACS was applied to analyze the rate of CD28+, CD152+, CD4+CD28+, CD8+CD28+, CD4+CD152+ and CD8+CD152+ cells in splenic lymphocytes and ELISA method was employed to measure the amount of IL-2 and IFN-γ in serum of mice. RESULTS:GPIF increased the percentage of CD28+, CD4+CD28+ and CD8+CD28+ cells (P<0.05, P<0.01), and decreased the percentage of CD152+ (P<0.05, P<0.01), CD4+CD152+ cells (P<0.05, P<0.01) in splenic lymphocytes of immunosuppressive mice significantly. GPIF increased the content of IL-2 and IFN-γ in serum of mice simultaneously (P<0.01). CONCLUSION:Immuno-enhancing effect of GPIF facilitates the costimulation of CD28 pathway, which can activate T cells and accelerate the course of renewing T cell activity. The function of GPIF may have close relationship with an immune network formed by the secretion of IL-2 and IFN-γ and the expression of CD28 and CD152.     

Molecular mechanism of miR-1246 enhancing radiosensitivity of cervical cancer cells

AIM: To investigate the molecular mechanism of microRNA-1246(miR-1246) enhancing radiosensitivity of cervical cancer cells. METHODS: Cervical cancer lines HeLa, CaSki, C33A and SiHa were transfected with miR-1246 mimic and negative control mimic (NC-mimic) using Lipofectamine 2000 kit, and the expression level of miR-1246 in cervical cancer tissue, normal tissue, cervical cancer cell lines and endometrial epithelium cell line ESC was detected by real-time PCR. The transfected cells were exposed to X-ray radiation. The cell viability and migration rate were measured respectively by MTT assay and Transwell method. The protein levels of γH2AX, ATM, p-ATM and p-p53 were monitored by immunofluorescence and Western blot. RESUITS: Higher miR-1246 level was found in normal tissue and ESC cells, while lower miR-1246 level was found in HeLa, SiHa, C33A and Caski cells and cervical cancer tissues. The expression level of miR-1246 in the cells transfected with miR-1246 mimic was significantly higher than that in the cells transfected with NC-mimic (P<0.05). The cell viability and migration rate of the cervical cancer cells with miR-1246 over-expression were notably lower than those of the cells transfected with NC-mimic (P<0.05) under the same conditions. The results of immunofluorescence indicated that the protein expression level of γH2AX significantly increased in the cervical cancer cells with miR-1246 over-expression exposed to radiation compared with the negative control (P<0.05). The protein expression level of γH2AX was significantly increased in the cervical cancer cells with miR-1246 over-expression, while the protein levels of p-ATM and p-p53 were significantly decreased as compared with the negative control group (P<0.05). CONCLUSION: miR-1246 is highly expressed in normal tissue and normal endometrial epithelial cells, while is low expressed in the cervical cancer tissues or cells. miR-1246 over-expression inhibits growth and migration, and significantly enhances radiosensitivity of cervical cancer cells. The molecular mechanism is possibly related to inhibiting ATM pathway and DNA damage repair.     

Expression of human papillomavirus L1 capsid protein in cervical cells and its clinical application

AIM: To investigate the effect of human papillomavirus (HPV) L1 capsid protein on the malignant transformation and cellular immunity of cervical cells, and to analyze the clinical application value of HPV L1 capsid protein detection in cervical cancer. METHODS: The data and samples of 280 women in the Gynaecology Clinic were collected from Yingtan People's Hospital from July 2012 to December 2014. All patients were enrolled for liquid-based cytology test (LCT). At the same time, the protein expression of HPV L1 in exfoliated cells was detected by CytoReact^® cell/tissue L1 capsid immunocytochemical staining. The Cervista HPV detection system was used for HPV detection, and the pathological results of cervical biopsy were used as a baseline for comparison. According to the degree of lesions, the tissues were divided into 5 groups:negative intraepithelial lesion (NILM) group, atypical squamous cell (ASC) group, low-grade squamous intraepithelial lesion (LSIL) group, high-grade squamous intraepithelial lesion (HSIL) group, and squamous-cell carcinoma (SCC) group. The positive expression rates of HPV L1 protein in different degrees of lesions were compared and analyzed. The levels of interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α) in the cells were detected by ELISA. Flow cytometry was used to analyze the immune cell subsets in the blood. RESULTS: The positive rate of HPV L1 capsid protein was decreased with the severity of cervical lesions determined by cervical biopsy, and was 0 in SCC group. The positive expression rate of HPV L1 capsid protein in each group was statistically different (P<0.05). The level of IL-2 was decreased with the increase in HPV L1 capsid protein expression, and the level of TNF-α was increased with the increase in HPV L1 capsid protein expression with statistical significance (P<0.05). The positive expression of HPV L1 capsid protein was accompanied by the decrease in immune-activated cell subsets, and the increase in immunosuppressive immune cell population with statistical significance (P<0.05), and the strong correlation was observed. CONCLUSION: The detection of HPV L1 capsid protein expression in cervical cells is highly applicable for judging the malignant transformation and the cellular immune status of the cells, which is worthy of clinical use.     

Shikonin induces apoptosis and autophagy of human cervical cancer HeLa cells by PI3K/Akt/mTOR signaling pathway

AIM:To observe the effects of shikonin on the apoptosis and autophagy of human cervical cancer HeLa cells, and to explore the possible role of PI3K/Akt/mTOR signaling pathway in these processes. METHODS:The HeLa cells were treated with shikonin, and the cell viability was detected by CCK-8 assay. The apoptosis was detected by Annexin V/PI double staining. The autophagosome was observed by transfection with GFP-LC3 into the HeLa cells. After the treatment with shikonin combined with autophagy inhibitor 3-methyladenine (3-MA) or apoptosis inhibitor Z-DEVD-FMK, the protein levels of autophagy-and apoptosis-related molecules microtuble-associated protein 1 light chain 3 (LC3) and cleaved caspase-3 in the HeLa cells were determined by Western blot. The protein levels of phosphorylated PI3K (p-PI3K), phosphorylated Akt (p-Akt) and phosphorylated mTOR (p-mTOR) were also determined by Western blot. RESULTS:Shikonin significantly inhibited the viability of HeLa cells (P<0.05). Compared with control group, shikonin significantly induced apoptosis of HeLa cells (P<0.05). The results of GFP-LC3 plasmid transfection analysis showed that green dot-like congregate autophagosomes appeared in the cytoplasm of the HeLa cells after shikonin treatment, while the autophagosomes were rarely observed in control group. Compared with shikonin group, LC3-Ⅱ/LC3-I was significantly decreased and cleaved caspase-3 was significantly increased in shikonin+3-MA group (P<0.05). Compared with shikonin group, LC3-Ⅱ/LC3-I was significantly increased and cleaved caspase-3 was significantly decreased in shikonin+Z-DEVD-FMK group (P<0.05). Compared with control group, shikonin significantly decreased the protein levels of p-PI3K, p-Akt and p-mTOR (P<0.05). CONCLUSION:The apoptosis and autophagy of the HeLa cells are induced by shikonin, these two processes are complementary. The mechanism may be related to inhibition of PI3K/Akt/mTOR signaling pathway.     

Effect of Linc00152 targeting miR-376c-3p on viability,apoptosis and radiosensitivity of cervical cancer cells

AIM: To investigate the effect of Linc00152 on the viability, apoptosis and radiosensitivity of cervical cancer cells. METHODS: RT-qPCR was used to detect the expression levels of Linc00152 and microRNA-376c-3p(miR-376c-3p) in human cervical cancer HeLa cells and SiHa cells, and normal cervical Ect1/E6E7 cells. The cervical cancer HeLa cells with low Linc00152 expression or miR-376c-3p over-expression were established. MTT assay, flow cytometry, colony formation assay and Western blot were used to determine the cell viability, apoptosis, radiosensitivity and related protein expression. The dual-luciferase reporter assay was used to verify the regulatory relationship between Linc00152 and miR-376c-3p in the HeLa cells. RESULTS: Compared with the Ect1/E6E7 cells, Linc00152 was up-regulated in the HeLa cells and SiHa cells, and miR-376c-3p was down-regulated (P < 0.05). Low expression of Linc00152 or over-expression of miR-376c-3p inhibited the viability of HeLa cells, induced apoptosis, enhanced the radiosensitivity, inhibited the protein expression of cyclin D and Bcl-2, and promoted the protein expression of P21 and Bax (P < 0.05). Linc00152 negatively regulated miR-376c-3p expression in the HeLa cells, and inhibition of miR-376c-3p expression reversed the effect of low expression of Linc00152 on HeLa cell viability, apoptosis and radiosensitivity. CONCLUSION: Linc00152 is highly expressed in the cervical cancer cells. Linc00152 affects the viability, apoptosis and radiosensitivity of HeLa cells by targeting miR-376c-3p, which is a potential diagnosis and treatment target for cervical cancer.     

Silencing of TKTL1 gene by siRNA down-regulates HIF-1α expression and activity of glycolytic key enzymes in human cervical cancer cells

AIM：To explore the relationship between the expression of transketolase-like gene 1 (TKTL1) and glycolysis metabolism in human cervical cells. METHODS：The changes of hypoxia-inducible factor 1α (HIF-1α) expression and the activity of glycolytic key enzymes, hexokinase Ⅱ (HK-Ⅱ) and lactate dehydrogenase (LDH), under hypoxia in human cervical cell line HeLa were observed after TKTL1 was knockdown by siRNA. The specific siRNA expression vector targeting TKTL1 gene was constructed, and the recombinant plasmid was transfected into HeLa cells. The effects of TKTL1 silencing were evaluated by detecting transketolase (TKT) activity and TKTL1 mRNA expression using RT-PCR. The changes of HIF-1α expression and HK-Ⅱ expression, and HK-Ⅱ and LDH activity were also observed in transfected HeLa cells. RESULTS：The mRNA expression of TKTL1 and the activity of TKT decreased significantly (P<0.01) after TKTL1 silencing. Meanwhile, all HIF-1α expression, HK-Ⅱexpression, and HK-Ⅱ and LDH activity decreased significantly compared with the untransfected cells (P<0.01). CONCLUSION：Silencing of TKTL1 gene in human cervical cancer cells by siRNA down-regulates HIF-1α expression and the activity of glycolytic key enzymes, thus changing the malignant phenotype of carcinoma cells.     

Immune function of dendritic cells in patients with hepatocellular carcinoma

AIM: To investigate the immune function of dendritic cells (DCs) in patients with hepatocellular carcinoma(HCC). METHODS: The DCs were cultured from human peripheral blood mononuclear cells (PBMC) by using GM-CSF and IL-4 for 7 days. Surface molecules CD86, HLA-DR of DCs were detected by flow cytometry. IL-12 production by DCs and IFN-γ production by T cells was measured with ELISA and ELISPOT, respectively. Allogenic mixed lymphocyte reaction was detected by MTT assay. RESULTS: CD86 expression in DCs in HCC patients were markedly lower than that in health control (91.7％ vs 83.5%, P<0.05). IL-12 production by DCs had no significant difference between the HCC patients and the health control ［(324.6±171.0)ng/L vs (436.5±142.7)ng/L, P>0.05］. However, after stimulated DCs with LPS, IL-12 production in HCC patients was significantly lower than that in health control ［(478.6±142.7)ng/L vs (630.0±151.9)ng/L, P<0.05］. IFN-γ production by T cells and T cell proliferation index (PI) in the HCC patients were all significantly lower than those in health control ［(IFN-γ: 133.4±51.2)103U/L vs (183.0±60.2)103U/L, P<0.05; PI: 2.3±0.7 vs 3.5±0.8, P<0.01］. CTL killing activity assay indicated that DC-induced CTL killing activity in HCC group was significantly lower than that in health group when the E/T ratio was 10∶1 and 20∶1, respectively. CONCLUSION: The immune function of DCs and T cells in the patients with HCC are significantly decreased. The CTL killing activity of HCC group is also markedly decreased.     

Mechanism of miR-30c over-expression inhibiting malignant phenotypes of cervical cancer cells

AIM:To investigate the molecule mechanism of microRNA (miR)-30c over-expression inhibiting malignant phenotypes of cervical cancer cells. METHODS:Cervical cancer cell lines C33A, HeLa, SiHa and CaSki were transfected with pGenesil-1-miR-30c plasmid using Lipofectamine 2000 kit, and the expression of miR-30c was determined by TaqMan real-time PCR. The cell viability inhibition rate, colony formation ability, migration rate and apoptotic rate were measured by MTT assay, colony formation assay, Transwell experiment, and flow cytometry with Annexin V-FITC staining. The protein expression of Bax, Bcl-2, matrix metalloproteinase (MMP)-9, MMP-13 and tissue inhibitor of metalloprotei-nase-1 (TIMP-1) was detected by Western blot. RESULTS:The expression levels of miRNA-30c in the cervical cancer cell lines transfected with pGenesil-1-miR-30c plasmid were significantly higher than those in negative control groups (cell lines transfected with pGenesil-1 plasmid) (P<0.01). Significantly increased cell viability inhibition rate, and decreased colony formation ability and migration rate were found in the cervical cancer cell lines over-expressing miR-30c as compared with negative control groups (P<0.05). The apoptotic rate in the cervical cancer cell lines over-expressing miR-30c was dramatically higher than that in control groups (P<0.05). Over-expression of miR-30c in cervical cancer cells promoted the protein expression of Bax and TIMP-1, and decreased the protein expression of Bcl-2 and MMP-13 (P<0.05 or P<0.01). CONCLUSION:Over-expression of miR-30c significantly inhibits the viability and migration, and induces apoptosis of cervical cancer cells. The mechanism may be related to activating apoptosis pathway and inhibiting MMP-13 protein expression.     

Antitumor effect of imperatorin enhances cytotoxicity of doxorubicin to HeLa cells

AIM: To determine whether imperatorin would enhance the effect of doxorubicin therapy on cervical cancer in vitro.METHODS: The viability of HeLa cells treated with imperatorin and doxorubicin was determined by MTT assay in vitro. The expression of Bcl-2 protein family(Mcl-1, Bcl-2, Bcl-xL, Bad and Bax) in HeLa cells treated with imperatorin and doxorubicin was evaluated by Western blot analysis. The apoptosis and mitochondrial membrane potential(ΔΨ_m) in the HeLa cells treated with imperatorin and doxorubicin were analyzed by flow cytometry. A Mcl-1 expression vector was constructed, and its role in the cytotoxicity of imperatorin plus doxorubicin to HeLa cells was detected by MTT assay.RESULTS: Addition of imperatorin significantly enhanced the cytotoxicity of doxorubicin to HeLa cells in vitro. Mcl-1 expression was down-regulated by imperatorin but was not influenced by doxorubicin in the HeLa cells. A combination of imperatorin and doxorubicin induced apoptosis and ΔΨ_m collapse more significantly compared with the treatment with imperatorin or doxorubicin alone. Furthermore, the imperatorin-induced sensitization for doxorubicin cytotoxicity to HeLa cells was abolished by the transfection with Mcl-1 expression plasmid.CONCLUSION: The combination of doxorubicin with imperatorin enhances the antitumor effect of doxorubicin on cervical cancer cells via targeting Mcl-1.     

Effect of berberine on the adhesion between human umbilical vein endothelial cells and human pulmonary carcinoma cells

AIM: To study the mechanism of berberine on the adhesion between human pulmonary carcinoma cells (PG cells) and HUVECs. METHODS: The effect of berberine (2.5-40 mg/L) on the proliferation of HUVECs was detected by MTT method. Further, PG cells were treated with berberine at doses of 2.5, 5, 10 mg/L for 6, 12, 24 h. The adhesion between PG cells and HUVECs was determined by rose bengal staining. The expression of CD44s on PG cells were determined by fluorescence antibody staining. Fluorescence anisotropy imaging system was used to assay the fluidity of PG cell membrane. RESULTS: Berberine at concentrations of 2.5, 5, 10 mg/L were the safety doses to the proliferation of HUVECs treated for 6, 12, 24 h. Berberine inhibited the adhesion between PG cells and HUVECs significantly in a dose-dependent manner (P<0.05 or P<0.01). Meanwhile, berberine increased the expression of CD44s on PG cells (P<0.05 or P<0.01). Berberine decreased the fluidity of PG cell membrane in a dose-dependent manner after 24 h incubation. CONCLUSION: Berberine inhibits the adhesion between PG cells and HUVECs by regulating the expression of adhesion molecules and the fluidity of cell membrane on PG cells.     

Study on the activation of blood platelets by propylene-acidamide grafted polypropylene membrane in vitro

AIM: To evaluate the blood compatibility of a new bioartificial reactor membranous material (propylene-acidamide grafted polypropylene membrane, PP-g-AAm) in vitro. METHODS: Contacted PP-g-AAm membrane and PP (polypropylene) membrane with platelet-rich plasma in a swing bed, 37 ℃, to simulate the conditions in vivo, and another group of PRP without any membranes was set as control group. ELISA was used to study the expression of β-thromboglobulin, and flow cytometry was used to study CD62P and CD63 expression of the activated blood platelets after contacting the two kinds of membranes with PRP. Scanning electrical microscopy was used to study the configuration and numbers of platelet cells adhered on the membranes. RESULTS: After contacting with PRP 30 min, β-TG expression showed marked difference between the two kinds of material groups and the control group (P<0.01, P<0.05), and the difference between the two kinds of membrane groups was also significant (P<0.05). There were obviously differences on the expression of CD62P and CD63 between the two kinds of membranes after contacting with PRP for 30 min (P<0.05，P<0.01). When enlarged 10 000 times, the disfiguration of the platelet cells adhered on the two kinds of membranes after one hour were found by scanning electrical microscopy, and the numbers of platelets on the PP membrane were more than the PP-g-AAm membrane markedly. CONCLUSION: The PP-g-AAm membrane has better blood compatibility than the PP membrane.     

Expression of SCD-1 in cervical carcinoma and effect of its down-regulation on proliferation and apoptosis of cervical carcinoma cells

AIM:To examine the expression of stearoyl-CoA desaturase-1 (SCD-1) in normal cervical tissues, cervical squamous cell carcinoma tissues, and cervical carcinoma cell lines HeLa, SiHa and CaSki, and to investigate the effect of down-regulation of SCD-1 on the proliferation and apoptosis of cervical carcinoma cells. METHODS:The expression of SCD-1 was detected by Western blotting in normal cervical tissues, cervical squamous cell carcinoma tissues, and cervical carcinoma cell lines HeLa, SiHa and CaSki. SCD-1 siRNA and control siRNA were utilized to transfect CaSki cells by Lipofectamine 2000, and SCD-1 protein level was determined by Western blotting after transfection. Furthermore, CCK-8 and flow cytometry were utilized to investigate the changes of cell proliferation and apoptosis after transfection with SCD-1 siRNA in CaSki cells. Subsequently, the activities of caspase-3 and caspase-9 were analyzed by Caspase-Glo3/7 and 9 detection kit after transfection with SCD-1 siRNA in CaSki cells. Finally, the protein expression of Bcl-2 and Bax was detected by Western blotting. RESULTS:The protein expression of SCD-1 in cervical squamous cell carcinoma tissues was significantly higher than that in normal cervical tissues, and the protein expression of SCD-1 in the 3 cervical carcinoma cell lines was obviously higher than that in normal cervical tissues, in which CaSki cells displayed the highest SCD-1 protein level. In addition, the protein expression of SCD-1 in SCD-1 siRNA group was significantly lower than that in untreated group and control siRNA group. Compared with untreated group and control siRNA group, the proliferation of CaSki cells was markedly inhibited in SCD-1 siRNA group. Early apoptotic rate in SCD-1 siRNA group was evidently higher than that in untreated group and control siRNA group. The activities of caspase-3 and caspase-9, and the level of Bax protein were significantly elevated, and the protein level of Bcl-2 was obviously reduced after transfection with SCD-1 siRNA in CaSki cells. CONCLUSION: SCD-1 may play an important role in the occurrence and development of cervical carcinoma, and its down-regulation, which mediates cell proliferation inhibition and apoptosis, may be tightly associated with the activities of caspase-3 and caspase-9, and the protein expression of Bcl-2 and Bax.