Blockade of autophagy aggravates endoplasmic reticulum stress and improves Paclitaxel cytotoxicity in human cervical cancer cells.

PURPOSE: Autophagy is one of the ways to degrade unfolded proteins after endoplasmic reticulum (ER) stress. The purpose of this study is to determine whether a blockade of autophagy leads to aggravated endoplasmic reticulum stress, which then induces cells apoptosis in HeLa cells treated with paclitaxel. MATERIALS AND METHODS: Autophagy activation and the proapoptotic effects were characterized using monodansylcadaverine labeling and Hoechest staining, respectively. A Western blot analysis was used to detect the expression of apoptotic and autophagy-related genes. A flow cytometry was used to assess the cell apoptosis ratio. RESULTS: Paclitaxel exposure induced the aggregation of autophagosomes in the cytoplasms of cervical cancer HeLa cells. The expression of Beclin 1 and LC3 II were upregulated, but p62 was downregulated, which suggests that autophagy was promoted by paclitaxel. On the other hand, the expression of GRP78 obviously increased, suggesting that ER stress was induced after paclitaxel treatment. The cell proliferation assay indicated that a knockdown of Beclin 1 sensitized HeLa cells to paclitaxel. Furthermore, paclitaxel-mediated apoptotic cell death was further potentiated by the pretreatment with autophagy inhibitor chloroquine or small interfering RNA against Beclin 1. These results suggest that an induction of autophagy by paclitaxel may induce cell survival rather than cell death in HeLa cells; moreover, inhibition of autophagy led to an aggravated ER stress and an induction of downstream apoptosis. CONCLUSION: Our results reveal autophagy induced by paclitaxel conferred protection of tumor cells against apoptosis, and blockade of autophagy subsequently aggravated ER stress, enhancing the apoptosis associated with paclitaxel treatment in HeLa cells.

Expression of Derlin-1 and its effect on expression of autophagy marker genes under endoplasmic reticulum stress in lung cancer cells.

BACKGROUND: Recent findings indicated that Derlin-1 has an important function in tumour progression. In this study, we aimed to determine whether Derlin-1 has an oncogene function as a cross-talk molecule with autophagy. METHODS: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot. Autophagy was analysed by fluorescence microscopy after staining the cancer cells with monodansylcadaverine. The interaction between Derlin-1 and other proteins was identified using co-immunoprecipitation assay. RESULTS: Our study demonstrated high Derlin-1 expression levels in most non-small lung cancer cell lines. Derlin-1 expression was enhanced under endoplasmic reticulum (ER) stress. Previous studies revealed that TM triggers the initiation of autophagy by activating Beclin 1, converting LC3I to LC3II and degrading p62. Knockdown of Derlin-1 did not affect Beclin 1 and LC3II expression but disrupted the degradation of p62 under ER stress, which resulted in the blockage of autophagy flux. Furthermore, Derlin-1 and p62 were observed to interact under ER stress. CONCLUSION: This study is the first report about the interaction between Derlin-1 and p62. Derlin-1 may function in tumour progression partially by interacting with p62.

Inhibition of autophagy-potentiated chemosensitivity to cisplatin in laryngeal cancer Hep-2 cells.

OBJECTIVE: The purposes of this study were to determine whether autophagy was involved in cisplatin (CDDP) resistance and to investigate the role of the autophagy in the regulation of chemosensitivity to CDDP in laryngeal cancer Hep-2 cells. METHODS: A WST-1 assay was performed to determine cell viability and cell proliferation. Autophagy activation and proapoptotic effects were characterized using monodansylcadaverine labeling and Hoechest staining, respectively. Western blot analysis was used to detect the expression of apoptotic and autophagy-related genes. Flow cytometry was used to assess cell apoptosis ratio. RESULTS: Exposure to CDDP induced the aggregation of autophagosomes in the cytoplasms of Hep-2 cells and up-regulated the expression of Beclin 1 and LC3II. However, CDDP treatment could not lead to obvious inhibition of cell proliferation, which implies that the autophagy may protect CDDP-treated cells from undergoing cell death. Meanwhile, the WST-1 assay indicated that knockdown of the autophagic gene Beclin 1 sensitized Hep-2 cells to CDDP. Furthermore, CDDP-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine or small interfering RNA against Beclin 1. For the definite mechanism of Beclin 1-enhancing chemosensitivity to CDDP, we found that Beclin1 augmented CDDP-induced apoptotic signaling via enhancing caspase-9 and caspase-3 activity but not caspase-8. CONCLUSION: Our results suggest that functional autophagy in response to CDDP may lead to cell survival in Hep-2 cells, whereas defective autophagy may contribute to CDDP-induced apoptosis in Hep-2 cells. Thus, modulators of autophagy may be used beneficially as adjunctive therapeutic agents during the treatment of laryngeal cancer with CDDP therapy.

Radical trachelectomy versus radical hysterectomy for the treatment of early cervical cancer: a systematic review.

OBJECTIVE: To assess the efficacy and safety of radical trachelectomy (RT) and radical hysterectomy (RH) for patients with early cervical cancer. DESIGN: Systematic review with meta-analysis. POPULATION: Women who had early cervical cancer. METHODS: Prospective controlled clinical trials comparing RT with RH were identified using a predefined search strategy. Recurrence, five-year recurrence-free survival rate, five-year overall survival rate, postoperative mortality, intraoperative and postoperative complications between the two operations were compared by using the methods provided by the Cochrane Handbook for Systematic Reviews of Interventions. RESULTS: Three controlled clinical trials involving 587 participants were included. Meta-analysis showed that there was no significant difference between the two groups in recurrence rate [1.38; 95% confidence interval (CI) 0.58-3.28, p=0.47], five-year recurrence-free survival rate (1.17; 95% CI 0.54-2.53, p=0.69), five-year overall survival rate (0.86; 95% CI 0.30-2.43, p=0.78), postoperative mortality (1.14; 95% CI 0.42-3.11, p=0.80), intraoperative complications (1.66; 95% CI 0.11-25.28, p=0.72), postoperative complications (0.52; 95% CI 0.11-2.48, p=0.41), blood transfusion (0.29; 95% CI 0.06-1.36, p=0.12) and number of harvested lymph nodes. However, RT, compared with RH, reduced blood loss and shortened duration to normal urine residual volume and postoperative hospital stay. Moreover, RT may achieve to normal conception rates, while RH makes patients sterile. CONCLUSIONS: Radical trachelectomy has similar efficacy and safety to RH as the surgical treatment for early cervical cancer. Moreover, it reduced blood loss and shortened the duration to normal urine residual volumes and postoperative hospital stay. Radical trachelectomy can be used to treat early stage cervical cancer as an alternative operation for patients who wish to preserve fertility.

Clinicopathologic correlations between human papillomavirus 16 infection and Beclin 1 expression in human cervical cancer.

Our earlier study showed that the autophagy gene Beclin 1 could affect cell proliferation in a cervical cancer HeLa cell line. In this study, we examined Beclin 1 protein expression in 81 specimens of cervical squamous carcinoma by immunohistochemistry. Meanwhile, we detected E6 and E7 genes of human papillomavirus 16 in these tissues by polymerase chain reaction. Beclin 1 expression significantly decreased in samples of malignant cervical cancer tissues than in those of normal or cervical intraepithelial neoplasia tissues. The expression of Beclin 1 was associated with pelvic lymph node metastasis and histological grade, but did not correlate with International Federation of Gynecology and Obstetrics stage, age, depth of cervical infiltration, tumor size, and gross type of cervical lesion. The expression of Beclin 1 was not obviously correlated with E6 and E7 genes statistically. Therefore, decreased expression of Beclin 1 may be related to tumorigenesis and the development of cervical cancer, but is not significantly relevant with human papillomavirus 16 infection.

[Effect and mechanism of an autophagy gene beclin 1 on cervical cancer HeLa cells].

OBJECTIVE: To investigate the inhibitory effects and the mechanism of autophagy gene beclin 1 on cervical cancer HeLa cells. METHODS: The eukaryotic expression vector and short hairpin RNA (shRNA) expression vector of beclin 1 were transfected via lipofectamine into HeLa cells. Experimental cells were classified into 5 groups: pcDNA3.1(+)-beclin 1 group, pSUPER-beclin 1 group, pcDNA3.1(+) group, pSUPER group and HeLa group. Real time-PCR and western blot were used for detecting expression of mRNA and protein of beclin 1 and caspase-9 in transfected cells. Flow cytometry was employed to observe the effect of transfection on the apoptosis, and autophagy of HeLa, while proliferation was analyzed by methyl thiazolyl tetrazolium (MTT) assay. The ultrastructural analysis of autophagic vacuoles was under the electron microscope. Five groups cells were seeded subcutaneously on nude mice. The carcinogenic and growth activities of cancer cells in vivo were observed, and immunohistochemistry was used to detect the protein expression of beclin 1 in tumor tissue. RESULTS: (1) The mRNA expression of beclin 1 and caspase-9: pcDNA3.1(+)-beclin 1 group were 994.72 ± 468.76 and 12.88 ± 2.71, pSUPER-beclin 1 group were 0.18 ± 0.63 and 0.11 ± 0.08, pcDNA3.1(+) group were 0.57 ± 0.12 and 4.28 ± 3.25, pSUPER group were 0.67 ± 0.29 and 2.77 ± 1.27, and HeLa group were 0.74 ± 0.25 and 3.67 ± 3.78, respectively. The eukaryotic expression vector pcDNA3.1(+)-beclin 1 significantly improved the expression of mRNA of beclin 1 and caspase-9 in HeLa cells (P < 0.05), and the shRNA expression vector inhibited the expression of mRNA of beclin 1 and caspase-9(P < 0.05). (2) The cell proliferations: pcDNA3.1(+)-beclin 1 vector significantly inhibited the growth of HeLa cells, while pSUPER-beclin 1 vector significantly improved the growth of HeLa cells (P < 0.05). (3) The rate of apoptosis: pcDNA3.1(+)-beclin 1 group was (28.2 ± 2.3)%, pcDNA3.1(+) group was (14.6 ± 4.6)%, pSUPER-beclin 1 group was (5.7 ± 2.0)%, pSUPER group wa (16.2 ± 3.1)%, and HeLa group was (11.2 ± 3.0)%. The pcDNA3.1(+)-beclin 1 vector significantly increased the apoptosis rate, while the pSUPER-beclin 1 vector significantly decreased the apoptosis rate (P < 0.05). (4) The activity of autophagy: more autophagy cells were identified in pcDNA3.1(+)-beclin 1 group; the rate of autophagy of five group were (10.3 ± 1.5)% in pcDNA3.1(+)-beclin 1 group, (3.6 ± 0.8)% in pcDNA3.1(+) group, (1.2 ± 0.3)% in pSUPER-beclin 1 group, (3.2 ± 1.2)% in pSUPER group and (2.2 ± 1.1)% in HeLa group, there was statistical significances between test groups and control groups (P < 0.05). (5) Carcinogenic activity of HeLa cells in nude mice: the duration of tumorigenesis was the longest in pcDNA3.1(+)-beclin 1 group and the shortest in pSUPER-beclin 1 group among all groups. The tumor size began to grow larger from 7th day after injection in pSUPER-beclin 1 group than in control groups (P < 0.05). The tumor size was smaller from 21st day after injection in pcDNA3.1(+)-beclin 1 group than in control groups (P < 0.05). From 28th day after injection, the tumor weigh was (0.52 ± 0.08) g in pSUPER-beclin 1 group, apparently more than HeLa group (0.37 ± 0.12) g and pSUPER group (0.34 ± 0.24) g (P < 0.05). While in pcDNA3.1(+)-beclin 1 group the tumor weighed (0.18 ± 0.12)g, which was lower than HeLa group and pcDNA3.1(+) group(0.34 ± 0.18) g (P < 0.05). CONCLUSIONS: Autophagy gene beclin 1 overexpression can inhibit proliferation and growth of HeLa cells in vitro and in vivo. Beclin 1 not noly participate in the regulation of autophagy signaling, but also play an important role in the regulation of endogenous apoptosis signaling through caspase-9. So it might be one of the new strategies for gene therapy of cervical carcinoma.

Combination of IL-24 and cisplatin inhibits cervical cancer growth in a xenograft nude mice model.

IL-24/mda-7 delivery augments the sensitivity of several tumor types to cisplatin but the underlying mechanism(s) are unclear. Here, we used a cervical cancer xenograft model in nude mice to further elucidate the interaction between IL-24 and cisplatin. Nude mice were inoculated subcutaneously in the left axilla with Hela cells and randomly grouped into 5 treatment schedules: PBS (I); pDC316 vector (II); pDC316-hIL-24 (III); cisplatin (IV); and pDC316-hIL-24 combined with cisplatin (V). Groups III, IV and V showed significant reduction at mean tumor weight by 43%, 50% and 72%, respectively, after 4 weeks in comparison to thePBS and vector control groups. Mitotic counts in groups III, IV and V were also significantly reduced and expression of tumor suppressor gene nm23-H1 protein was significantly higher in groups III and V than in the cisplatin (IV), PBS (1), and vector (II) cases. The cisplatin group exhibited significantly greater weight loss than the other four groups. The mean weight loss of the combined group, while significantly more than in the controls and the IL-24 group, was significantly less than that of the cisplatin group. The IL-24 group and the combined therapy group exhibited enhancing effects on the tumor suppressor gene nm23H1expression.

[Effect of autophagy gene Beclin 1 on the growth of cervical cancer HeLa cells in vitro and vivo].

OBJECTIVE: To investigate the effects of autophagy gene Beclin 1 on growth of cervical cancer HeLa cells in vitro and vivo. METHODS: The eukaryotic expression vector of Beclin1 was constructed and transfected via lipofectamine into HeLa cells. The experimental cells were classified into 3 groups: pcDNA3.1(+)-Beclin1 group,pcDNA3.1(+) group and HeLa group. Real time-ploymerase chain reaction and Western blot were used for detecting expression of Beclin1 mRNA and protein in the transfected cells. Flow cytometry (FCM) was employed to observe the effect of transfection on the apoptosis of HeLa cells, and proliferation was analyzed by MTT assay. The formation of autophagic vacuoles was measured by MDC staining. HeLa cells transfected with plasmid pcDNA3.1(+)-Beclin1 and pcDNA3.1(+) were inoculated subcutaneously in nude mice. The carcinogenic and growth activities of cancer cells in vivo were observed. RESULTS: Eukaryotic expression vector pcDNA3.1(+)-Beclin1 was constructed successfully. It significantly improved the expression of Beclin1 mRNA and protein in HeLa cells. The proliferation of HeLa cells was inhibited, and the inhibition rate was 58.7%. FCM investigation showed that the apoptotic rate was (28.22 ± 2.34)% of pcDNA3.1(+)-Beclin1 group, significantly higher than the (14.6 ± 4.6)% in the pcDNA3.1(+) group and (11.2 ± 3.0)% in the HeLa group (P < 0.05). The monodansylcadaverin (MDC) staining showed significantly more autophagic vacuoles in the pcDNA3.1(+)-Beclin1 group (10.9%) than that in the pcDNA3.1(+) group (3.1%) and HeLa group (2.5%) (P < 0.05). After transfected with vector pcDNA3.1(+)-Beclin1, the carcinogenic activity of HeLa cells was decreased in nude mice, and the inhibition rate of tumor growth was 52.2%. CONCLUSIONS: Autophagy gene Beclin 1 overexpression can inhibit the proliferation and growth of HeLa cells in vitro and vivo,while promote autophagy and apoptosis of HeLa cells. So it might be one of new gene therapy strategies for cervical carcinoma.

[Size distribution of particles collected by passive sampler].

Airborn particulate matters were sampled by two duplicate glass slides coated with thin layer of vaseline laid at the bottom of sampling cylinder of passive sampler for collecting both gaseous and particulate phase semi-volatile organic pollutant. Their size distribution was analyzed and found to be influenced by wind speed and coverage of the fine-screen-mesh (300 mesh) wrapping around the outside of sampling cylinder. In a windless (indoor) and semi-static windy conditions (sealed courtyard), diffusion of coarse particles (> 50 microm) was reduced effectively by covering sampling cylinder with the fine-screen-mesh, and accumulated size distribution curve of PM10 was similar with those collected by an active size-fractionated sampler (cascade impactor). In windy conditions (outdoor), coarse particles entered the sampling cylinder randomly, which is independent with wind speed, while the percentage of fine particulate with size of 3-5 microm decreased and those with size of 6-9 microm increased significantly.

[Growth inhibitory effects of Beclin1 gene on epithelial ovarian cancer SKOV3 cells].

OBJECTIVE: To explore the effect of Beclin1 overexpression on the growth of ovarian carcinoma cell line SKOV3 in vitro and in vivo. METHODS: The recombinant plasmid pcDNA3.1/Beclin1 was constructed and transfected into SKOV3 cells via lipofectamine 2000. MTT assay was used to evaluate the effect of Beclin1 overexpression on the proliferation and growth of the transfected cells, whose apoptosis and autophagy were analyzed by flow cytometry. SKOV3 cells transfected with the plasmids pcDNA3.1/Beclin1 or pcDNA3.1 were inoculated subcutaneously in nude mice, and their carcinogenic and growth activities in vivo were evaluated. RESULTS: MTT assay showed that transfection with pcDNA3.1/Beclin1 significantly inhibited the proliferations of SKOV3 cells, with a cell inhibition rate of 58.68% (P<0.05). The transfection also resulted in a cell apoptosis rate of (21.26-/+3.89)%, significantly higher than that of pcDNA3.1 trasnfection (P<0.05). Flow cytomerty showed that pcDNA3.1/Beclin1 transfection of SKOV3 cells produced a significantly higher MDC fluorescent intensity than pcDNA3.1 transfection. The SKOV3 cells transfected with vector pcDNA3.1/Beclin1 also showed decreased carcinogenic activity in nude mice, with a growth inhibition rate of 50.27%. CONCLUSION: Beclin1 overexpression can inhibit the proliferation and growth of SKOV3 cells in vitro and vivo, suggesting its potential role in gene therapy of ovarian carcinoma.

[Size distribution and shape characteristics of subaerial airborne particles].

This research sampled airborne particles in the typical air polluted city of Shijiazhuang to measure the particle size and shape by the instrument of the CIS-50 and the scan electronic microscope in the non-heating period and heating period. The results show that the subaerial airborne particle size distribution mode is coarse with the size range of 0.8-120 microm, mostly under 10 microm, and the semi-square & square like particle shape is dominant, the sphere like lesser, the acute-angle and lathy like sparse. There exist particle size and shape difference in the non-heating period and heating period influenced greatly by the ground emission. When in the heating period, the particle size average value increases by 53.2% principally in the size range of 5-8 microm, and 10-30 microm secondly. Meanwhile, the number of particles with semi-sphere & sphere like shape increases obviously. These semi-sphere particles are agglomerate of finer spheres derived from combustion in the SEM images. The relationship between particle size and shape is demonstrated by that the percentage of PM5 and the one of the semi-square & square like particles are positively correlative with the r of 0.9458; the one of the semi-sphere & sphere like particles negatively correlative with the r of -0.972 6 respectively.

Beclin 1-mediated macroautophagy involves regulation of caspase-9 expression in cervical cancer HeLa cells.

OBJECTIVE: To investigate the role of Beclin 1 in HeLa cells and to obtain further insight into the relationship between autophagy and apoptosis. METHODS: Beclin 1 silencing was achieved using RNA interference. The expression of gene was measured using quantitative real time RT-PCR and Western blotting. The percentage of apoptotic cells and cell cycle analysis and cell proliferation were assessed by flow cytometry and MTT assay. The ultrastructural analysis was under the electron microscope. RESULTS: In pSUPER-Bec transfectants (Beclin 1 gene partially silenced) the expression of mRNA and protein of Beclin 1 were significantly suppressed in comparison to pSUPER-non (scramble RNA control) or untreated cells in HeLa cells. The growth of transfected cells was promoted, and less apoptosis cells were identified in pSUPER-Bec transfectants compared with pSUPER-non transfectants. Meanwhile pcDNA3.1-Bec transfectants (Beclin 1 gene overexpressed) showed reduction of cell proliferation but augmentation of cell programmed death compared with vector vehicle. The autophagy-promoting activity of beclin 1 in HeLa cells is associated with inhibition of HeLa cellular proliferation, in vivo tumorigenesis in nude mice. The expression pattern of caspase-9 was extraordinarily similar to that of Beclin 1in siRNA against Beclin 1 transfectants and constructive expression of Beclin 1transfectants. CONCLUSION: siRNA against Beclin 1 transfectants promoted the cell proliferation but overexpression of Beclin 1 promoted the autophagy cell death, and in the process of autophagy triggered by Beclin 1 expression followed accordingly the regulation of the expression of caspase-9. We conjecture that the autophagy gene Beclin 1 may be the critical molecular switch that plays an important role in fine tuning the autophagy and apoptosis through caspase-9, and defection of autophagy or apoptosis may be an important mechanism in tumorigenesis.

[Construction of shRNA expression vectors for autophagy gene Beclin 1 and effect of the vectors on transfected HeLa cells in vitro].

OBJECTIVE: Autophagy gene Beclin 1 plays an important role in several types of human cancer. In this study, RNA interference (RNAi) technique was employed to determine the effect of inhibiting Beclin 1 on the growth of tumor cells. METHODS: According to the encoding sequence of mRNA of Beclin 1, the target site for the RNAi technique was designed and the vector for shRNA (short hairpin RNA) expression in tumor cells was constructed. The HeLa cell line was transfected with the sfRNA to inhibit the expression of Beclin 1. RESULTS: The constructed vector significantly inhibited the expression of the mRNA and protein of Beclin 1 in the HeLa cells. The growth of the transfected cells was promoted, and less apoptosis cells were identified in these cells. CONCLUSIONS: The shRNA expression vector can effectively inhibit the expression of Beclin 1 in the HeLa cells, and promote the growth of HeLa cells.

[Expression and involved signal transduction pathway of autophagy gene Beclin 1 in epithelial ovarian cancer].

OBJECTIVE: To investigate the relationship between the autophagy gene Beclin 1 involving the PI3K/PKB signaling pathway and the occurrence, development of epithelial ovarian carcinoma. METHODS: The expression of Beclin 1, Class I PI3K (p110alpha), Class III PI3K (hvps34) or p-PKB was, by immunohistochemistry, detected respectively in 25 normal ovarian tissues, 25 benign neoplasia tissues, 19 borderline tissues, and 69 epithelial ovarian carcinoma tissues. RESULTS: The higher expressions of Beclin 1 and hvps34 were found in normal and benign ovarian neoplasia tissues; the expressions were reduced in the borderline lesion tissue; and the lowest level of expressions could be detected in the ovarian carcinoma tissue (P < 0.05). The expressions of p110alpha and p-PKB increased slightly in borderline ovarian tissue, and were higher in the epithelial ovarian carcinoma tissue than other three groups (P < 0.05). Beclin 1 expressions in the epithelial ovarian cancer tissues with stage I - II, high-middle grade differentiation and negative lymph node metastasis were higher than those with stage III - IV, low grade differentiation and positive lymph node metastasis, but the expressions of p110alpha and p-PKB in were lower (P < 0.05). CONCLUSION: Beclin 1 expression is down-regulated in epithelial ovarian cancer tissue while the p110alpha, hvps34 and p-PKB are having the abnormal expressions on PI3K/PKB signaling pathway, which may be correlated with the occurrence and development of epithelial ovarian carcinoma.

[Correlation of autophagy gene Beclin1 to tumorigenesis and development of epithelial ovarian cancer].

BACKGROUND & OBJECTIVE: Some studies have showed that autophagy suppression may result in malignant transformation, and the inactivation of autophagy gene Beclin1 induces malignancy. This study was to investigate the role of Beclin1 in the tumorigenesis and development of epithelial ovarian carcinoma, and to explore the effect of Beclin1 overexpression on the growth of ovarian carcinoma cell line SKOV3 in vitro. METHODS: The expression of Beclin1 in 25 specimens of normal ovarian tissue, 25 specimens of benign ovarian neoplasia, 19 specimens of borderline ovarian tissue, and 69 specimens of epithelial ovarian carcinoma was detected by immunohistochemistry. Eukaryotic expression vector pcDNA3.1/Beclin1 was constructed and transfected into SKOV3 cellsû plasmid pcDNA3.1 was used as control. The effect of Beclin1 overexpression on the proliferation of SKOV3 cells was evaluated by MTT assay. Cell apoptosis was measured by flow cytometry (FCM). RESULTS: The expression of Beclin1 was high in normal and benign ovarian neoplasia tissues, and there was no significant difference between the 2 groups (P>0.05). Reduced Beclin1 expression was observed in borderline lesions, and the lowest level was detected in ovarian carcinoma tissues (P<0.05). The inhibition rate was significantly higher in pcDNA3.1/Beclin1-SKOV3 cells than in pcDNA3.1-SKOV3 cells [(68.75+/-5.10)% vs. (10.91+/-4.20)%, P<0.05]. At 72 h after transfection, the apoptosis rate was significantly higher in pcDNA3.1/Beclin1-SKOV3 cells than in pcDNA3.1-SKOV3 cells and SKOV3 cells [(19.07+/-0.65)% vs. (4.30+/-0.50)% and (3.87+/-0.84)%, P<0.05]. CONCLUSIONS: Beclin1 expression is down-regulated in epithelial ovarian cancer tissues, which may relate to tumorigenesis and development of epithelial ovarian cancer. Beclin1 overexpression can inhibit proliferation and induce apoptosis of SKOV3 cells.

[Expression and clinical significance of autophagy gene Beclin 1 in cervical squamous cell carcinoma].

OBJECTIVE: Autophagy gene Beclin 1 plays an important role in several types of human cancers. So we, in this study, employed the immunohistochemical manner to detect the Beclin 1 gene expression and explore its clinical significance in cervical aquamous cell carcinoma. METHODS: SP immunohistochemistry technique was used to detect the expression of Beclin 1 gene in specimens of 81 cervical squamous cell carcinoma, 20 cervical intraepithelial neoplasm (CIN, II - III), and 20 normal cervix. Correlations between the expressions of Beclin 1 gene and the clinicopathologic factors of cervical squamous cell carcinoma were statistically analyzed. RESULTS: The rates of negative, weak, strong expression of Beclin 1 in cervical squamous cell carcinoma were 43.2% (35/81), 34.6% (28/81) or 22.2% (18/81) respectively, and the significantly lower than those in normal cervix and CIN II - III (P = 0.011). The Beclin 1 expressions did not associate with FIGO stage, age, depth of cervical infiltration, tumor size, and gross type of cervical lesion (P < 0.05), but were related to pelvic lymph node metastases and histological tumor grade (P < 0.05). CONCLUSION: s Expression of autophagy gene Beclin 1 decreases in cervical aquamous cell carcinoma, and is closely related to pelvic lymph node metastases and histological tumor grade.