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Objective@#To explore effect of AMP-activated protein kinase (AMPK) /mammalian target of rapamycin (mTOR) /ribosomal protein S6 kinase-1 (S6K1) signaling pathways and the insulin-sensitizing effect by adiponectin in endometrial cancer HEC-1B cells.@*Methods@#The experiments were divided into 4 groups, adiponectin (Ad) group (HEC-1B cells treated with 20 μg/ml adiponectin for 30 minutes) , inhibitor group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes) , inhibitor+ Ad group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes following incubation with 20 μg/ml adiponectin for 30 minutes) , control group (only added the culture medium without serum DMEM) . (1) Real-time quantitative PCR and western blot analysis were used to detect the level of mRNA and protein of adiponectin receptor (AdipoR) 1 and AdipoR2. (2) Western blot analysis were used to detect phosphorylation of AMPK, mTOR, S6K1 or insulin receptor substrate 1 (IRS1) protein expression with stimulation in different concentrations of adiponectin (2.5, 5, 10, and 20 μg/ml) , or following incubation with insulin 50 nmol/L for 5 minutes; or treated with 20 μg/ml adiponectin for different times (15, 30, 45, and 60 minutes) , or following incubation with insulin 50 nmol/L for 5 minutes. (3) Cell counting kit-8 (CCK-8) assay was performed to investigate the cell proliferation, and transwell chamber assay was used to detect the cell migration in different groups.@*Results@#(1) The relative expression level of AdipoR1 mRNA and protein were higher than AdipoR2 in HEC-1B cell (8.50±0.09 to 1.00±0.00, and 0.91±0.03 to 0.69±0.03; P<0.05) . (2) The phosphorylation level of p-AMPK was significantly induced, and the phosphorylation level of p-mTOR and p-S6K1 proteins, and 20 μg/ml adiponectin at 30 minutes, AMPK protein had the highest level of activation. (3) Adiponectin induces increased tyrosine phosphorylation of IRS1 in a time-and concentration-dependent manner. (4) The proliferation inhibition ratio in Ad group (0.68±0.34) % was much more than that in inhibitor+Ad group (0.24±0.04) % (t=17.88, P<0.05) . The number of cell migration in Ad group (77±8) was much more than that in inhibitor+Ad group (132±13; t=-7.34, P<0.05) .@*Conclusions@#Adiponectin maybe inhibit proliferation and migration of endometrial cancer cells through AMPK/mTOR/S6K1 signal pathway. Adiponectin insensitizes insulin signaling may by regulating by the AMPK/S6K1/IRS1 pathway.
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Objective@#To evaluate the short-term and long-term outcomes after laparoscopic surgery compared with traditional laparotomy in cases of stage ⅠA2-ⅡA2 cervical cancer.@*Methods@#We conducted a retrospective study on the clinical data of 1 863 patients diagnosed as FIGO stages ⅠA2-ⅡA2 cervical cancer in 6 third-grade class-A hospitals in Guangxi province between January 2007 and May 2014. One thousand and seventy-one received laparoscopy, and 792 received laparotomy. T-test, U-test and χ2 test were used to compare the short-term and long-term outcomes. The short-term outcomes included surgical related outcomes and operative complications, and the long-term outcomes included quality of life (pelvic floor functions and sexual functions), survival and recurrence. Pelvic floor function and sexual function were assessed with the International Consultation on Incontinence Quesonnaire Female Lower Urinary tract(ICIQ-FLUTS) and the Female Sexual Function Inventory (FSFI), respectively. Survival rates were estimated by Kaplan-Meier analysis. The survival curves were compared with Log-rank test. Cox regression analysis was used to evaluaterisk factors for prognosis.@*Results@#(1)The short-term outcomes : There were significant difference in operative time([(257±69) vs(238±56)min], estimated blood loss[(358±314) vs(707±431)ml], anus exhausting time[(2.5±0.9) vs (2.9±0.8)d], preserved days of catheter[(15±7) vs(18±9)d], and post-operative length of stay[(19±16) vs (30±21)d] between the laparoscopic surgery group and the opensurgery group(P<0.05). There was no significant difference in lymph nodes yielded[(21±9) vs (21±11)], left parametrial width[(2.5±0.8) vs (2.7±0.7)cm], right parametrial width [(2.6±0.3) vs (2.7±0.2)cm], vaginal cuff length[(2.4±0.7) vs (2.2±0.7)cm] between the laparoscopic surgery group and the opensurgery group(P>0.05). The intra-operative complications occurred in 8.1%(87/1 071)in the laparoscopic surgery group and in 10.7%(85/792)in the open surgery group(P>0.05). However, the complications of vascular injury in the laparoscopic surgery group[2.6%(28/1 071)]was lower than that in the open surgery group[7.7%(61/792), P<0.001]. The laparoscopic surgery exhibited lower post- operative complication rate [33.8%(362/1 071)vs 40.2%(318/792), P<0.05] and poorer wound healing rate [0.7%(7/1 071)vs 4.0%(32/792), P<0.05]. (2)The long-term outcomes(Hierarchical analysis): The overall incontinence in ICIQ-FLUTS questionnaire in nerve-sparing laparoscopic group [28.4%(67/236)] was lower than that in the open surgery group [35.9%(71/198), P=0.004] . However, There was no significant difference in degree of incontinence between the two groups(P>0.05). The overall sexual dysfunction in FSFI questionnaire after 12 months of postoperative in the nerve-sparing laparoscopic group [47.0%(111/236)]was lower than that in the open surgery group [58.6%(116/198), P=0.001], and the six different dimension scores in the laparoscopic surgery group were higher than that in the open surgery group (P<0.05). The recurrence rate was 3.5%(35/1 007)in the laparoscopicsurgery group and 4.7%(35/740)in the open surgery group(P>0.05). The 5-year OS was 94.0% for the laparoscopic surgery group and 90.2% for the open surgery group(P>0.05), and the 5-year DFS was 93.9% for the laparoscopic surgery group and 89.1% for the open surgery group(P>0.05). (3) Prognostic fators: In univariate analysis, tumor dimension, clinical stage, deep stromal invasion, LVSI, and retroperitoneal lymph node metastasis signficantly affected 5-year OS and 5-year DFS(P<0.05); In multivariate analyses, LVSI, deep stromal invasion and LN metastasis were independent prognostic factors(P<0.05).@*Conclusions@#Laparoscopy can reduceestimated blood loss, accelerate postoperative recovery and improve the quality of life after surgery compared to laparotomy, and it ensures the same oncological results as open surgery. Laparoscopic approach is a safe and effective treatment for early-stage cervical cancer.
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Objective To discuss the risk factors and prognosis of gynecologic cancer patients with deep venous thrombosis(DVT). Methods Data from gynecologic cancer patients diagnosed by cytology or histopathology in Affiliated Tumor Hospital of Guangxi Medical University between Jan. 1994 and Sep. 2014 were collected,including 106 cases in the DVT group, according to 1:1 proportion by the computer random method to selecting patients without DVT as the control group. The follow-up deadline was March 31, 2015. The median follow-up time of DVT group was 27.0 months (range, 1 to 169 months), while the control groupwas 33.5 months (range,1 to 125 months). Univariate analysis was performed by two independent sample t test or χ2 test. Multivariate analysis was performed by logistic regression analysis. The Kaplan-Meier curve was used to estimate the survival analysis. Results (1) The univariate analysis showed that body mass index (BMI), hypertension, diabetes, history of thrombosis, tumor stage, blood transfusion, stimulating factor, white blood cell (WBC), platelet (PLT), prothrombin time (PT) and fibrinogen (FIB) were statistically significant associated with DVT (P<0.05). Multivariate analysis showed that tumor stage, stimulating factor, WBC, PT and FIB may be the independent risk factors of gynecologic cancer with DVT (P<0.05). (2) The median survival time in DVT group was 66 months, while the control group was 102 months(χ2=7.039, P=0.008). The overall survival and progression-free survival in the DVT group were statistically significant lower than those in the control group (P<0.05). The tumor stage, the scope of DVT (whether with pulmonary embolism) and the treatment of DVT were the effective factors influenced the prognosis of gynecologic oncology patients with DVT (P<0.05). Cox regression model showed that tumor stage and the scope of DVT were the independent risk factors (P<0.01). Conclusions Gynecologic cancer with DVT is the common effect of various risk factors. We should identify the risk factors for high-risk patients and take preventive measures actively to reduce the deep venous thromboembolism, then improve the survival of patients and their prognosis.
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Objective To explore the effects of mitogen-activated protein kinase (MAPK) pathway by estradiol induced vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in endometrial cancer Ishikawa cells.Methods The experiments were divided into 4 groups:E2 group (Ishikawa cells treated with 1 p mol/L estradiol for 30 minutes); inhibitor group:including Ishikawa cells treated with 10 μmol/L Bibf1 120 (Bibf1 120 group),or treated with 2.5 μmol/L Ponatinib (Ponatinib group),or treated with 10 p mol/L U0126 (U0126 group) for 60 minutes; inhibitor + E2 group:including Ishikawa cells treated with 10 μmol/L Bibf1120 (Bibf1120 + E2 group),or treated with 2.5 μmol/L Ponatinib (Ponatinib + E2 group),or treated with 10 μmol/L U0126 (U0126+ E2 group) for 60 minutes following incubation with 1 μmol/L estradiol for 30 minutes; control group:only adding the culture medium without serum DMEM.(1) Western blot analysis was used to detect phosphorylation extracellular signal-regulated kinase 1/2(p-ERK 1/2) protein expression with stimulation in different concentrations of estradiol (0.01,0.1,1,10,100 μmol/L).(2) Quantitative fluorescent reverse transcription (qRT)-PCR and western blot analysis was used to test the level of mRNA and protein of VEGF,bFGF,MAPK kinase 1/2 (MEK1/2),extracellular signal-regulated kinase 1/2 (ERK1/2),p-ERK1/2 and phosphorylation MEK1/2 (p-MEK1/2).Flow cytometry were used to examine the cell cycle,and transwell chamber assay were used to detect the cell migration in different groups.Results The expression of the p-ERK1/2 protein at 0.01,0.1,1,10,100 μ mol/L were 0.16±0.03,0.10±0.03,0.41 ±0.04,0.19±0.03,0.19±0.03,there were significantly higher than that in control group(0.05±0.00,P＜0.05),and which was more obvious at the concentration of 1 μmol/L estradiol.The expression level of VEGF,bFGF mRNA and protein in E2 group were higher than those in the control group (P＜O.05).VEGF mRNA and protein in Bibf1120+E2 group were higher than those in E2 group.The expression of MEK1/2,ERK1/2 mRNA protein in E2 group were higher than those in control group (P＜0.05).The expression of MEK1/2,ERK1/2 mRNA or p-MEK1/2,p-ERK1/2 protein in Bibf1120 + E2 group,Ponatinib+E2 group or U0126+E2 group were lower than those in E2 group(all P＜0.05).Percentage of G1 phase [(53.6±3.2)％] and S phase[(29.2±4.2)％] in E2 group was significantly different with those in control group respectively(P＜0.05).Percentage of G1 phase[(66.8±2.6)％,(63.1±2.6)％ and (63.3±0.4)％] and S phase [(25.4±1.9)％,(25.0±3.8)％ and(23.8±0.5)％] in U0126+E2 group,Bibf1120+E2 group or Ponatinib +E2 group was also significantly different with those in control group (all P＜0.05); percentage of G1 phase and S phase in U0126+E2 group was significant difference with those in Bibf1120+E2 group or ponatinib+E2 group (P＜0.05).The number of cell colony in E2 group (110± 17) was more than those in control group (65±8) ;the number of cell colony in U0126+E2 group(28±4),Bibf1120+E2 group(38±5) or Ponatinib+E2group(42±6) were significant different with those in E2 group (P＜0.05),the number of cell colony in U0126+E2 group was significant difference with those in Bibf1 120+E2 group or Ponatinib+E2 group (all P＜0.05).The results shown that the abilities of proliferation and cell migration were significantly increased in cells after estradiol stimulation.Conclusion Estradiol inducing the production of VEGF and bFGF could activate MAPK pathway through ER-independent manner,further promote development.
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<p><b>OBJECTIVE</b>The aim of this study was to explore whether estradiol induces the expression of VEGF and bFGF in the endometrial cancer Ishikawa cells by activation of NF-κB via AKT pathway, and its effect on cell proliferation.</p><p><b>METHODS</b>Western blot was used to detect the AKT protein expression in Ishikawa cells after stimulation with estradiol, and the effect of AKT inhibitor or ER inhibitor on the activation of AKT. TransAM kit was used to detect the NF-κB p65 activity. qPCR and Western blot were used to detect the expression of VEGF and bFGF mRNA and proteins in the Ishikawa cells after estradiol treatment (E2 group), and pretreated with AKT inhibitor (AKT group) or ER inhibitor (ER group) or NF-κB inhibitor (NF-κB group), following the estradiol treatment. Flow cytometry and CFSE (carboxyfluorescein diacetate, succinimidyl ester) staining were used to examine the cell proliferation. Transwell was used to detect the migration ability of Ishikawa cells.</p><p><b>RESULTS</b>Expression of p-AKT protein in the Ishikawa cells was markedly higher than that in the control group (P < 0.05). Expressions of p-AKT protein in the AKT and ER groups were significantly decreased than that in the E2 group (P < 0.05). The NF-κB activity was highest after stimulation with 1×10(-6) mol/L estradiol for 30 min to 1 h. AKT inhibitor significantly reduced the NF-κB activity (P < 0.05). The expressions of VEGF and bFGF mRNA and proteins in the E2 group were significantly increased than that in the control group (P < 0.05), and their expression in the AKT, ER and NF-κB groups were significantly decreased than that in the E2 group (P < 0.05). The proliferation and migration abilities of the Ishikawa cells were significantly increased after estradiol stimulation.</p><p><b>CONCLUSIONS</b>Estradiol induces the production of VEGF and bFGF through activating NF-κB via AKT pathway, and enhances the proliferation and migration ability of cancer cells.</p>
Subject(s)
Female , Humans , Cell Line, Tumor , Cell Proliferation , Endometrial Neoplasms , Estradiol , Metabolism , NF-kappa B , Metabolism , Neovascularization, Pathologic , Metabolism , RNA, Messenger , Signal TransductionABSTRACT
Background and purpose:The occurrence of endometrial cancer may be related to the persistent stimulus of endogenous and exogenous estrogen without progesterone antagonist. But how does estrogen regulate cell proliferation is still unknown. AKT pathway is the most important signal transduction way to mediate proliferation in the cells. The main aim was to study whether estradiol induces the expression of VEGF, bFGF and IL-8 in the endometrial cancer HEC-1A cells by activating AKT, and its effect on proliferation. Methods:Western blot was used to detect the expression of AKT protein in HEC-1A cells after estradiol stimulation, AKT inhibitor or ER inhibitor stimulation followed by estradiol. Real-time PCR and ELISA were used to detect the gene and protein expression of VEGF, bFGF and IL-8 in different inhibitors. Cell colony formation assay, lfow cytometry and CFSE assay were used to examine the proliferation in HEC-1A cells. Results:The expression of p-AKT protein in HEC-1A cells after stimulation with estradiol was markedly higher than that in the control group (P=0.006 2);the expression of p-AKT protein in AKT inhibitor group and ER inhibitor group were signiifcantly decreased than that in estradiol group (P=0.006 0, P=0.006 4). qPCR and ELISA showed the mRNA and protein expression of VEGF, bFGF, IL-8 in estradiol group were signiifcantly increased than that in control group (P<0.05);The expressions of VEGF, bFGF, IL-8 in AKT inhibitor group and ER inhibitor group were signiifcantly decreased than that in estradiol group (P<0.01). The abilities of proliferation and cell cycle were signiifcantly increased in HEC-1A cells after estradiol stimulation. Conclusion:Estrogen induces the production of VEGF, bFGF and IL-8 through activating AKT signal pathway.
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Objective To compare intraoperative,pathologic,postoperative outcomes and quality of life of laparoscopic radical hysterectomy and pelvic lymphadenectomy ( LRH + LPL) with abdominal radical hysterectomy and pelvic lymphadenectomy ( ARH + APL) for patients with early-stage cervical cancer.Methods The consecutive cases with International Federation of Gynecology and Obstetrics (FIGO) stages Ⅰ a2 - Ⅱ a cervical cancer who underwent surgery from Jan.1,2002 to Jan.1,2011 were documented,including 85 patients underwent LRH + LPL,and 85 patients underwent ARH + APL as control group.The clinical data of intraoperative,pathologic,postoperative outcomes and quality of life were compared between two groups.Survival data were estimated using Kaplan-Meier survival curves and compared with the log-rank test.Cox proportional hazards model was used for multivariate analysis.Results All but 2 surgical procedures were completed laparoscopically because of right common ihac vein vessel injuries.Mean operative time,it was longer for LRH + LPL than that for ARH + APL [ (242 ±74) minutes vs.( 190 ±61 ) minutes,P =0.000 ].Mean recovery time of intestines function was less for LRH + LPL than that for ARH + APL [ (45 ± 7 ) hours vs.(63 ± 1 1 ) hours,P =0.000 ].Mean estimated blood loss was less for LRH + LPL than that for ARH + APL[ (367 ±252) ml vs.(460 ±220) ml,P =0.006].Mean recovery time of urinary function was less that for LRH + LPL than that for ARH + APL [ ( 19 ±4) days vs.(21 ±4) days,P =0.000 ].There were no significant difference in numbers of the pelvic lymph nodes resected,the extent of parametrial tissue,vaginal cuff,negative margins obtained and complications.The median follow-up was 32 months (range 4 to 105 months),there was no significant difference in the recurrence rate (7％ vs.5％,P=0.540) and mortality rate (7％ vs.5％,P=0.540),5 years disease-free survival(90％ vs.94％,P =0.812),5 years over survival ( 90％ vs.95％,P =0.532 ).There were not significant difference in quality of life between ARH + APL group and LRH + LPL group( P ＞ 0.05 ).Only lympho-vascular space invasion was an independent prognostic factor by multivariate analysis (P =0.016).Conclusions For early stage cervical cancer,LRH + LPL has similar outcomes compared with ARH + APL.Laparoscopic treatment by experienced surgeons should be an ideal altemative.
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Objective To evaluate the clinical value of autoantibody spectrum against ovarian cancer associated antigens combine CA125 in detecting and monitoring ovarian cancer. Methods Circulating IgG, IgM autoantibodies against ovarian cancer associated antigens which included TM4SF1, C1D,TIZ, OV-142,FXR1 and OV-189 were measured by indirect ELISA in serum from 126 patients with ovarian cancer (prior treatment), 42 patients with benign ovarian masses, 142 healthy women. Cut off value of IgG, IgM autoantibodies were determined by receive operating characteristic (ROC) curve. CA125 was measured in serum by immunoradiometric assay (IRMA). We evaluated the clinical value of combining multiple autoantibodies (autoantibody spectrum ), combining autoantibody spectrum with CA125 by binary logistic regresion. The positive ratio of autoantibody spectrum in serum (prior and post treatment ) of 24 synchronization patients with ovarian cancer was analyzed to evaluate the value in monitoring state of illness.Results Our data indicated that serum contains IgG, IgM autoantibodies against ovarian cancer associated antigens. The positive ratio of IgG autoantibodies in serum from ovarian cancer patients and cancer-free patients were 34. 1% - 47. 6% and 13.0% - 19. 0%, respectively ( P ＜ 0. 05 ). The positive ratio of IgM autoantibodies in serum from ovarian cancer patients and cancer-free patients were 39. 7% - 53.2% and 12. 0% -33.2%, respectively (P ＜0. 05). The positive ratio of IgG autoantibodies against FXR1 and IgM autoantibodies against TIZ,FXR1 and OV-189 in early stage ( Ⅰ - Ⅱ ) ovarian cancer(55.3% ,63.8%,61.7% and 66. 0% ) were significantly higher than those in advanced ( Ⅲ - Ⅳ )ovarian cancer( 34. 2%,39. 2% ,26. 6% ,45.6%; all P ＜ 0. 05 ). Combining five autoantibodies ( TM4SF1 IgG, TM4SF1 IgM, C1D IgG, FXR1 IgG and TIZ IgM ) showed significantly improved sensitivity (75.4%, P ＜ 0. 05 ), lower specificity (78. 3% ,P ＜ 0. 05 ) and similar accuracy (77. 1%, P ＞ 0. 05 ) in detecting ovarian cancer compared to those of CA125 (61.1% ,88.0% ,77. 1% ). But the autoantibody spectrum showed significantly improved sensitivity in classifying early stage (76. 6% ), compared to those of CA125 (51.1% ,P ＜ 0. 05 ).Combining autoantibody spectrum with CA125 showed significantly improved sensitivity ( 85.7% ), specificity (90. 8% )and accuracy (88.7%) in detecting ovarian cancer compared to those of autoantibody spectrum alone ( all P ＜ 0. 05 ), while CA125 ( 61.1%, P ＜ 0. 05; 88. 0%, P ＞ 0. 05; 77. 1%, P ＜ 0. 05 ). The positive ratio of combine the autoantibody spectrum with CA125 was significantly lower in 24 post-treatment serum (42%) compared to the pairing prior treatment serum ( 88%, P ＜ 0. 05 ). Conclusion Combining the autoantibody spectrum against ovarian cancer associated antigens with CA125 can improve sensitivity,specificity and accuracy in detecting early ovarian cancer and may be used to monitoring state of illness.
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Objective To analyse the clinico-pathologic characteristics,diagnosis,therapy and prognostic of small cell neuroendocrine carcinoma of the cervix(SCNCC).Methods The clinic-pathological features of 12 patients with SCNCC treated in Tumor Hospital of Guangxi Medical University,admitted during March 2006 to July 2010,were analyzed retrospectively.Results Of 12 patients,the mean age was 38.7 years(rang 28-57 years),6 had stages Ⅰ b1-Ⅱa,6 had stagesⅡb-Ⅳ.Among 8 patients(Ⅰ b1-Ⅲb)underwent surgery,4 of them received neoadjuvant chemotherapy,8 of them received adjuvant chemotherapy and(or)radiotherapy.All had greater than one-half stromal invasion,4 patients had positive pelvic lymph nodes metastases.The positive ratio of the chromogranin(CgA),synaptophysin,neuronspecific enolase(NSE),cytokeratins(CK),CD56 tested by immunohistochemical staining were 8/12,9/10,4/4,4/4,4/4,respectively.Median follow-up period was 3 months(1-22 months).Among 8 patients underwent surgery,2 patients developed lung metastases,1 patient developed liver and lung metastases,1 patient developed liver metastases concurrently with bone metastases,disease-free survival (DFS)were 3 months(Ⅰ b2 with positive lymph nodes),4.6 months(Ⅱ a),7 months(Ⅰ b1),17 months (Ⅰ b2);2 patient died(8.5 and 11.3 months,respectively)after surgery;4 patients are alive and show no evidence of disease.Among 4 patients untreated,1 patients received concurrent chemoradiation and are alive for 10.1 months.Two patient untreated(Ⅲb,Ⅳ)died after 0.6 and 1.3 months final diagnosis,respectively.One patient Was lost follow-up.Conclusions SCNCC is a highly malignant tumor with rare morbility,propensity for distant spread and dismal prognosis.Final diagnosis of SCNCC depends on pathomorphology and immunohistochemical analysis.Combined therapeutic modalities may in favor of survival in some patients.
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Objective To explore the relationship between WWOX gene and attachment and adhesion of ovarian cancer. Methods The expression of WWOX mRNA was detected by RT-PCR, the expression of the WWOX protein was evaluated by western blot in WWOX-transfected PEO1 cells (H6, H7, H8 cell) and vector-transfected control cells (vec-1, vec-2 cell). Attachment assay was used to assess the adhesion of the tranafection in PEOI cells via culturing the cells on the pre-coated fibronectin wells. RNA interference (RNAi) was used to knockdown the endogenous expression of WWOX in the A2780 ovarian cancer cell line by liposome. Attachment assay was detected the adhesion to fibronectin after gene silencing. Restdts RT-PCR showed that expression of mRNA WWOX in exon9 was in all transfection cells (H6, H7, H8, vec-1, vec-2 cell ). Western blot showed that expression of WWOX protein was in the WWOX-transfected cells (H6, H7, H8 cell ), but not in the vector-transfected cells (vec-1, vec-2 cell ). Attachment assay showed that H6, H7, H8 cell (0.098±0.003, 0.091±0.004, 0.099±0.003) adhered more slowly to fibronectin than vec-1, vec-2 cell (0.185±0.003, 0.175±0.006) and non-transfected PEO1 cell (0.211±0.007), and demonstrated significantly reduced adhesion after 2 hours (P ＜ 0.01). A2780 adhesive cells that WWOX gene be knockdown was 0.059±0.005, adhered more significantly rapid than those untreated cells that was 0.029±0.003 after treated 30 minutes (P ＜ 0.05 ). Conclusions WWOX gene can suppress adhesion to fibronectin in ovarian cancer cells. This suggests an important role for loss of WWOX gene in promoting attachment and adhesion of ovarian cancer cells on loco-regional peritoneum, and further resulting in enhancing loco-regional peritoneal tumor invasiveness and spread.
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Objective To investigate the value of autoantibody of breast cancer susceptibility 1 associated RING domain (BARD1) splice variant (OV-142) in detection of ovarian cancer.Methods We cloned OV-142 gene into plasmid pET-30b(+).The recombinant protein of OV-142 was expressed in pET30b(+) system and purified. The autoantibody of OV-142 was detected by indirect enzyme-linked immunosorbent assay (ELISA).Results We successfully constructed the recombinant plasmid of OV-142.The recombinant protein was expressed in pET-30b(+) system and purified.The purification rate of the recombinant protein was up to 90%.The relative amount of autoantibody of OV-142 detected by indirect ELISA was analyzed by receiver operating characteristic curve (ROC) and the cutoff value was determined.Combination of the autoantibody IgG of OV-142 and CA125 was analyzed by logistic regression. The sensitivity,specificity and accuracy was 71.4%,89.1%,and 81.9%,respectively,which were higher than IgG (41.3%,84.2%,66.8% ) and CA125( 61.1%,88.0%,77.1% ) when used alone each.Conclusions OV-142 is a splice variant of BARD1.It may be a potential immunotherapy target of ovarian cancer.Detection of autoantibody of OV-142 is a potent complementary tool of CA125 in ovarian cancerdiagnosis.
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To explore a new mode of teaching activities and management of clinical practice, our hospital adopted various methods, including computer training and exams, selecting practice guiding experts among the three level specialties, establishing labs for the operation of basic skills, using credit books for trainees and adopting integrated education on disease entities. In the past, teachers could teach and set exams in whatever way they liked and students did not have enough opportunities to come across various disease entities or to operate with their hands. Now such shortcomings have been overcome. Students can receive comprehensive, systematic and standard training in clinical operations. At the same time, their quality with regard to professional knowledge and ethics has also been enhanced.