Objective To investigate the role of extracellular regulated kinase (ERK1/2) pathway in cisplatin-induced apoptosis in human ovarian carcinoma cells. Methods Cisplatin-induced apoptosis were stained with DAPI and was ...Objective To investigate the role of extracellular regulated kinase (ERK1/2) pathway in cisplatin-induced apoptosis in human ovarian carcinoma cells. Methods Cisplatin-induced apoptosis were stained with DAPI and was assessed microscopically in human epithelial adenocarcinoma ovarian cell line SKOV3 cells. ERK activation was determined by Western blotting using an anti-phospho-ERK antibody to detect ERK activity. The effect of PD98059 on ERK activity induced by cisplatin was detected by MTT assay. Results Marked apoptosis of SKOV3 cells resulted from 48 hours treatment with 20 μg/mL cisplatin. Strong activation of ERK was led to by 15 μg/mL cisplatin. Dose response and time course of cisplatin induced apoptosis in SKOV3 cells. Cisplatin-induced ERK activation occurred at 12 hours and increased to highest induction at 24 hours by Western blotting. The effect of PD 98059 on ERK activity induced by cisplatin at the concentration of 100 μmol/L PD 98059. Statistically significant decreased in cell survival were observed with 100 μmol/L PD 98059 at 15 and 20 μg/mL cisplatin (P< 0.05). Conclusions Cisplatin activates the ERK signaling pathway in ovarian cancer cell line SKOV3. Inhibition of ERK acti-vity enhances sensitivity to cisplatin cytotoxity in ovarian cancer cell line SKOV3. Evaluation of ERK activity could be useful in predicting which ovarian cancer will response most favorably to cisplatin therapy.展开更多
The effects of antisense oligonucleotide to insulin-like growth factor 11 (IGFII) to induce apoptosis in human ovarian cancer cells were evaluated. Antiproliferation effects of antisense to IGFII in ovarian cancer AO ...The effects of antisense oligonucleotide to insulin-like growth factor 11 (IGFII) to induce apoptosis in human ovarian cancer cells were evaluated. Antiproliferation effects of antisense to IGFII in ovarian cancer AO cells were determined by 3H-thymidine incorporation. Apoptosis of the IGFll antisense-treated cells was quantitated by both nuclear condensation and flow cytometry after cells were stained with propidium iodide. IGFII antisense (4.5μM)treatment of 48 h maximally inhibited proliferation of AO cells. More than 25% of IGFII antisense-treated cells (4.5PM for 24 h) had undergone apoptosis, whereas less than 3% of the cells were apoptotic in either IGFII sense-treatedcells or untreated cells. Antisense oligonucleotide to IGFII significantly inhibited cell proliferation and induced apoptosis in human ovarian cancer AO cell. These data suggest that IGFII may be a potential target in treatment of ovarian cancer and antisense oligonucleotide to IGFⅡmay serve as a therapeutic approach.展开更多
Objective: The aim of the study was to investigate the mechanism of gemcitabine (GEM) combination with radiation on the high metastasis human ovarian cancer cell line (HO-8910PM). Methods: Human ovarian cancer c...Objective: The aim of the study was to investigate the mechanism of gemcitabine (GEM) combination with radiation on the high metastasis human ovarian cancer cell line (HO-8910PM). Methods: Human ovarian cancer cell line HO- 8910PM was treated with different concentrations of gemcitabine for 24 h, then the cells were counted. In the study of GEM combination with radiation, an efficiency of colony formation was observed; the cell cycle and apoptosis were analyzed by flow cytometry; the experiment of depend on the time and its radio sensitivity were observed by using mitotic index with the cells for each 24, 48, 72 and 96 h after experiment. Results: It suggested that the GEM had an inhibition effect on the human ovarian cancer cell line. The alive cell numbers were decreased by following a height of GEM concentration. When GEM in combina- tion with a radiation, the suppression was significantly increased than that of single GEM therapy. The efficiency of colony formation was significantly lower, under this condition the cell could be arrested at G0-G1 phase and could be decreased to enter into the S phase; the apoptosis percentage could be significantly increased; especially, under the 4 Gy and 6 Gy doses the cell apoptosis was more obvious. GEM combination with radiation had depended on the time to the cells; mitotic index of the calls in combination group was observed significantly lower than that of single GEM therapy or single radiation, and this showed that it had an effect of radiosensitivity. Conclusion: The GEM has a significant growth inhibition on the human ovarian cancer cells, GEM combination with radiation could induce HO-8910PM cell occurred arrested and apoptosis. It has depended on the time and has a radiosensitivity effect. The result shows that it is a better method to treat the human ovarian cancer by using radiotherapy combined with gemcitabine.展开更多
A chemosensitivity test for ovarian cancer using tritiated thymidine incorporation assay was carried out. A dose-response relationship for cisplatin and potentiation of verapamil in increasing vincristine inhibition t...A chemosensitivity test for ovarian cancer using tritiated thymidine incorporation assay was carried out. A dose-response relationship for cisplatin and potentiation of verapamil in increasing vincristine inhibition to ovarian cancer were investigated. A 5- fold increase of cisplatin density converted the tumors which were initially resistance to standard-dose cisplatin Into drug-sensitive ones. Vera-pamil was found to be able to overcome vincristine-resistance of some tumors in vitro. These results suggest that using high dose cisplatin therapy or increasing local drug concentration by using other administration way, we could expect some ovarian cancers that had failed to standard dose cisplatin therapy to be effective. Combination of vincristine with verapamll may be helpful in treating some vincristineresistant cases.展开更多
Inactivation of tumor suppressor genes is a key factor in cancer regulation. N-myc downstream regulated gene 1 (NDRG1) is a tumor suppressor gene well known to be involved in carcinogenesis of numerous cancer types. T...Inactivation of tumor suppressor genes is a key factor in cancer regulation. N-myc downstream regulated gene 1 (NDRG1) is a tumor suppressor gene well known to be involved in carcinogenesis of numerous cancer types. The present study was designed to investigate the role of NDRG1 in human ovarian cancer, using SKOV-3 and SW626 (moderately and well differentiated cancer cells, respectively). Our results revealed that over-expressed NDRG1 significantly up-regulated the differentiation marker p21, in the ovarian cancer cell lines. This regulation led to decrease in cell viability and DNA synthesis rates in SW626 cells (83% and 89.5%, respectively). However, no effect on viability or on DNA synthesis was observed in SKOV-3 NDRG1-transfected cells. These findings prove that NDRG1 is indubitably functional in human ovarian cancer cells, as it up-regulated p21 expression. Nevertheless, this regulation showed differential effect on cell viability and DNA formation thus promoting the perception that downstream regulation of p21 could be inefficient in some cancer cells, a concept that needs to be further explored in order to understand its disability to play as regulator of cell cycle progression.展开更多
Using the tetrazolium (MTT) assay, we examined the cytotoxicities of recombinant human tumor necrosis factor (rhTNF) and five chemotherapeutic agents, namely CTX, 5-FU, VCR, DDP and KSM, on human ovarian cancer cell l...Using the tetrazolium (MTT) assay, we examined the cytotoxicities of recombinant human tumor necrosis factor (rhTNF) and five chemotherapeutic agents, namely CTX, 5-FU, VCR, DDP and KSM, on human ovarian cancer cell lines OVCAR3 and CAOV3. The results showed that the cytotoxicities of rhTNF at concentrations of 50-50 000 U / ml on OVCAR3 cell line and CAOV3 cell line exposed to rhTNF for 24 hours were from 14.2% ± 6.8% to 67.2%± 3.0% and from 8.2%± 4.3% to 60.9%±1.3%, respectively. The cytotoxicities of all five chemotherapeutic agents tested on the two cell lines were much lower than that of rhTNF. We also studied the combined antitumor potential of rhTNF with the five chemotherapeutic agents and the results showed that there were various degrees of synergism in cytotoxicities of rhTNF in combination with DDP or KSM on the two cell lines. Based on experiments in vitro, the in vivo antitumor activities of rhTNF, both alone and in combination with KSM, were examined in OVCAR3 cancer transplanted in nude mice. The results showed a considerable antitumor effect of rhTNF when it was used alone and a marked synergistic effect when it was used in combination with KSM on the xenograft tumors.展开更多
Peroxisome proliferator-activated receptor gamma (PPAR),) coactivator-1 alpha (PGC-1α) coactivates multiple transcription factors and regulates several metabolic processes. The current study investigated the rol...Peroxisome proliferator-activated receptor gamma (PPAR),) coactivator-1 alpha (PGC-1α) coactivates multiple transcription factors and regulates several metabolic processes. The current study investigated the role of PGC-1α in the induction of apoptosis in human epithelial ovarian cancer cells. The PGC-1α mRNA level between human ovaries and human ovarian epithelial tumors was examined by quantitative RT-PCR. Less PGC- 1α expression was found in the surface epithelium of malignant tumors compared with normal ovaries. Overexpression of PGC-1α in human epithelial ovarian cancer cell line Ho-8910 induced cell apoptosis through the coordinated regulation of Bcl-2 and Bax expression. Microarray analyses confirmed that PGC-1α dramatically affected the apoptosis-related genes in Ho-8910 cells. Mitochondrial functional assay showed that the induction of apoptosis was through the terminal stage by the release of cytochrome c. Furthermore, PG-C- 1 α-induced apoptosis was partially, but not completely, blocked by PPAR), antagonist (GW9662), and suppression of PPAR), expression by siRNA also inhibited PGC-1α-induced apoptosis in Ho-8910 cells. These data suggested that PGC-1α exerted its effect through a PPARγ-dependent pathway. Our findings indicated that PGC-1α was involved in the apoptotic signal transduction pathways and downregulation of PGC-1α may be a key point in promoting epithelial ovarian cancer growth and progression.展开更多
Objective:To investigate effect and possible mechanisms of silencing human WFDC2(HE4) gene on biological behavior changes as cell proliferation,apoplosis,movement and invasion of human serous ovarian cancer cell lin...Objective:To investigate effect and possible mechanisms of silencing human WFDC2(HE4) gene on biological behavior changes as cell proliferation,apoplosis,movement and invasion of human serous ovarian cancer cell line SKOV3.Methods:Lentiviral WFDC2 gene sequence of small interfering siRNA was stablely transfected into SKOV3 identified by Q-PCR and western-blot. Obtained SKOV3 stable strains with silenced HE4 were measured by proliferation,apoplosis, migration,and invasion.Results:Gene sequencing showed that the oligonucleotides were successfully inserted into the expected site.After silencing HE4 in the SKOV3,proliferation was significandy inhibited(P【0.05).G<sub>0</sub>/G<sub>1</sub> phase was arrested by the cell cycle(P【0.01) and capacity of the migration and invasion decreased significandy(P【0.01).Slight early apoptosis ratio and no change of late apoplosis were found without change of Caspase-3 or Bcl-2 protein.Proteins involed in ERK pathway as phosphorylated protein as p-EGFR,p- ERK decreased and protease protein involved in tissue remoding as matrix metalloproteinases MMP-9,MMP-2 and cathepsin B decreased compared with control group.Conclusions:HE4 gene plays an important role in regulating proliferation,apoptosis,migration,invasion of serous ovarian cancer cells by ERK pathway and protease system.Its role in apoptosis needs to be further explored,and it may be a potential target for serous ovarian cancer.展开更多
Objective: Human epididymis protein 4(HE4) is a promising biomarker of epithelial ovarian cancer(EOC). But its role in assessing the primary optimal debulking(OD) of EOC remains unknown. The purpose of this stu...Objective: Human epididymis protein 4(HE4) is a promising biomarker of epithelial ovarian cancer(EOC). But its role in assessing the primary optimal debulking(OD) of EOC remains unknown. The purpose of this study is to elucidate the ability of preoperative HE4 in predicting the primary cytoreductive outcomes in advanced EOC, tubal or peritoneal carcinoma.Methods: We reviewed the records of 90 patients with advanced ovarian, tubal or peritoneal carcinoma who underwent primary cytoreduction at the Department of Obstetrics and Gynecology of Peking University People's Hospital between November 2005 and October 2010. Preoperative serum HE4 and CA125 levels were detected with EIA kit. A receiver operating characteristic(ROC) curve was used to determine the most useful HE4 cut-off value. Logistic regression analysis was performed to identify significant preoperative clinical characteristics to predict optimal primary cytoreduction.Results: OD was achieved in 47.7%(43/48) of patients. The median preoperative HE4 level for patients with OD vs. suboptimal debulking was 423 and 820 pmol/L, respectively(P〈0.001). The areas under the ROC curve for HE4 and CA125 were 0.716 and 0.599, respectively(P=0.080). The most useful HE4 cut-off value was 473 pmol/L. Suboptimal cytoreduction was obtained in 66.7%(38/57) of cases with HE4 ≥473 pmol/L compared with only 27.3%(9/33) of cases with HE4 〈473 pmol/L. At this threshold, the sensitivity, specificity, positive predictive value(PPV) and negative predictive value(NPV) for diagnosing suboptimal debulking were 81%, 56%, 67%, and 73%, respectively. Logistic regression analysis showed that the patients with HE4 ≥473 pmol/L were less likely to achieve OD(odds ratio =5.044, P=0.002).Conclusions: Preoperative serum HE4 may be helpful to predict whether optimal cytoreductive surgery could be obtained or whether extended cytoreduction would be needed by an interdisciplinary team.展开更多
基金Supported by Heilongjiang Province Natural Science Funds (D03-55) and Heilongjiang Province Sanitary Bureau Science Funds (2003-003)
文摘Objective To investigate the role of extracellular regulated kinase (ERK1/2) pathway in cisplatin-induced apoptosis in human ovarian carcinoma cells. Methods Cisplatin-induced apoptosis were stained with DAPI and was assessed microscopically in human epithelial adenocarcinoma ovarian cell line SKOV3 cells. ERK activation was determined by Western blotting using an anti-phospho-ERK antibody to detect ERK activity. The effect of PD98059 on ERK activity induced by cisplatin was detected by MTT assay. Results Marked apoptosis of SKOV3 cells resulted from 48 hours treatment with 20 μg/mL cisplatin. Strong activation of ERK was led to by 15 μg/mL cisplatin. Dose response and time course of cisplatin induced apoptosis in SKOV3 cells. Cisplatin-induced ERK activation occurred at 12 hours and increased to highest induction at 24 hours by Western blotting. The effect of PD 98059 on ERK activity induced by cisplatin at the concentration of 100 μmol/L PD 98059. Statistically significant decreased in cell survival were observed with 100 μmol/L PD 98059 at 15 and 20 μg/mL cisplatin (P< 0.05). Conclusions Cisplatin activates the ERK signaling pathway in ovarian cancer cell line SKOV3. Inhibition of ERK acti-vity enhances sensitivity to cisplatin cytotoxity in ovarian cancer cell line SKOV3. Evaluation of ERK activity could be useful in predicting which ovarian cancer will response most favorably to cisplatin therapy.
文摘The effects of antisense oligonucleotide to insulin-like growth factor 11 (IGFII) to induce apoptosis in human ovarian cancer cells were evaluated. Antiproliferation effects of antisense to IGFII in ovarian cancer AO cells were determined by 3H-thymidine incorporation. Apoptosis of the IGFll antisense-treated cells was quantitated by both nuclear condensation and flow cytometry after cells were stained with propidium iodide. IGFII antisense (4.5μM)treatment of 48 h maximally inhibited proliferation of AO cells. More than 25% of IGFII antisense-treated cells (4.5PM for 24 h) had undergone apoptosis, whereas less than 3% of the cells were apoptotic in either IGFII sense-treatedcells or untreated cells. Antisense oligonucleotide to IGFII significantly inhibited cell proliferation and induced apoptosis in human ovarian cancer AO cell. These data suggest that IGFII may be a potential target in treatment of ovarian cancer and antisense oligonucleotide to IGFⅡmay serve as a therapeutic approach.
文摘Objective: The aim of the study was to investigate the mechanism of gemcitabine (GEM) combination with radiation on the high metastasis human ovarian cancer cell line (HO-8910PM). Methods: Human ovarian cancer cell line HO- 8910PM was treated with different concentrations of gemcitabine for 24 h, then the cells were counted. In the study of GEM combination with radiation, an efficiency of colony formation was observed; the cell cycle and apoptosis were analyzed by flow cytometry; the experiment of depend on the time and its radio sensitivity were observed by using mitotic index with the cells for each 24, 48, 72 and 96 h after experiment. Results: It suggested that the GEM had an inhibition effect on the human ovarian cancer cell line. The alive cell numbers were decreased by following a height of GEM concentration. When GEM in combina- tion with a radiation, the suppression was significantly increased than that of single GEM therapy. The efficiency of colony formation was significantly lower, under this condition the cell could be arrested at G0-G1 phase and could be decreased to enter into the S phase; the apoptosis percentage could be significantly increased; especially, under the 4 Gy and 6 Gy doses the cell apoptosis was more obvious. GEM combination with radiation had depended on the time to the cells; mitotic index of the calls in combination group was observed significantly lower than that of single GEM therapy or single radiation, and this showed that it had an effect of radiosensitivity. Conclusion: The GEM has a significant growth inhibition on the human ovarian cancer cells, GEM combination with radiation could induce HO-8910PM cell occurred arrested and apoptosis. It has depended on the time and has a radiosensitivity effect. The result shows that it is a better method to treat the human ovarian cancer by using radiotherapy combined with gemcitabine.
文摘A chemosensitivity test for ovarian cancer using tritiated thymidine incorporation assay was carried out. A dose-response relationship for cisplatin and potentiation of verapamil in increasing vincristine inhibition to ovarian cancer were investigated. A 5- fold increase of cisplatin density converted the tumors which were initially resistance to standard-dose cisplatin Into drug-sensitive ones. Vera-pamil was found to be able to overcome vincristine-resistance of some tumors in vitro. These results suggest that using high dose cisplatin therapy or increasing local drug concentration by using other administration way, we could expect some ovarian cancers that had failed to standard dose cisplatin therapy to be effective. Combination of vincristine with verapamll may be helpful in treating some vincristineresistant cases.
文摘Inactivation of tumor suppressor genes is a key factor in cancer regulation. N-myc downstream regulated gene 1 (NDRG1) is a tumor suppressor gene well known to be involved in carcinogenesis of numerous cancer types. The present study was designed to investigate the role of NDRG1 in human ovarian cancer, using SKOV-3 and SW626 (moderately and well differentiated cancer cells, respectively). Our results revealed that over-expressed NDRG1 significantly up-regulated the differentiation marker p21, in the ovarian cancer cell lines. This regulation led to decrease in cell viability and DNA synthesis rates in SW626 cells (83% and 89.5%, respectively). However, no effect on viability or on DNA synthesis was observed in SKOV-3 NDRG1-transfected cells. These findings prove that NDRG1 is indubitably functional in human ovarian cancer cells, as it up-regulated p21 expression. Nevertheless, this regulation showed differential effect on cell viability and DNA formation thus promoting the perception that downstream regulation of p21 could be inefficient in some cancer cells, a concept that needs to be further explored in order to understand its disability to play as regulator of cell cycle progression.
文摘Using the tetrazolium (MTT) assay, we examined the cytotoxicities of recombinant human tumor necrosis factor (rhTNF) and five chemotherapeutic agents, namely CTX, 5-FU, VCR, DDP and KSM, on human ovarian cancer cell lines OVCAR3 and CAOV3. The results showed that the cytotoxicities of rhTNF at concentrations of 50-50 000 U / ml on OVCAR3 cell line and CAOV3 cell line exposed to rhTNF for 24 hours were from 14.2% ± 6.8% to 67.2%± 3.0% and from 8.2%± 4.3% to 60.9%±1.3%, respectively. The cytotoxicities of all five chemotherapeutic agents tested on the two cell lines were much lower than that of rhTNF. We also studied the combined antitumor potential of rhTNF with the five chemotherapeutic agents and the results showed that there were various degrees of synergism in cytotoxicities of rhTNF in combination with DDP or KSM on the two cell lines. Based on experiments in vitro, the in vivo antitumor activities of rhTNF, both alone and in combination with KSM, were examined in OVCAR3 cancer transplanted in nude mice. The results showed a considerable antitumor effect of rhTNF when it was used alone and a marked synergistic effect when it was used in combination with KSM on the xenograft tumors.
基金This work was supported by grants from the National Natural Science Foundation of China (No. 30225037, 30400538, 30471991,30570731);the 973 Program of China (No. 2006CB503909, 2004CB518603);the "111" Project, and the Natural Science Foundation of Jiangsu Province (No. BK2004082, BK2006714).
文摘Peroxisome proliferator-activated receptor gamma (PPAR),) coactivator-1 alpha (PGC-1α) coactivates multiple transcription factors and regulates several metabolic processes. The current study investigated the role of PGC-1α in the induction of apoptosis in human epithelial ovarian cancer cells. The PGC-1α mRNA level between human ovaries and human ovarian epithelial tumors was examined by quantitative RT-PCR. Less PGC- 1α expression was found in the surface epithelium of malignant tumors compared with normal ovaries. Overexpression of PGC-1α in human epithelial ovarian cancer cell line Ho-8910 induced cell apoptosis through the coordinated regulation of Bcl-2 and Bax expression. Microarray analyses confirmed that PGC-1α dramatically affected the apoptosis-related genes in Ho-8910 cells. Mitochondrial functional assay showed that the induction of apoptosis was through the terminal stage by the release of cytochrome c. Furthermore, PG-C- 1 α-induced apoptosis was partially, but not completely, blocked by PPAR), antagonist (GW9662), and suppression of PPAR), expression by siRNA also inhibited PGC-1α-induced apoptosis in Ho-8910 cells. These data suggested that PGC-1α exerted its effect through a PPARγ-dependent pathway. Our findings indicated that PGC-1α was involved in the apoptotic signal transduction pathways and downregulation of PGC-1α may be a key point in promoting epithelial ovarian cancer growth and progression.
基金supported by Young Researcher Koundation from Education Department of Jiangxi Province(Grant No.GJJ12161)
文摘Objective:To investigate effect and possible mechanisms of silencing human WFDC2(HE4) gene on biological behavior changes as cell proliferation,apoplosis,movement and invasion of human serous ovarian cancer cell line SKOV3.Methods:Lentiviral WFDC2 gene sequence of small interfering siRNA was stablely transfected into SKOV3 identified by Q-PCR and western-blot. Obtained SKOV3 stable strains with silenced HE4 were measured by proliferation,apoplosis, migration,and invasion.Results:Gene sequencing showed that the oligonucleotides were successfully inserted into the expected site.After silencing HE4 in the SKOV3,proliferation was significandy inhibited(P【0.05).G<sub>0</sub>/G<sub>1</sub> phase was arrested by the cell cycle(P【0.01) and capacity of the migration and invasion decreased significandy(P【0.01).Slight early apoptosis ratio and no change of late apoplosis were found without change of Caspase-3 or Bcl-2 protein.Proteins involed in ERK pathway as phosphorylated protein as p-EGFR,p- ERK decreased and protease protein involved in tissue remoding as matrix metalloproteinases MMP-9,MMP-2 and cathepsin B decreased compared with control group.Conclusions:HE4 gene plays an important role in regulating proliferation,apoptosis,migration,invasion of serous ovarian cancer cells by ERK pathway and protease system.Its role in apoptosis needs to be further explored,and it may be a potential target for serous ovarian cancer.
基金supported by Natural Science Foundation of China(NSFC-81172454)the Specialized Research Fund for Doctoral Program of Higher Education(SRFDR-20100001110079)
文摘Objective: Human epididymis protein 4(HE4) is a promising biomarker of epithelial ovarian cancer(EOC). But its role in assessing the primary optimal debulking(OD) of EOC remains unknown. The purpose of this study is to elucidate the ability of preoperative HE4 in predicting the primary cytoreductive outcomes in advanced EOC, tubal or peritoneal carcinoma.Methods: We reviewed the records of 90 patients with advanced ovarian, tubal or peritoneal carcinoma who underwent primary cytoreduction at the Department of Obstetrics and Gynecology of Peking University People's Hospital between November 2005 and October 2010. Preoperative serum HE4 and CA125 levels were detected with EIA kit. A receiver operating characteristic(ROC) curve was used to determine the most useful HE4 cut-off value. Logistic regression analysis was performed to identify significant preoperative clinical characteristics to predict optimal primary cytoreduction.Results: OD was achieved in 47.7%(43/48) of patients. The median preoperative HE4 level for patients with OD vs. suboptimal debulking was 423 and 820 pmol/L, respectively(P〈0.001). The areas under the ROC curve for HE4 and CA125 were 0.716 and 0.599, respectively(P=0.080). The most useful HE4 cut-off value was 473 pmol/L. Suboptimal cytoreduction was obtained in 66.7%(38/57) of cases with HE4 ≥473 pmol/L compared with only 27.3%(9/33) of cases with HE4 〈473 pmol/L. At this threshold, the sensitivity, specificity, positive predictive value(PPV) and negative predictive value(NPV) for diagnosing suboptimal debulking were 81%, 56%, 67%, and 73%, respectively. Logistic regression analysis showed that the patients with HE4 ≥473 pmol/L were less likely to achieve OD(odds ratio =5.044, P=0.002).Conclusions: Preoperative serum HE4 may be helpful to predict whether optimal cytoreductive surgery could be obtained or whether extended cytoreduction would be needed by an interdisciplinary team.