A Predictive Model for Endometrial Carcinoma Based on Hysteroscopic Data.

Objective: The purpose is to establish a model to predict endometrial carcinoma and assess its value in the preliminary diagnosis of endometrial carcinoma. Methods: The data of 381 patients undergoing hysteroscopy were incorporated into the model, including 282 cases in the training cohort and 99 cases in the validation cohort. Significant morphological indexes were selected using the chi-square test and subjected to the binary logistic regression analysis. Besides, the scoring interval was set, and the nomogram of the prediction model was established. Model calibration curves were drawn using the data from the validation cohort. The study was approved by the Ethics Committee of the Affiliated Sir Run Run Hospital of Nanjing Medical University, and written informed consent was obtained from the patients. Results: The sensitivity, specificity, positive predictive value, and negative predictive value of the model were 96.7%, 92.3%, 77.3%, and 99.0%, respectively. Analysis of the receiver operating characteristic curve in the training cohort showed an area under the curve of 0.984 (95% CI: 0.974-0.995). The receiver operating characteristic curve in the validation cohort revealed an area under the curve of 0.976 (95% CI: 0.950-1.000). The calibration curve indicated that the probability in the actual setting was consistent with that predicted by the nomogram in the training cohort. Conclusion: Our model has high sensitivity and specificity in predicting endometrial carcinoma, and helps clinicians to make accurate diagnosis.

Giant cyst in heterotopic pregnancy: A case report.

BACKGROUND: The coexistence of a heterotopic pregnancy with a giant ovarian cyst is an incredibly rare abnormal pregnancy in cases of natural conception. The incidence of this condition has increased significantly as a result of the continuous development of assisted reproductive technologies. When this type of pregnancy occurs, both the continuation of intrauterine pregnancy and the life of the pregnant woman are severely threatened. Early diagnosis and treatment using safe and effective methods are paramount in this situation. CASE SUMMARY: A 30-year-old primigravida at a gestation age determined as 8 wk 4 d by scan was admitted to the hospital with heterotopic pregnancy and a right ovarian cyst. Laparoscopic resection of the ectopic pregnancy was performed, but the intrauterine pregnancy and ovarian cyst were preserved. CONCLUSION: The approach to a patient with heterotopic pregnancy and a giant ovarian cyst is individualized base on the fertility requirements. We recommend the following: (1) If the patient satisfies parity and has no fertility requirement, a laparoscopic salpingectomy should be performed and the giant ovarian cyst and intrauterine pregnancy removed; (2) If the patient has fertility requirements wishes to have more children in the future, laparoscopic salpingectomy or salpingostomy should be performed and the intrauterine pregnancy preserved. Serial ovarian cyst aspiration can be performed under ultrasound and resection can be done after delivery; and (3) Heterotopic pregnancy should be diagnosed early by active surveillance during antenatal visits using ultra sound as this is important for the avoidance of catastrophic complications.

Long Non-coding RNA UCA1a Promotes Proliferation via PKM2 in Cervical Cancer.

Cervical cancer is a common malignancy that affects women worldwide. The long non-coding RNA (lncRNA) urothelial cancer-associated 1a (UCA1a) is reported to be significantly upregulated in cervical cancer. However, the exact role of UCA1a in cervical cancer remains unknown. This study aimed to identify two core promoter regions in UCA1a, which are essential for CEBPA-dependent transcription and FOXL1-, FOXL4-, and FOXL6-dependent activation, respectively. RNA sequencing results showed that overexpression of UCA1a resulted in extensive changes in the gene expression profile of HeLa cells, especially in the signaling pathway that regulates tumorgenesis. Mass spectrometry assay was conducted to show that pyruvate kinase M2 (PKM2) was a UCA1a-interacting protein. The 400 ~ 800 nt long region of UCA1a at the 5' end and the A1B domain of PKM2 were critical for the UCA1a-PKM2 interaction. Functional assays were performed to show that PKM2 was sufficient and necessary for UCA1a-induced proliferation of HeLa cells, which was partly due to the regulating of nuclear translocation and stabilization of PKM2. These findings provide a novel mechanism for UCA1a to regulate Hela cells by ubiquitination degradation of PKM2 and suggest that UCA1a may play a key role in the progression of cervical cancer.

Peptidome analysis of human intrauterine adhesion tissues and the identification of antifibrotic peptide.

Intrauterine adhesion (IUA) is a common clinical endometrial disease, which can severely damage the fertility and quality of life in women. This study aims to find the differentially expressed endogenous peptides and their possible roles in IUA. Liquid chromatography-mass spectrometry was used to identify the peptidomic profiling of IUA tissues, and the differentially expressed peptides were screened out. Using real-time quantitative PCR, Western blotting, and immunocytochemistry staining, the function of six endogenous peptides was verified in vitro. It was found that peptide 6 (T6) (peptide sequence: TFGGAPGFPLGSPLSSVFPR) could inhibit the expression of TGF-ß1-induced cell fibrosis in human endometrial stromal cell line and primary human endometrial stromal cell at a concentration of 50 µmol/L. This study provides new targets for further clarifying the formation and prevention of IUA.

Yikang decoction facilitates embryo implantation in mice with implantation dysfunction via upregulation of LIF expression.

OBJECTIVE: The present study investigates the effects and mechanisms of Yikang decoction on embryo implantation in mice. METHODS: Totally, mature female mice were randomly divided into four groups: normal, implantation failure (mifepristone treatment), Yikang decoction treatment (mifepristone and Yikang decoction treatment), and control (mifepristone and physiological saline treatment) groups. The efficacy of Yikang decoction was evaluated by the adhesion of uterine endometrial cells. The expression of leukemia inhibitory factor (LIF) and integrin αvß3 in the endometrium were detected by real-time quantitative PCR and western blot. In addition, mouse endometrial cells were transfected with LIF specific siRNA-1, and the expression of LIF and αvß3 were detected. RESULTS: The number of embryos markedly decreased after mifepristone treatment. The adhesion of endometrial cells in the Yikang decoction treatment group significantly increased, when compared to the control group. The expression of LIF and integrin αvß3 was significantly reduced by mifepristone, but the attenuated expression of LIF and αvß3 was markedly reversed by treatment with Yikang decoction. In addition, after LIF siRNA-1 transfection, the expression of integrin αvß3 significantly decreased (P < 0.01). The correlation analysis revealed a significant positive correlation between LIF and αvß3 protein expression. CONCLUSION: Yikang decoction can regulate the expression of αvß3 and increase cell adhesion by upregulating the expression of LIF, thereby improving embryo implantation in mice. These data suggest that Yikang decoction may have therapeutic effect in treating infertility.

Autotransplantation of the ovarian cortex after in-vitro activation for infertility treatment: a shortened procedure.

STUDY QUESTION: Is it possible to establish a new in-vitro activation (IVA) protocol for infertility treatment? SUMMARY ANSWER: A new IVA procedure is an efficient and easily performed approach for infertility treatment of patients with diminished ovarian reserve (DOR). WHAT IS KNOWN ALREADY: IVA of primordial follicles with or without stimulators has been developed to treat patients with primary ovarian insufficiency (POI) successfully. However, the efficiency of the procedure is still very low. There is a requirement to optimize the protocol with increased efficiency for clinical application. STUDY DESIGN, SIZE, DURATION: Newborn mouse ovaries were used to establish a new 1-h IVA protocol with the mechanistic target of rapamycin (mTOR) stimulator phosphatidic acid (PA, 200 µM) and the phosphatidylinositol-3-kinase (PI3K) stimulator 740Y-P (250 µg/ml); a prospective observational cohort study in POI patients was performed on 15 POI patients and 3 poor ovarian response (POR) patients in three different centers of reproductive medicine in China. PARTICIPANTS/MATERIALS, SETTING, METHODS: One-third of ovarian cortex was removed and processed into bigger strips (1 × 1 cm2, 1-2 mm thickness). Strips were then sutured back after treatment. The new approach only requires one laparoscopic surgery. MAIN RESULTS AND THE ROLE OF CHANCE: Follicular activation and development increased in cultured mouse and human ovarian tissues after 1 h of stimulator treatment. Compared with tiny ovarian cortex pieces (1 × 1 mm2), large ovarian strips (1 × 1 cm2) showed the lowest apoptotic signals after incubation. We applied the orthotropic transplantation procedure with large strips in the clinic, and 9 of 15 POI patients showed at least one-wave follicular growth during the monitoring period. One patient was reported with one healthy delivery after natural conception and another patient with a healthy singleton delivery after IVF. All the contacted patients (n = 13) responded with no side effects on their health 2-4 years after IVA procedure. LIMITATIONS, REASONS FOR CAUTION: Further clinical trials with a large number of well-defined patients are required to compare different IVA protocols. A long-term follow-up system should be set up to monitor patient's health in the future cohort study. WIDER IMPLICATIONS OF THE FINDINGS: By using stimulators, the findings in the study provide a more efficient IVA protocol for the treatment of patients with DOR. It requires only one laparoscopic surgery and thus minimizes patients' discomfort and costs. This strategy could be useful for patients diagnosed with POI and desire pregnancy as soon as possible after the operation. STUDY FUNDING/COMPETING INTEREST(S): This work was supported by the National Key Research and Development Program of China (2018YFC1003703 and 2018YFC1004203); the National Natural Science Foundation of China (81871221); Co-construction of Provincial Department (201601006). The authors have no conflict of interest to disclose. TRIAL REGISTRATION NUMBER: ChiCTR2000030872.

Activation of COL11A1 by PRRX1 promotes tumor progression and radioresistance in ovarian cancer.

PURPOSE: Although radiotherapy is a common treatment option for all kinds of cancer patients, including ovarian cancer, a major obstacle limiting its application in the development of resistance. Therefore, it is urgently needed to clarify the mechanism of radiosensitivity modulation. MATERIALS AND METHODS: We obtained open datasets and analyzed the expression of collagen type XI alpha 1 (COL11A1) in ovarian cancer patients with different stages. Meanwhile, the correlation of COL11A1 and survival outcomes is determined by Kaplan-Meier analysis. The role of COL11A1 in cell proliferation was observed in an in vitro knockdown system. SKOV3 radioresistant cells were established to determine the role of COL11A1 on radioresistant in ovarian cancer. RESULTS AND DISCUSSION: COL11A1 were highly enriched in late-stage ovarian cancer tumor tissues and negatively correlated with survival outcomes in ovarian cancer. The functional analysis found that COL11A1 promoted ovarian cancer cell proliferation in vitro. Importantly, COL11A1 decreased radiosensitivity in ovarian cancer by AKT activation. Paired related homeobox 1 (PRRX1) acted as an upstream transcription factor to regulate COL11A1 expression in ovarian cancer. Increased COL11A1 expression is related to low survival outcomes and radiosensitivity in ovarian cancer. CONCLUSIONS: Targeting COL11A1 is a promising strategy for improving radiotherapy efficiency.

Long non-coding RNA SNHG25 promotes epithelial ovarian cancer progression by up-regulating COMP.

Long non-coding RNAs (lncRNAs) play a pivotal role in the genesis and development of cancer. The role and molecular mechanisms of SNHG25 in epithelial ovarian cancer (EOC) have not been investigated. In the present study, we showed that SNHG25 expression was up-regulated in EOC tissues relative to normal ovarian tissues. In vitro, functional experiments demonstrated that high expression of SNHG25 promoted proliferation, migration and invasion, and decreased apoptosis, in ovarian cancer cell lines. In vivo, downregulation of SNHG25 inhibited the growth (tumor volume) of subcutaneous xenografts in nude mice. High-throughput sequencing and western blot analysis showed a significant decrease in the expression of COMP mRNA and protein in SNHG25 knockdown compared to control ovarian cancer cells. These data suggest that SNHG25 promotes EOC progression by regulating COMP, serving as a potential biomarker for EOC.

Enhancing solar-thermal energy conversion with silicon-cored tungsten nanowire selective metamaterial absorbers.

This work experimentally studies a silicon-cored tungsten nanowire selective metamaterial absorber to enhance solar-thermal energy harvesting. After conformally coating a thin tungsten layer about 40 nm thick, the metamaterial absorber exhibits almost the same total solar absorptance of 0.85 as the bare silicon nanowire stamp but with greatly reduced total emittance down to 0.18 for suppressing the infrared emission heat loss. The silicon-cored tungsten nanowire absorber achieves an experimental solar-thermal efficiency of 41% at 203°C during the laboratory-scale test with a stagnation temperature of 273°C under 6.3 suns. Without parasitic radiative losses from side and bottom surfaces, it is projected to reach 74% efficiency at the same temperature of 203°C with a stagnation temperature of 430°C for practical application, greatly outperforming the silicon nanowire and black absorbers. The results would facilitate the development of metamaterial selective absorbers at low cost for highly efficient solar-thermal energy systems.

The protective effects of rapamycin pretreatment on ovarian damage during ovarian tissue cryopreservation and transplantation.

Ovarian tissue cryopreservation and transplantation (OCT) has been sufficiently proven effective and feasible to preserve fertility for women especially for prepubertal girls suffering from cancer with radiotherapy and chemotherapy. However, grafts' survival, significant follicle loss and a delay of revascularization during OCT still need to be resolved no matter what kind of cryopreserved method being used. Different from previous reports about additives treatment on recipient after ovarian transplantation, we here report a new vitrification protocol with pretreatment of rapamycin, an inhibitor of the mTOR signaling pathway. The rapamycin treatment has been shown to inhibit the activation of mTOR signaling pathway in fresh thawed ovaries or in ovaries shortly grafted in the recipient mice. Further study revealed increased percentage of primordial follicles and reduced apoptosis after 5 days of transplantation. Long-term follow up of ovarian development demonstrated the increase of ovarian survival rates in rapamycin treated ovaries after 2 weeks of transplantation. Although follicular development showed a slight delay with more secondary and early antral follicles found in rapamycin treated ovaries, follicular development was not blocked as manifested by the ovarian morphology after 5 weeks of transplantation. Taken together, the pretreatment of rapamycin before vitrification is a good method for clinical application with its effectiveness on preserving follicle reserve and promoting ovarian survival during the process of OCT.

miR-29a in Exosomes from Bone Marrow Mesenchymal Stem Cells Inhibit Fibrosis during Endometrial Repair of Intrauterine Adhesion.

BACKGROUND AND OBJECTIVES: Bone marrow mesenchymal stem cells (BMSCs) is an ideal source of stem cells in the treatment of intrauterine adhesion. Exosomes are a type of membrane vesicle and the diameter is 30∼100 nm. Exosomes can take their contents into the target cells, releasing and exerting their functions. In this study, we intend to study the role of human BMSC-derived exosomes (BMSC-Exo) in promoting endometrial damage repair in the treatment of IUA. METHODS: We used the magnetic bead affinity method to extract BMSC-Exo and analyzed its biological character. Then we co-cultured the BMSCs-Exo with endometrial cells to detect its effect. We injected BMSCs-Exo into the IUA mouse model. We over-expressed miR-29a in BMSCs-Exo by transient transfection, then used RT-PCR to analyze the expression of the related genes. RESULTS: BMSCs-Exo expressed exosome-specific proteins CD9, CD63, and CD81. BMSCs-Exo could bring the contents into the target cells. BMSCs-Exo can promote endometrial repair in vitro or in vivo. BMSCs-Exo overexpressing miR-29a can reduce αSMA, Collagen I, SMAD2, and SMAD3. CONCLUSIONS: In this study, we successfully isolated BMSCs-Exo and proved its character and biological activity. BMSCs-Exo can promote cell proliferation and cell migration in vitro and can repair damaged endometrium in the IUA model. The presence of miR-29a in BMSCs-Exo may be an important factor in its resistance to fibrosis during endometrial repair of IUA. This study provides new ideas for the treatment of patients with IUA and has important clinical research significance.

Wilms' tumor 1 (WT1) promotes ovarian cancer progression by regulating E-cadherin and ERK1/2 signaling.

Wilms' tumor 1 (WT1) is reported to play an important role in tumor invasion and metastasis, two hallmarks of ovarian cancer (OC) that influence treatment efficacy and prognosis. However, the specific roles and underlying mechanisms of WT1 in OC have not been fully understood. Here, we investigated the potential function and signaling pathways of WT1 in OC cells. We showed that WT1 was significantly upregulated in human OC tissues and closely associated with OC type, grade and FIGO stage. In cultured cells and xenograft mouse models, WT1 depletion significantly inhibited cell migration and invasion, reversed epithelial-mesenchymal transition (EMT), and prevented metastasis of OC cells. We further demonstrated that WT1 inhibited E-cadherin expression via targeting E-cadherin gene promoter by chromatin immunoprecipitation and luciferase reporter assay. Moreover, ERK1/2 activation was suppressed upon WT1 silencing. Inhibiting ERK1/2 phosphorylation increased E-cadherin expression and suppressed WT1-induced OC cell migration and invasion. Taken together, our study reveals WT1 exerts a tumor-promoting role in OC, enhancing EMT through negative modulation of E-cadherin expression via ERK1/2 signaling. WT1 may represent a novel therapeutic target that may improve the prognosis of OC.

A preliminary study on the immune responses of HPV16-E7 by combined intranasal immunization with lymphotoxin.

OBJECTIVES: Human papillomavirus (HPV) ranks the first cause of cervical cancer. Cervical cancer has high prevalence rates in women around the world. The HPV-E7 oncoprotein is expressed in cervical cancer and is a target of developing immunotherapies against HPV-associated tumors. However, the antigenicity of this protein is low. Due to this reason, potent adjuvants are required to enhance its therapeutic efficacy. This preliminary study aims to evaluate whether lymphotoxin (LT) could act as an effective immune adjuvant for HPV infection in mice models. MATERIAL AND METHODS: Intranasal immunization was used to explore the effect of HPV-E7 and/or LT immune response. After the third intranasal immunization, the titer for the HPV-E7 antibody was detected in serum and vaginal washing fluid. Also, we assessed the expression of chemokine ligand 13 (CXCL13) and Peripheral Node Addressin (PNAd) in the lymph nodes after intranasal immunization with immunohistochemical analysis. RESULTS: compared to HPV-E7 immunization, intranasal immunization with HPV-E7 plus LT significantly increased HPV-E7-specific serum IgG and vaginal IgA titers. Furthermore, the combined use of HPV-E7 and LT strongly induced E7-specific CTL responses. CONCLUSIONS: LT can be effective for intranasal immunized HPV-E7 to improve E7-specific immune responses to HPV infection. It is new approach to eradicate chronic HPV infection capable of inducing an effective anti-infection method.

Decreased microRNA-125b-5p disrupts follicle steroidogenesis through targeting PAK3/ERK1/2 signalling in mouse preantral follicles.

BACKGROUND: Hyperandrogenism is one of the major characteristics of polycystic ovary syndrome (PCOS). Abnormal miR-125b-5p expression has been documented in multiple diseases, but whether miR-125b-5p is associated with aberrant steroidogenesis in preantral follicles remains unknown. METHODS: Steriod hormone concentrations and miR-125b-5p expression were measured in clinical serum samples from PCOS patients. Using a mouse preantral follicle culture model and a letrozole-induced PCOS mouse model, we investigated the mechanism underlying miR-125b-5p regulation of androgen and oestrogen secretion. RESULTS: The decreased miR-125b-5p expression was observed in the sera from hyperandrogenic PCOS (HA-PCOS) patients. In mouse preantral follicles, inhibiting miR-125b-5p increased the expression of androgen synthesis-related genes and stimulated the secretion of testosterone, while simultaneously downregulating oestrogen synthesis-related genes and decreasing oestradiol release. Ectopically expressed miR-125b-5p reversed the effects on steroidogenesis-related gene expression and hormone release. Mechanistic studies identified Pak3 as a direct target of miR-125b-5p. Furthermore, inhibiting miR-125b-5p facilitated the activation of ERK1/2 in mouse preantral follicles, while inhibiting Pak3 abrogated this activating effect. These results were recapitulated in letrozole-induced PCOS mouse ovaries. Of note, inhibiting PAK3 antagonised the positive effect of miR-125b-5p siRNA on the expressions of androgen synthesis-related enzymes and testosterone secretion. Luteinizing hormone (LH) inhibited miR-125b-5p expression, and stimulated Pak3 expression. CONCLUSION: High serum LH concentrations in PCOS patients repress miR-125b-5p expression, which further increases Pak3 expression, leading to activation of ERK1/2 signalling, thus stimulating the expression of androgen synthesis-related enzymes and testosterone secretion in HA-PCOS.

Sexual function after total laparoscopic hysterectomy or transabdominal hysterectomy for benign uterine disorders: a retrospective cohort.

The objective of this study was to evaluate changes in sexual function after total laparoscopic hysterectomy (TLH) or transabdominal hysterectomy (TAH). This retrospective cohort study included patients with benign uterine tumors that were divided into TLH group and TAH group based on the hysterectomy technique used. Baseline, intraoperative, and postoperative characteristics were compared between groups. Postoperative sexual function was assessed using the Brief Index of Sexual Functioning for Women. The TLH and TAH groups contained 119 patients (age, 51.5±6.1 years) and 126 patients (age, 50.0±4.7 years), respectively. Baseline characteristics were comparable between groups, although uterine size was larger in the TAH group (P<0.001). Compared with the TAH group, the TLH group had a longer operative time (130.0±36.2 vs 107.3±28.5 min, P<0.001), lower pain index at 24 h (2.0±1.6 vs 4.0±2.6, P<0.001), and shorter hospitalization time (5.7±1.1 vs 8.1±1.2 days, P<0.001). Many patients in the TLH and TAH groups reported decreased satisfaction with their sexual life (67.5 and 56.0%, respectively), reduced frequency of sexual activity (70.1 and 56.0%, respectively), decreased libido (67.5 and 56.0%, respectively), orgasm dysfunction (42.9 and 42.9%, respectively), and increased dyspareunia (77.9 and 85.7%, respectively). However, there was no significant difference between groups in any of the indexes of postoperative sexual function (P>0.05). Both TLH and TAH had comparable negative effects on sexual function in women treated for benign uterine tumors in China, with a decreased frequency of sexual activity, reduced libido, orgasm dysfunction, and increased dyspareunia.

PNMA5 knockdown suppresses the proliferation, invasion, and metastasis of epithelial ovarian cancer cells.

BACKGROUND: Ovarian cancer is a severe gynecological malignancy. Paraneoplastic Ma antigen 5 (PNMA5) is a confirmed tumor onconeural antigen, which has been screened as a female fertility factor. PNMA5 overexpression might serve as a marker of poor prognosis in colon cancer. Our earlier study showed that PNMA5 was essential for meiosis in mouse oocytes. In this study, we investigate the role and probable mechanism of PNMA5 in the occurrence and development of epithelial ovarian cancer (EOC). METHODS: Immunochemistry and western blot analyses were used to verify PNMA5 overexpression in clinical EOC tissues and EOC cell line HO8910. A specific siRNA was used to reduce PNMA5 levels, and several proliferation and migration-related indexes were assessed. We also examined mitochondria, microfilaments, and several essential kinases. RESULTS: We found that the expression of PNMA5 in EOC tissues was significantly higher than that in benign ovarian tumors and healthy normal ovarian tissues and that this was strictly related to the FIGO stage and histological grade. PNMA5 expression in ovarian cancer cell line HO8910 was higher than that in the normal healthy ovarian cell line Moody. PNMA5 knockdown in HO8910 cells not only inhibited the proliferation, migration, invasion, cell cycle, and F-actin polymerization of HO8910 cells but also promoted early apoptosis and led to abnormal distribution and accumulation of mitochondria. PNMA5 phosphorylation was found to be positively regulated by Src activity, and PNMA5 phosphorylation promoted the downstream glycogen synthase kinase-3ß (GSK-3ß) signaling pathway. CONCLUSIONS: PNMA5 plays a pivotal role in the occurrence and development of EOC and is a potential marker of this disease.

Sexual function after total laparoscopic hysterectomy or transabdominal hysterectomy for benign uterine disorders: a retrospective cohort

The objective of this study was to evaluate changes in sexual function after total laparoscopic hysterectomy (TLH) or transabdominal hysterectomy (TAH). This retrospective cohort study included patients with benign uterine tumors that were divided into TLH group and TAH group based on the hysterectomy technique used. Baseline, intraoperative, and postoperative characteristics were compared between groups. Postoperative sexual function was assessed using the Brief Index of Sexual Functioning for Women. The TLH and TAH groups contained 119 patients (age, 51.5±6.1 years) and 126 patients (age, 50.0±4.7 years), respectively. Baseline characteristics were comparable between groups, although uterine size was larger in the TAH group (P<0.001). Compared with the TAH group, the TLH group had a longer operative time (130.0±36.2 vs 107.3±28.5 min, P<0.001), lower pain index at 24 h (2.0±1.6 vs 4.0±2.6, P<0.001), and shorter hospitalization time (5.7±1.1 vs 8.1±1.2 days, P<0.001). Many patients in the TLH and TAH groups reported decreased satisfaction with their sexual life (67.5 and 56.0%, respectively), reduced frequency of sexual activity (70.1 and 56.0%, respectively), decreased libido (67.5 and 56.0%, respectively), orgasm dysfunction (42.9 and 42.9%, respectively), and increased dyspareunia (77.9 and 85.7%, respectively). However, there was no significant difference between groups in any of the indexes of postoperative sexual function (P>0.05). Both TLH and TAH had comparable negative effects on sexual function in women treated for benign uterine tumors in China, with a decreased frequency of sexual activity, reduced libido, orgasm dysfunction, and increased dyspareunia.

Microtubule­severing protein Katanin p60 ATPase­containing subunit A­like 1 is involved in pole­based spindle organization during mouse oocyte meiosis.

Microtubule­severing proteins (MTSPs) are a group of microtubule­associated proteins essential for multiple microtubule­related processes, including mitosis and meiosis. Katanin p60 ATPase­containing subunit A­like 1 (p60 katanin­like 1) is an MTSP that maintains the density of spindle microtubules at the poles in mitotic cells; however, to date, there have been no studies about its role in female meiosis. Using in vitro­matured (IVM) oocytes as a model, it was first revealed that p60 katanin­like 1 was predominant in the ovaries and oocytes, indicating its essential roles in oocyte meiosis. It was also revealed that p60 katanin­like 1 was concentrated at the spindle poles and co­localized and interacted with γ­tubulin, indicating that it may be involved in pole organization. Next, specific siRNA was used to deplete p60 katanin­like 1; the spindle organization was severely disrupted and characterized by an abnormal width:length ratio, multipolarity and extra aster microtubules out of the main spindles. Finally, it was determined that p60 katanin­like 1 knockdown retarded oocyte meiosis, reduced fertilization, and caused abnormal mitochondrial distribution. Collectively, these results indicated that p60 katanin­like 1 is essential for oocyte meiosis by ensuring the integrity of the spindle poles.

MicroRNA-218 regulates the chemo-sensitivity of cervical cancer cells through targeting survivin.

Background: Cervical cancer is one of the most lethal malignancies among women in the world. Every year about 311,365 women die because of cervical cancer. Chemo-resistance is the main reason of the lethal malignancies, and the mechanism of chemo-resistance in cervical cancer still remains largely elusive. Purpose: Previous studies reported that microRNAs played important biological roles in the chemo-resistance in many types of cancers, in the present study we tried to investigate the biological roles of microRNA-218 in chemo-resistance in cervical cancer cells. Results: Real-time PCR results indicated microRNA-218 was downregulated in cisplatin-resistant HeLa/DDP and SiHa/DDP cells compared with the mock HeLa and SiHa cells. CCK-8 assay results showed upregulation of microRNA-218 enhanced the cisplatin sensitivity of cervical cancer cells; while downregulation of microRNA-218 decreased the cisplatin sensitivity of cervical cancer cells. Dual-luciferase assay indicated survivin was a direct target of microRNA-218. Western blotting and PCR results indicated the expression of survivin in HeLa/DDP and SiHa/DDP cells was significantly increased compared with HeLa and SiHa cells. Further study indicated induction of microRNA-218 decreased the expression of survivin while inhibition of microRNA-218 increased the expression of survivin in cervical cancer cells. Cell apoptosis results indicated induction of microRNA-218 induced the cell apoptosis in cervical cancer cells. Conclusion: Our data revealed microRNA-218 enhanced the cisplatin sensitivity in cervical cancer cells through regulation of cell growth and cell apoptosis, which could potentially benefit to the cervical cancer treatment in the future.

Knocking down of LINC01220 inhibits proliferation and induces apoptosis of endometrial carcinoma through silencing MAPK11.

Background: Endometrial carcinoma (EC) still threatens the health of women. Thus, to explore how long intergenic non-protein coding RNA 01220 regulates the development of EC.Methods: Whole genome expression profile data of EC and paracancerous tissues in TCGA database were downloaded. LINC01220 expression in EC and paracancerous tissues of patients in our hospital were detected by qRT-PCR. Furthermore, the relationship between LINC01220 expression and clinicopathological features of EC patients was analyzed. After transfection with sh-LINC01220 and pcDNA-MAPK11 (mitogen-activated protein kinase) in EC cells, proliferative, colony formation abilities and apoptosis were determined by cell counting kit-8 (CCK-8), colony formation assay and flow cytometry, respectively. Western blot was conducted to determine the regulatory role of LINC01220 on MAPK11.Results: TCGA data showed that LINC01220 expression is markedly higher in EC tissues than that of paracancerous tissues, which was consistent without detection in EC patients of our hospital. LINC01220 expression was positively correlated to pathological grade and International Federation of Gynecology and Obstetrics (FIGO) stage of EC patients. After knockdown of LINC01220 in EC cells, proliferative and colony formation abilities decreased, whereas apoptotic rate increased. Cor function analysis revealed the positive correlation between LINC01220 and MAPK11 in EC. MAPK11 expression was regulated by LINC01220 in EC cells. Overexpression of MAPK11 can reverse the tumor suppressing effect of LINC01220 on EC.Conclusions: LINC01220 promotes EC development by stimulating proliferation and inhibiting apoptosis of EC cells through up-regulating MAPK11.