Clinical Effect of Uterosacral and Cardinal Ligament Fixation versus Sacrospinous Ligament Fixation of Vaginal Vault Prolapse: A Retrospective Analysis.

Objective: This study aimed at comparing sacrospinous ligament fixation (SSLF) with uterosacral and cardinal ligament fixation (USCLF) concerning complications and outcomes in patients with pelvic organ prolapse (POP). Methods: A retrospective analysis was performed on the clinical data of patients with POP stage III or above uterine prolapse treated at Wenzhou People's Hospital from January 2013 to December 2019. Patients were divided into two groups: USCLF group and SSLF group. The perioperative indicators, postoperative complications, pelvic organ prolapse quantification (POP-Q), Pelvic Floor Distress Inventory-20 (PFDI-20), and POP/Urinary Incontinence Sexual Questionnaire-12 (PISQ-12) scores of the groups were analyzed and compared. Results: (1) The operative time and intraoperative blood loss in the USCLF group were lower than those in the SSLF group, with statistical significance (p < 0.05). (2) The incidence of postoperative buttock pain in the SSLF group was 10.7% (6/56), higher than that in the USCLF group (0/56) (Fisher's exact test, p = 0.027). (3) At one year of follow-up, significant improvement in Aa, Ba, C, Ap, and Bp values was observed in both groups (p < 0.05). The values of the Aa and Ba sites in the USCLF group were lower than those in the SSLF group one year after surgery (p < 0.05). (4) The PFDI-20 and PISQ-12 scores of the groups one year after surgery were lower than those before surgery (p < 0.05). Conclusion: Uterosacral and cardinal ligament suture fixation leads to less bleeding and better postoperative quality of life than preoperative and may be better than SSLF at preventing the recurrence of anterior wall prolapse after surgery.

A Functional Variant rs2072915 is Associated with the Susceptibility and Mortality of Cervical Squamous Cell Carcinoma.

PURPOSE: Genetic variant has been demonstrated to be a risk factor for the occurrence and outcome of cervical squamous cell carcinoma (CSCC). From previous genome wide association studies, 6p21.32 has been identified as a susceptibility locus of CSCC. The purpose of this study was to investigate the association of a polymorphism rs2072915 located in 6p21.32 with the risk of CSCC and examine the potential mechanism of the rs2072915 in CSCC pathogenesis. PATIENTS AND METHODS: The rs2072915 was genotyped using polymerase chain reaction (PCR)-restriction fragment length polymorphism. miR-637 and RXRB mRNA expression levels in CSCC patients were examined using quantitative PCR. miR-637 target site was determined using the dual-luciferase reporter assay. RESULTS: The rs2072915 was associated with a significantly increased risk (AA vs TT: adjusted OR = 2.48, 95% CI, 1.57-3.94, P < 0.001; AT/AA vs TT: adjusted OR = 1.38, 95% CI, 1.06-1.80, P = 0.018; A vs T: adjusted OR = 1.49, 95% CI, 1.21-1.84, P < 0.001, respectively) and shorter survival time of CSCC (P = 0.03). Patients with the rs2072915 AA genotype displayed lower levels of RXRB that is a target of miR-637. CONCLUSION: These findings suggest that the rs2072915 T > A change might augment the binding energy of miR-637 to RXRB, result in lower levels of RXRB, and thus contribute to the risk of CSCC.

LINC00261 functions as a competing endogenous RNA to regulate BCL2L11 expression by sponging miR-132-3p in endometriosis.

Endometriosis is a benign disease but manifests with malignant features and limited treatment options. Women with endometriosis should not be ignored or patronized by the medical profession and society. In this regard, a major cultural change and searching for the optimum therapeutic regimen from multiple perspectives is needed in China even in the whole world. Long non-coding RNAs are crucial for various human diseases while its potential functions and mechanisms are largely unknown in endometriosis. LINC00261 was significantly downregulated in endometriosis tissues and our study indicated that it suppresses proliferation and invasion of endometriosis cells functionally in vitro. Insights of the mechanism of competitive endogenous RNAs were obtained from bioinformatic analysis, RIP, RNA pull-down and luciferase assays, which further confirmed that LINC00261 functions as a molecular sponge to regulate BCL2L11 expression by binding to miR-132-3p directly. These data defined LINC00261/miR-132-3p/BCL2L11 regulatory networks may be a novel therapeutic target for endometriosis.

Upregulation of long noncoding RNA TUG1 by EGR1 promotes adenomyotic epithelial cell migration and invasion through recruiting EZH2 and suppressing TIMP2.

Emerging studies showed that lncRNA taurine upregulated 1 (TUG1) plays important roles in diverse biological processes. However, there is no previously published research reporting the regulatory role of lncRNAs in the progression of adenomyosis. In the present study, we found that TUG1 is upregulated in human adenomyosis, and the overexpression of TUG1 is associated with the transcription factor early growth response 1 (EGR1). Functionally, the knockdown of TUG1 inhibited adenomyotic epithelial cell migration and invasion but not growth. The mechanistic experiments demonstrated that the function of TUG1 in adenomyotic epithelial cell invasion is, at least in part, through recruiting the enhancer of zeste homolog 2 (EZH2) to the promoter of tissue inhibitor of metalloproteinases 2 (TIMP2) and negatively regulating its expression. Our study demonstrated that TUG1 promotes the migration and invasion of human adenomyotic epithelial cells, and EGR1/TUG1/EZH2/TIMP2 may be a potential therapeutic target for adenomyosis.

Clinical efficacy of pelvic autologous tissue reconstruction in treating pelvic organ prolapse in 36 patients.

This study aims to search for a new, economic, convenient, and low recurrence rate operation for the surgical management of pelvic organ prolapse (POP). The clinical value of the operation for treating POP was determined through retrospective case series. The new operation was called, pelvic autologous tissue reconstruction.Women with symptomatic uterine prolapse, who required surgery, were recruited. A total of 97 women [stage III to IV, according to POP quantification (POP-Q) staging] were collected from January 2010 to December 2016. Among these women, 61 women underwent a traditional operation (TO, vaginal hysterectomy and vaginal anterior and posterior wall repair), while the remaining women underwent pelvic autologous tissue reconstruction.First, there was no statistically significant difference in intraoperative blood loss, indwelling urethral catheter time, in-hospital time, and the time of passage of gas through the anus between the pelvic autologous reconstruction (PAR) and TO groups (P > .05). The average operation time in the PAR group was significantly longer than that in the TO group (P < .05). Second, ultrasonic parameters before and after the operation between the 2 groups were compared. The postoperative rotation angle of the urethra (UR), posterior vesicourethral angle (PVA), and bladder neck descent (BND) significantly decreased in the PAR group (P < .05). There was no statistically significant difference in UR between before and 12 months after surgery in the TO group (P > .05). Furthermore, BND increased in the TO group at 12 months after the operation, compared with that at 3 months after the operation (P < .05). There was no significant difference in PVA and UR before the surgery and at 3 and 12 months after the surgery between the 2 groups (P > .05). In addition, BND was significantly smaller in the PAR group than in the TO group at 3 and 12 months after the surgery (P < .05). Third, there was no statistically significant difference in PFIQ-7 and PISG-12 in both groups after surgery.The stability of the pelvic floor structure was better in the PAR group than in the TO group. Furthermore, PAR is better for preventing the occurrence of pelvic floor prolapse and stress urinary incontinence after surgery.

Long non-coding RNA LINC00261 inhibits cell growth and migration in endometriosis.

AIM: A previous study reported that LINC00261 is significantly downregulated in human ectopic endometrial tissues. The present study aimed to explore whether LINC00261 is functional in endometriosis cell proliferation, apoptosis and migration. METHODS: By transfecting human endometriosis cell line CRL-7566 with plasmids containing LINC00261, we successfully established the cell CRL-7566/LINC00261 with a high LINC00261 expression level. Cell-counting kit-8 and colony formation assays were conducted to evaluate the effect of LINC00261 on cell proliferation, and flow cytometry analysis and transwell migration assay were conducted to evaluate its effect on cell apoptosis and cell migration, respectively. RESULTS: Cell-counting kit-8 and colony formation assays both indicated that LINC00261 could inhibit cell proliferation in CRL-7566. Flow cytometry analysis confirmed that LINC00261 mediated inhibition of cell proliferation, which might be a consequence of inducting apoptosis. Furthermore, transwell migration assay indicated that LINC00261 could inhibit cell migration in endometriosis. CONCLUSION: LncRNA LINC00261 is capable of inhibiting cell growth and migration in endometriosis.

[Experimental study on anti-metastasis effect of emodin on human pancreatic cancer].

OBJECTIVE: To investigate the anti-metastasis effect of emodin on the pancreatic cancer in vitro and in vivo. METHOD: Human pancreatic cancer cell line SW1990 was treated with different concentrations of emodin (10, 20, 40 micromol x L(-1)) for 2 h, the effects of emodin on the migration and invasion of SW1990 cells were examined by using wound assay and matrigel counting. Western blot was used to detect the protein expression of NF-kappaB and MMP-9 in SW1990 cells after various concentrations of emodin (10, 20, 40 micromol x L(-1)) treatment for 48 h. Metastatic model simulating human pancreatic cancer was established by orthotropic implantation of histologically intact human tumor tissue into pancreatic wall of nude mice, and then divided into three groups: control group, low-dose emodin group (L-EMO) and high-dose emodin group (H-EMO). Eight weeks after implantation, the presences of metastasis were evaluated respectively after the mice were sacrificed. Immunohistochemistry was used to detect the positive expression of CD34, NF-kappaB and MMP-9 in the tumors. RESULT: Emodin suppressed the migration and invasion of SW1990 cells in a dose-dependent manner. Western bolt assay indicated that emodin down-regulated the expression of NF-kappaB and MMP-9 proteins in SW1990 cells. The incidences of metastasis were decreased significantly in L-EMO group and H-EMO group as compared with that in control group. The percentage of CD34, NF-kappaB and MMP-9-positive cells in the tumors were significantly reduced by the administration of emodin. CONCLUSION: Emodin exerts anti-metastatic activity in pancreatic cancer both in vitro and in vivo, which may be related to down-regulation of NF-kappaB and MMP-9.