The effect of pelvic floor muscle training for women with pelvic organ prolapse: a meta-analysis.

INTRODUCTION AND HYPOTHESIS: This study was aimed at evaluating the effect of pelvic floor muscle training (PFMT) as a conservative treatment for patients with pelvic organ prolapse (POP). METHODS: A comprehensive search to identify eligible randomized controlled trial (RCT) studies was conducted using electronic databases including PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), and Embase up to 10 June 2021. Results were presented as risk ratio (RR), the weighted mean difference (WMD), with 95% confidence interval (95% CI) using the random effects model. Outcome variables were pooled using Review Manager version 5.3. RESULTS: Thirteen studies were included. Our results demonstrated that women who received PFMT intervention had a greater improvement than controls in prolapse symptom score (POP-SS; mean difference [MD] -1.66, 95% CI -2.36 to -0.97, p < 0.00001] and POP stages (risk ration [RR] 1.51, 95% CI 1.14-2.01, p = 0.004). The number of participants who felt better after PFMT was higher (RR 1.98, 95% CI 1.21-3.24, p = 0.006). Subgroup analysis showed that the symptoms of prolapse and the degree of prolapse were improved significantly in the short term, but there was no significant difference in the long-term effect. In addition, there was no significant difference in the impact of PFMT on the elderly and the quality of life. More RCTs are needed to evaluate the effect of PFMT on the elderly and whether the quality of life can be improved. CONCLUSIONS: We found that PFMT can improve subjective symptoms and objective POP severity. More research is needed on the long-term effect.

Three adiponectin rs1501299G/T, rs822395A/C, and rs822396A/G polymorphisms and risk of cancer development: a meta-analysis.

Many epidemiological studies have studied the associations between adiponectin rs1501299G/T, rs822395A/C, and rs822396A/G polymorphisms and risk of cancer development, while conflicting results have been reported. Therefore, we conducted a meta-analysis to assess the associations. We retrieved the following databases: Medline, Embase, Web of Science, and Wanfang, and the latest update date was 15th of August 2012. Odds ratio (OR) and corresponding 95 % confidence interval (95 % CI) were calculated by using fixed- or random-effect model. Overall, there were 13 case-control studies consisting of 7,902 subjects for adiponectin rs1501299G/T, seven studies consisting of 6,209 subjects for rs822395A/C, and seven studies consisting of 5,791 subjects for rs822396A/G polymorphism in this study. Combined analyses indicated that neither adiponectin rs822395A/C nor rs822396A/G was associated with risk of cancer incidence (OR (95 % CI) 0.91 (0.77-1.77), P z test = 0.26 for CC vs. AA and 0.96 (0.87-1.05) for C carriers vs. A carriers, P z test = 0.33 for rs822395A/C; 0.88 (0.53-1.47) for GG vs. AA, P z test = 0.63 and 0.94 (0.84-1.04) for G carriers vs. A carriers, P z test = 0.24 for rs822396A/G polymorphism). Similarly, combined analysis also indicated that adiponectin rs1501299G/T polymorphism was not associated with risk of cancer development (OR (95 % CI) 0.86 (0.73-1.01) for TT vs. GG, P z test = 0.07 and 1.17 (0.98-1.39), P z test = 0.08). However, when stratified analyses were conducted, the result indicated that T allele was significantly associated with increased cancer risk for Caucasians (OR (95 % CI) 1.28 (1.06-1.64) and P z test = 0.01 for G carriers vs. T carriers) and associated with increased risk of colorectal cancer development while with decreased risk of prostate cancer incidence compared to G allele (OR (95 % CI) 1.34 (1.14-1.57), P z test < 0.01 for G carriers vs. T carriers for colorectal cancer; 0.80 (0.65-0.97), P z test = 0.03 for TG vs. GG for prostate cancer). In summary, this meta-analysis indicated that adiponectin rs1501299G/T, rather than rs822395A/C and rs822396A/G polymorphism, was associated with risk of cancer development, especially for colorectal and prostate cancer.

[Retracted] microRNA­206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α­positive ovarian cancer cells.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 1A and Transwell cell migration data shown in Fig. 4A were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 9: 1703­1708, 2014; DOI: 10.3892/mmr.2014.2021].

[Retracted] MicroRNA­148a inhibits the proliferation and promotes the paclitaxel­induced apoptosis of ovarian cancer cells by targeting PDIA3.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the cell apoptosis assay data shown in Figs. 1C and 4D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12: 3923­3929, 2015; DOI: 10.3892/mmr.2015.3826].

[Retracted] MicroRNA­148a inhibits migration and invasion of ovarian cancer cells via targeting sphingosine­1­phosphate receptor 1.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 4A and B were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12: 3775­3780, 2015; DOI: 10.3892/mmr.2015.3827].

Tumor necrosis factor-alpha suppresses the invasion of HTR-8/SVneo trophoblast cells through microRNA-145-5p-mediated downregulation of Cyr61.

Deficiency in trophoblast invasion is causally linked to the pathogenesis of preeclampsia. Tumor necrosis factor-alpha (TNF-α) shows the ability to suppress the invasiveness of trophoblasts, while cysteine-rich 61 (Cyr61) exerts an opposite function in trophoblast invasion. This study was designed to check the hypothesis that cysteine-rich 61 (Cyr61) may be involved in the anti-invasive activity of TNF-α in trophoblasts. To this end, we examined the effect of TNF-α treatment on Cyr61 expression in HTR-8/SVneo trophoblast cells and investigated the mechanism for the regulation of Cyr61 by TNF-α. Gain-of-function experiments were performed to clarify the role of Cyr61 in TNF-α-dependent suppression of trophoblast invasion. It was found that TNF-α at 1 and 10 ng/mL reduced Cyr61 protein levels by 30 and 80%, respectively, in HTR-8/SVneo cells, but did not affect the mRNA expression of Cyr61. Mechanistically, microRNA (miR)-145-5p was stimulated by TNF-α and negatively regulated the expression of Cyr61 via interaction with its 3'-untranslated region. Functionally, overexpression of miR-145-5p significantly impaired the migration and invasion of HTR-8/SVneo cells. Depletion of miR-145-5p rescued HTR-8/SVneo cells from TNF-α-mediated invasion suppression, which coincided with prevention of Cyr61 downregulation by TNF-α. In addition, overexpression of Cyr61 partially restored the invasion of HTR8/SVneo cells co-transfected with miR-145-5p mimic or exposed to TNF-α. Taken together, miR-145-5p-mediated downregulation of Cyr61 is required for the anti-invasive effect of TNF-α on trophoblasts.

MicroRNA-148a inhibits the proliferation and promotes the paclitaxel-induced apoptosis of ovarian cancer cells by targeting PDIA3.

MicroRNAs (miRs) are a class of non-coding RNAs that function as key regulators of gene expression at the post-transcriptional level. miR-148a has been suggested to be associated with human ovarian cancer, however, the detailed functions of miR­148a in ovarian cancer remain to be fully elucidated. The present study aimed to investigate the regulatory mechanism of miR-148a in ovarian cancer cells. Reverse transcription­quantitative polymerase chain reaction and western blot analysis were conducted to examine the RNA and protein levels, respectively. The luciferase reporter assay was used to determine the target relationship. Cell proliferation and apoptosis assays were additionally conducted. The present study demonstrated that miR­148a inhibited cell proliferation and promoted the paclitaxel­induced apoptosis of ovarian cancer cells. Furthermore, protein disulfide isomerase family A, member 3 (PDIA3) was identified as a target gene of miR­148a. A fluorescent reporter assay was performed to confirm that miR­148a was able to directly bind to the 3'­untranslated region of PDIA3 mRNA. In addition, miR­148a was frequently downregulated in ovarian cancer tissue, whereas the expression levels of PDIA3 were increased. Knockdown of PDIA3 significantly inhibited the proliferation and promoted the paclitaxel­induced apoptosis of the ovarian cancer cells, whereas overexpression of PDIA3 had the opposite effects. Therefore, the results of the present study suggested that miR­148a inhibited the proliferation and promoted the paclitaxel­induced apoptosis of ovarian cancer cells, and this may be partly attributed to direct targeting of PDIA3.

MicroRNA-148a inhibits migration and invasion of ovarian cancer cells via targeting sphingosine-1-phosphate receptor 1.

MicroRNAs, a group of small non-coding RNA molecules that are involved in gene silencing, function as fine­tuning regulators during cancer progression. MicroRNA (miR)-148a has previously been demonstrated to be associated with ovarian cancer. However, whether miR­148a influences the migration and invasion of ovarian cancer cells has remained elusive. In the present study, reverse transcription­quantitative polymerase chain reaction and western blotting were conducted to examine mRNA and protein expression levels, respectively. Luciferase reporter assay was used to determine target relationship, and a Transwell assay was used to study cell migration and invasion. The results of the present study indicated that miR­148a expression was markedly downregulated in ovarian cancer tissues compared with that of their matched normal adjacent tissues. In addition, miR­148a expression levels were reduced in three ovarian cancer cell lines, SKOV3, OVCAR and A2780, when compared with those of HUM­CELL­0088 normal ovarian epithelial cells. Furthermore, sphingosine­1­phosphate receptor 1 (S1PR1), which is upregulated in ovarian cancer tissues and cell lines, was identified as a novel target of miR­148a in SKOV3 ovarian cancer cells. The protein expression of S1PR1 was negatively regulated by miR­148a in SKOV3 cells. Furthermore, overexpression of miR­148a or inhibition of S1PR1 suppressed SKOV3 cell migration and invasion, while restoration of S1PR1 expression reversed the suppressive effect of miR­148a upregulation on SKOV3 cell migration and invasion. In conclusion, it was hypothesized that miR­148a may potentially be used as a molecular agent for the prevention and treatment of invasion and metastasis in ovarian cancer, while S1PR1 may present a promising target for clinical applications.

microRNA-206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α-positive ovarian cancer cells.

The expression levels of estrogen receptor (ER α) are closely associated with estrogen-dependent growth, invasion and response to endocrine therapy in ERα-positive ovarian cancer. However, the underlying regulatory mechanisms remain to be fully understood. Previous studies have demonstrated that ERα is a direct target of microRNA (miR)-206. miR-206 has been found to be an important tumor suppressor in several cancer types, including ovarian, gastric and laryngeal cancer. However, the specific role of miR-206 in ovarian cancer remains unclear. The aim of the present study was to investigate the role of miR-206 in ER-a positive ovarian cancer in vitro. The present study demonstrated that miR-206 is significantly downregulated in ERα-positive but not ERα­negative ovarian cancer tissues, compared with normal ovarian epithelium tissue. It was also found that the expression of miR-206 was decreased in ERα-positive ovarian cancer cell lines, CAOV-3 and BG-1, compared with normal ovarian epithelium tissues. This suggests that miR-206 may play a role in ERα-positive ovarian cancer cells via an estrogen-dependent mechanism. Further analysis revealed that 17ß-E2 treatment significantly promoted cellular proliferation and invasion of estrogen-dependent CAOV-3 and BG-1 cells, which could be reversed by the introduction of miR-206 mimics. In conclusion, the present study suggests that miR-206 has an inhibitory role in estrogen-dependent ovarian cancer cells. Thus, miR-206 may be a promising candidate for the endocrine therapy of ERα-positive ovarian cancer.

High-dose aspirin consumption contributes to decreased risk for pancreatic cancer in a systematic review and meta-analysis.

OBJECTIVES: The aim of this study was to analyze the association between aspirin intake and its effect for chemoprevention of pancreatic cancer incidence by using a meta-analysis method. METHODS: The databases of MEDLINE, EMBASE, and Wangfang (Chinese database) were retrieved to identify eligible studies. Odds ratio (OR) and 95% confidence interval (CI) were calculated using a random-effects model. RESULTS: A total of 10 studies (4 case-control studies, 5 prospective cohort studies, and 1 randomized controlled trial) with 7,252 cases of pancreatic cancer and more than 120,0000 healthy control subjects were enrolled in the studies. Pooled analyses showed that high-dose aspirin intake was marginally associated with decreased risk for pancreatic cancer for overall analysis (OR, 0.88; 95% CI, 0.76-1.01) as well as for both cohort and case-control studies (OR, 0.70; 95% CI, 0.54-1.16, for the cohort studies; OR, 0.82; 95% CI, 0.62-1.02, for the case-control studies), without between-study heterogeneity. Stratified analysis for Americans showed a similar result (OR, 0.82; 95% CI, 0.65-1.02). In contrast, our study inferred that low-dose aspirin intake was not associated with risk for pancreatic cancer for the total and subgroup analyses. CONCLUSIONS: In summary, our study indicated that high-dose aspirin, rather than low-dose aspirin, might be associated with decreased risk for pancreatic cancer, especially for Americans.