Abstract:Catalpol is expected to possess diverse pharmacological actions including anti-cancer, anti-inflammatory and hypoglycemic properties. Matrix metalloproteinase-2 (MMP-2) is closely related to the pathogenesis of ovarian cancer. In addition, microRNA-200 (miR-200) can modulate phenotype, proliferation, infiltration and transfer of various tumors. Here, OVCAR-3 cells were employed to investigate whether the effect of catalpol (25, 50 and 100 μg/mL) promoted apoptosis of ovarian cancer cells and to explore the potential mechanisms. Our results demonstrate that catalpol could remarkably reduce the proliferation and accelerate the apoptosis of OVCAR-3 cells. Interestingly, our findings show that catalpol treatment significantly decreased the MMP-2 protein level and increased the miR-200 expression level in OVCAR-3 cells. Further, microRNA-200 was shown to regulate the protein expression of MMP-2 in OVCAR-3 cells. It is concluded that catalpol suppressed cellular proliferation and accelerated apoptosis in OVCAR-3 ovarian cancer cells via promoting microRNA-200 expression levels and restraining MMP-2 signaling.

Abstract. Primary ovarian leiomyosarcoma (POLMS) is a rare disease. To the best of our knowledge, only 72 cases, including the present case, have been reported in the English literature, while synchronous POLMS and fibroma in a single ovary have not previously been reported at all. In the present study, a 46-year-old premenopausal woman was diagnosed with a mass in the left ovary in 2005. A total of 5 years after the diagnosis of this mass, the patient was admitted to hospital exhibiting lower abdominal pain, and two masses were observed in the left ovary. An exploratory laparoscopy was performed. Frozen section analysis led to a diagnosis of fibroma. Furthermore, the observed second mass was hypothesized to be a malignant form of the original fibroma. A hysterectomy and bilateral salpingo-oophorectomy were performed. Pathological reports following surgery revealed concurrent stage Ic POLMS and fibroma in the left ovary. A total of 13 months after the initial surgery, recurrent leiomyosarcoma was detected. Although the patient underwent multiple cytoreductive surgeries and chemotherapy cycles, as well as interstitial brachytherapy and conventional therapy, a poor state of health ensued. Due to the rarity of POLMS, particularly in combination with ovarian fibroma, the current report presents a detailed overview of the literature and discusses a number of histogenetic and clinical issues.

Background: Tissue factor pathway inhibitor 2 (TFPI2) participates in carcinogenesis of various tumors, and is associated with poor survival of breast cancer patients. However, the effect and underlying mechanism of TFPI2 on breast cancer progression remains to be investigated. Methods: The expression level of TFPI2 in breast cancer tissues and cell lines was examined via qRT-PCR (quantitative real-time polymerase chain reaction) and immunohistochemistry. CCK8 (Cell Counting Kit-8), colony formation, wound healing or transwell assays were used to detect cell viability, proliferation, migration or invasion, respectively. In vivo subcutaneous xenotransplanted tumor model was established to detect tumorigenic function of TFPI2, and the underlying mechanism was evaluated by immunohistochemistry and western blot. Results: TFPI2 was down-regulated in breast cancer tissues and cell lines, and was associated with poor prognosis of patients diagnosed with breast cancer. Over-expression of TFPI2 inhibited cell viability, proliferation, migration and invasion of breast cancer cells. Mechanistically, Twist-related protein 1 (TWIST1) was negatively associated with TFPI2 in breast cancer patients, whose expression was decreased by TFPI2 over-expression or increased by TFPI2 knockdown. Moreover, TWIST1 could up-regulate integrin α5 expression. Functional assays indicated that the inhibition abilities of TFPI2 over-expression on breast cancer progression were reversed by TWIST1 over-expression. In vivo subcutaneous xenotransplanted tumor model also revealed that over-expression of TFPI2 could suppress breast tumor growth via down-regulation of TWIST1-mediated integrin α5 expression. Conclusions: TFPI2 suppressed breast cancer progression through inhibiting TWIST-integrin α5 pathway, providing a new potential therapeutic target for breast cancer treatment.

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AIMSSeveral epidemiological studies have reported inconsistent associations between insulin therapy and the risk of colorectal cancer (CRC) in patients with type 2 diabetes mellitus. We performed this meta-analysis of observational studies to evaluate the effect of insulin therapy on the risk of CRC. METHODSWe carried out a systematic search of PubMed, Embase and the Cochrane Library Central database between January 1966 and August 2013. Fixed-effects and random-effects models were used to estimate the pooled relative risk (RR) and corresponding 95% confidence interval (CI). RESULTSA total of 12 epidemiological studies were included in the present meta-analysis, involving a total of 7947 CRC cases and 491 384 participants. There was significant heterogeneity among the studies, but no publication bias. Insulin therapy significantly increased the risk of CRC [RR = 1.69, 95% CI (1.25, 2.27)]. When the various studies were stratified by study design, we found that insulin use was associated with a statistically significant 115% CONCLUSIONSThe present meta-analysis suggests that insulin therapy may increase the risk of CRC. More prospective cohort studies with longer follow-up durations are warranted to confirm this association. Furthermore, future studies should report results stratified by gender and race and should adjust the results by more confounders. WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• The association between insulin therapy and cancer growth is linked at the biological level through hyperinsulinemia. Although several observational studies have investigated the association between insulin therapy and risk of colorectal cancer; however, the results were inconsistent. WHAT THIS STUDY ADDS• The present meta-analysis suggested that insulin therapy may increase the risk of colorectal cancer.