BackgroundBreast cancer is the most common cancer among women worldwide and metastasis is the leading cause of death among patients with breast cancer. The transforming growth factor-β (TGF-β) pathway plays critical roles during breast cancer epithelial–mesenchymal transition (EMT) and metastasis. SMAD2, a positive regulator of TGF-β signaling, promotes breast cancer metastasis through induction of EMT.MethodsThe expression of miR-190 and SMAD2 in breast cancer tissues, adjacent normal breast tissues and cell lines were determined by RT-qPCR. The protein expression levels and localization were analyzed by western blotting and immunofluorescence. ChIP and dual-luciferase report assays were used to validate the regulation of ZEB1-miR-190-SMAD2 axis. The effect of miR-190 on breast cancer progression was investigated both in vitro and in vivo.ResultsmiR-190 down-regulation is required for TGF-β-induced EMT. miR-190 suppresses breast cancer metastasis both in vitro and in vivo by targeting SMAD2. miR-190 expression is down-regulated and inversely correlates with SMAD2 in breast cancer samples, and its expression level was associated with outcome in patients with breast cancer. Furthermore, miR-190 is transcriptionally regulated by ZEB1.ConclusionsOur data uncover the ZEB1-miR-190-SMAD2 axis and provide a mechanism to explain the TGF-β network in breast cancer metastasis.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0818-9) contains supplementary material, which is available to authorized users.

Advancing age is associated with endothelial dysfunction and reduced arterial elasticity. Reduced arterial elasticity parallels changes in impaired endothelium dependent vasodilation. It appears that reduced arterial elasticity may be used as a noninvasive measure for the determination of endothelial function.

Objective To assess the effect of a low carbohydrate diet (LCD) on women with polycystic ovary syndrome (PCOS). Methods Data from randomized controlled trials (RCTs) were obtained to perform a meta-analysis of the effects of LCD in PCOS patients. The primary outcomes included the changes in BMI, homeostatic model assessment for insulin resistance (HOMA-IR), and blood lipids, including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), follicle-stimulating hormone (FSH), luteotropic hormone (LH), total testosterone (T), and sex hormone-binding globulin (SHBG). Results Eight RCTs involving 327 patients were included. In comparison with the control group, the LCD decreased BMI (SMD = −1.04, 95% CI (−1.38, −0.70), P < 0.00001), HOMA-IR (SMD = −0.66, 95% CI (−1.01, −0.30), P < 0.05), TC (SMD = −0.68, 95% CI (−1.35, −0.02), P < 0.05), and LDL-C (SMD = −0.66, 95% CI (−1.30, −0.02), P < 0.05). Stratified analyses indicated that LCD lasting longer than 4 weeks had a stronger effect on increasing FSH levels (MD = 0.39, 95% CI (0.08, 0.71), P < 0.05), increasing SHBG levels (MD = 5.98, 95% CI (3.51, 8.46), P < 0.05), and decreasing T levels (SMD = −1.79, 95% CI (−3.22, −0.36), P < 0.05), and the low-fat and low-CHO LCD (fat <35% and CHO <45%) had a more significant effect on the levels of FSH (MD = 0.40, 95% CI (0.09, 0.71), P < 0.05) and SHBG (MD = 6.20, 95% CI (3.68, 8.72), P < 0.05) than the high-fat and low-CHO LCD (fat >35% and CHO <45%). Conclusion Based on the current evidence, LCD, particularly long-term LCD and low-fat/low-CHO LCD, may be recommended for the reduction of BMI, treatment of PCOS with insulin resistance, prevention of high LDL-C, increasing the levels of FSH and SHBG, and decreasing the level of T level. Together, the analyzed data indicate that proper control of carbohydrate intake provides beneficial effects on some aspects of PCOS and may represent one of the important interventions improving the clinical symptoms of affected patients.

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