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Yulangsan polysaccharide (YLSPS) is derived from the root of Millettia pulchra (Benth.) Kurz var. Recent studies have postulated YLSPS as a regimen for cancer treatment. However, the underlying mechanism anti-breast cancer is still poorly unknown. The aim of this study was to examine the suppressive and apoptosis effect of YLSPS on the growth of breast cancer cell 4T1 and its possible underlying mechanism. In this study, breast cancer cell 4T1 viability and apoptosis were assessed by CCK-8 and flow cytometry, relative quantitative real-time PCR and western blot after treated with drug-serum of YLSPS. Furthermore, therapy experiments were conducted using a Balb/c mouse transplanted tumor model of breast cancer. The number of apoptotic cells and microvascular density (MVD) in the tumor tissues were assessed by TUNEL and CD34 immunostaining. Immunohistochemical assays and ELISA were used to detect the expression of VEGF, Bcl-2, Bax and Caspase-3 in the tissues. The in vitro studies showed that the drug-serum of YLSPS significantly inhibition of proliferation and effectively induced apoptosis of 4T1 cells. Oral administration of YLSPS in the breast cancer models significantly reduced the tumor volume and weight. The enhanced antitumor efficacy was associated with decreased angiogenesis, an enhanced antioxidant capacity, an increased induction of apoptosis and an inhibition of lung metastasis. These findings indicate that YLSPS significantly inhibited mouse breast cancer growth in vitro and in vivo. These data suggest that YLSPS may serve as a potential therapeutic agent for breast cancer.

Ethnopharmacological relevance The root of Averrhoa carambola L. (Oxalidaceae), a traditional Chinese medicine, was mainly used in ancient times in the treatment of urinary calculi, recurrent headache and joint pain. Aim of the study Our aims were to explore the potential therapeutic effect of the extract of Averrhoa carambola L. (Oxalidaceae) roots (EACR) against hepatic fibrosis in CCl4-treated rats and to understand the underlying molecular mechanism. Materials and methods Six groups of male Sprague Dawley rats were treated as follows: vehicle (olive oil), CCl4 alone, CCl4+colchicine, CCl4+EACR 1.0 g/kg, CCl4+EACR 0.5 g/kg and CCl4+EACR 0.25 g/kg. At the end of the 12th week, biomarkers of liver function, liver fibrosis, hepatic oxidative stress and antioxidant status were assayed, and histopathological and immunohistochemical evaluation of liver tissue were conducted to investigate the liver damage and fibrosis degree. Furthermore, expressions of COL-1a1, α-SMA, TGF-β1, Smad2, smad3, Smad4 and TIMP2 were examined by qPCR and/or western blot. The expressions of apoptosis-related proteins were also detected using western blot analysis. Results EACR treatment markedly reduced the CCl4-induced elevation of serum aminotransferase activities, liver fibrosis indexes, and the extent of oxidative stress. EACR treatment also significantly reduced the accumulation of collagen and the immunostaining of α-SMA, TGF-β1 and Smad2, 4 and 7 in the liver of CCl4 treated rats. In addition, EACR treatment markedly reversed the CCl4-induced increase in mRNA expression of COL-1a1, α-SMA, TIMP2, TGF-β1, Smad2 and Smad4 and suppressed the expressions of α-SMA, TIMP2, TGF-β1, smad2, 3 and 4, BAX and cleaved caspase-3 proteins. Meanwhile, EACR treatment also significantly elevated the mRNA expression of Smad7 and the protein expression of Smad7 and Bcl-2. Conclusion These results suggest that EACR has protective activity against liver fibrosis. The anti-fibrotic activity of EACR in vivo is associated with enhanced antioxidant, apoptosis-inhibition and increased MMP-2/TIMP-2 expression ratio, and with modulation of TGF-β1/Smad signaling pathway.

Osteosarcoma has been reported as a severe and worldwide clinical problem, research focusing on osteosarcoma for overall analysis and understanding of the mechanism will be of great importance for theoretical basis and treatment of osteosarcoma. In the present study, we sought to explore the correlation of miR-200-3p with osteosarcoma proliferation, apoptosis and the related signaling pathway. MTT, flow cytometry, qRT-PCR and western blot were separately used to test the influence of miR-200-3p on cells proliferation, cells apopsotis and the FOXO expression. The results shown that miR-200-3p inhibits cell viability, and promotes apoptosis in Saos-2 and U2OS. The wertern blot results proved the overexpression of miR-200-3p can activate the FOXO signaling pathway by upregulating FOXO1 expression.

Activation of phosphatase and tensin homolog (PTEN) is known to induce cell apoptosis. MicroRNA-374a (miR-374a), which can suppress PTEN expression, has been found abnormally expressed in inflammatory bowel disease (IBD). Fortunellin is a citrus flavonoid that is a potential anti-inflammation agent in inflammatory diseases. The present study investigated the effects and mechanisms underlying fortunellin-induced inhibition of PTEN in IBD. Colitis was established in rats by the intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid to mimic human ulcerative colitis, which is the main type of IBD. miR-374a expression was measured by quantitative real-time polymerase chain reaction, and the regulation of PTEN by miR-374a was evaluated by dual luciferase reporter assay. Western blotting was used to measure the corresponding protein expression. Fortunellin ameliorated colitis symptoms, including excessive inflammation and oxidative stress. Fortunellin decreased epithelial cell apoptosis through inhibiting PTEN expression in colitis. Fortunellin-induced downregulation of PTEN could be counteracted by miR-374a depletion. Moreover, knockdown of miR-374a in vivo partly inhibited the effects of fortunellin on rat colitis. In conclusion, PTEN inhibition contributes to the amelioration effects of fortunellin on colitis. It was confirmed that fortunellin targets miR-374a, which is a negative regulator of PTEN. This study provides novel insights into the pathological mechanisms and treatment alternatives of colitis.

Curcumin has been proven to effectively inhibit tumor growth by both targeting tumor cells and angiogenesis; however, poor water solubility limits further clinical application. In the present study, we prepared water-soluble liposomal curcumin to investigate its anti-tumor effects and the underlying mechanism. The MTT assay was used to test the anti-proliferative activities for the MS1 murine endothelial and LL/2 Lewis lung cancer cell lines. Apoptosis and cell cycle arrest induced by liposomal curcumin were analysed by flow cytometry. Anti-angiogenic agents and the resulting anti-tumor effects were investigated in a murine lung cancer model. Zebrafish were used to investigate the anti-angiogenic effect of liposomal curcumin in the development of embryos. In vitro, liposomal curcumin inhibited the proliferation of MS1 cells and induced cell cycle arrest and apoptosis. Notably, LL/2 cells showed less sensitivity to the liposomal curcumin in vitro. In vivo, the systemic administration of liposomal curcumin resulted in significant inhibition of tumor growth. CD31 immunohistochemical analysis and alginate encapsulation assay revealed that angiogenesis was decreased by liposomal curcumin treatment. Angiogenesis was also suppressed in the development of zebrafish. Liposomal curcumin showed potent inhibitory activity against murine endothelial cells but not lung cancer cells. Liposomal curcumin treatment is capable of significantly inhibiting tumor growth in vivo, a process that may depend primarily on its anti-angiogenic effects. Our study also indicates that liposomal curcumin may be developed not only for cancer therapy, but also for the treatment of other angiogenesis-related diseases.