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Breast cancer is the second leading cancer diagnosed globally and every year about two million new incidences were accounted. Curcuma wenyujin, a rhizome grown abundantly in china and used in various traditional Chinese medicines. Recent times the research on anticancer property of Curcuma wenyujin is extensively on progress and it is proved by many researchers. The major drawback of herbal drugs are their limited bio-availability, to overcome this we formulated a herbal gold nanodrug with Curcuma wenyujin (CW-AuNPs) and examined its anticancer potential against breast cancer cells. The cytotoxic effect of synthesized CW-AuNPs against MDA-MB231/HER2 cell line was inspected by MTT assay and the dosage for further analysis was calculated. The apoptosis triggered by CW-AuNPs was investigated by intracellular ROS and caspases levels in CW-AuNPs treated MDA-MB231/HER2 cell line. Over expression of HER2/neu, oncogene leads to meager prognosis in most of the breast cancer patients. Therefore in the current exploration, we investigated the inhibitory potential of CW-AuNPs against the expression of HER2/neu in breast cancer cell line by immunocytochemical and immunoblotting analysis. Our results of UV-Spec, FTIR, TEM and Atomic force investigation confirms, the synthesized nanodrug CW-AuNPs satisfies the characteristic features of a nanodrug. The results authentically proves that CW-AuNPs possessed the potent anticancer activity, increases ROS in breast cancer cells which in turn inhibits the HER2/neu, key oncogene expression and inhibited the cancer cell proliferation.

Colorectal cancer (CRC) is one of the most common solid tumors worldwide and has an extremely poor prognosis. MicroRNA-429 (miR-429) has been reported to participate in the progression of CRC. However, the pathological mechanisms require further investigation. The aim of the present study was to investigate the association between miR-429 and high mobility group box 3 (HMGB3) in CRC and the associated mechanism. The mRNA expression levels of miR-429 and HMGB3 in 65 paired CRC and adjacent tissues were examined by reverse transcription-quantitative PCR. Furthermore, a dual-luciferase reporter assay was performed to identify the association between miR-429 and HMGB3. Finally, the effects of miR-429 and HMGB3 on the proliferation and apoptosis of CRC cells were detected. As a result, it was identified that miR-429 expression was downregulated and HMGB3 expression was upregulated in CRC tissues compared with in adjacent non-cancer tissues, and the expression levels of miR-429 were negatively associated with those of HMGB3. Notably, HMGB3 was demonstrated to be a direct target of miR-429 by dual-luciferase reporter assay. Furthermore, transfection with a miR-429 mimic significantly inhibited HMGB3 expression and led to decreased proliferation and increased apoptosis of CRC cells. On the other hand, transient overexpression of HMGB3 partially inhibited the antitumor effects of miR-429. To the best of our knowledge, the present study demonstrated for the first time that miR-429 regulated the proliferation and apoptosis of CRC cells via HMGB3, suggesting a specific tumor suppressive function of the miR-429/HMGB3 signaling pathway in CRC.

Background & Aims The secretory protein Slit2 and its receptor Robo1 are believed to regulate cell growth and migration. Here, we aimed to determine whether Slit2-Robo1 signaling mediates the pathogenesis of liver fibrosis. Methods Serum levels of Slit2 in patients with liver fibrosis were determined by ELISA. Liver fibrosis was induced in wild-type (WT), Slit2 transgenic ( Slit2 -Tg) and Robo1 +/− Robo2 +/− double heterozygotes ( Robo1/2 +/− ) mice by carbon tetrachloride (CCl 4 ). The functional contributions of Slit2-Robo1 signaling in liver fibrosis and activation of hepatic stellate cells (HSCs) were investigated using primary mouse HSCs and human HSC cell line LX-2. Results Significantly increased serum Slit2 levels and hepatic expression of Slit2 and Robo1 were observed in patients with liver fibrosis. Compared to WT mice, Slit2 -Tg mice were much more vulnerable to CCl 4 -induced liver injury and more readily develop liver fibrosis. Development of hepatic fibrosis in Slit2 -Tg mice was associated with a stronger hepatic expression of collagen I and α-smooth muscle actin (α-SMA). However, liver injury and hepatic expression of collagen I and α-SMA were attenuated in CCl 4 -treated Robo1/2 +/− mice in response to CCl 4 exposure. In vitro , Robo1 neutralizing antibody R5 and Robo1 siRNA downregulated phosphorylation of Smad2, Smad3, PI3K, and AKT in HSCs independent of TGF-β1. R5 and Robo1 siRNA also inhibited the expression of α-SMA by HSCs. Finally, the protective effect of R5 on the CCl 4 -induced liver injury and fibrosis was further verified in mice. Conclusions Slit2-Robo1 signaling promotes liver injury and fibrosis through activation of HSCs.