Colon cancer is one of the major prevailing types of cancer worldwide. It has been the most important public health difficulty. Thus, we planned phytoconstituents arbitrated synthesis of gold nanoparticles (AuNPs) and examined their curative efficacy against the colon cancer (HCT-116) cells. In this current study, we formulated the AuNPs by using Albizia lebbeck (AL) aqueous leaf extract by the green method and synthesized AL-AuNPs were distinguished by UV-visible spectroscopy (UV-vis), energy dispersive X-ray diffraction (XRD), selected area (electron) diffraction (SAED) pattern, Fourier transform infrared spectroscopy (FTIR) and high-resolution transmission electron microscopy (HR-TEM). Synthesized AL-AuNPs confirmed by the UV absorption highest at 535 nm and the crystal structure of AL-AuNPs was additionally established by XRD and SAED pattern. HR-TEM images explained the size and morphology allocation of nanoparticles. FTIR analysis confirmed the presence of alkynes, aromatic compounds, and alkenes of biomolecules in AL-AuNPs. Furthermore, AL-AuNPs induced cytotoxicity at the IC 50 concentration 48 mg/ml and also induced apoptosis by enhanced ROS production, decreased DWm, apoptotic morphological changes by AO/EtBr and altering pro and anti-apoptotic protein expressions were analyzed in HCT-116 colon cancer cells. The findings of this investigation proved that the AL-AuNPs were revealed the potential anticancer activity against colon cancer (HCT-116) cells.

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Purpose Colorectal cancer (CRC) is the third most common cancer in China and poses high morbidity and mortality. In recent years, increasing evidence has indicated that microRNAs played important functions in the occurrence and development of tumors. The purpose of this study was to identify the biological mechanisms of miR-362 in CRC. Materials and Methods Quantitative real-time PCR was carried out to assess the expression of miR-362 and SIX1. The Kaplan-Meier method was employed to evaluate the 5-year overall survival of CRC patients. The proliferative and invasive abilities of CRC cells were assessed by MTT and transwell assays. Results miR-362 was significantly decreased in CRC tissues and cell lines, compared to the normal tissues and normal cells. A significant connection was confirmed between the overall survival of 53 CRC patients and low expression of miR-362. Downregulation of miR-362 inhibited the proliferation and invasion through binding to the 3′-UTR of SIX1 mRNA in CRC. Additionally, we discovered that SIX1 was a direct target gene of miR-362 and that the expression of miR-362 had a negative connection with SIX1 expression in CRC. SIX1 could reverse partial functions in the proliferation and invasion in CRC cells. Conclusion miR-362 may be a prognostic marker in CRC and suppress CRC cell proliferation and invasion in part through targeting the 3′-UTR of SIX1 mRNA. The newly identified miR-362/SIX1 axis provides insight into the progression of CRC.

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Objective. Tong Xie Yao Fang (TXYF) is a classic and effective prescription in traditional Chinese medicine which is used to treat ulcerative colitis (UC). Our study investigated the effect of TXYF on Hippo pathway activation in UC-induced intestinal mucosa injury and explored the possible mechanism. Method. After ulcerative colitis was successfully induced by trinitrobenzene sulfonic acid (TNBS), 48 Sprague Dawley (SD) rats were randomly divided into a control group, model group, TXYF group, and sulfasalazine group and treated with the corresponding drugs for 28 days. The parameters including body weight, colon length, spleen index, and disease activity index (DAI) and histopathological characteristics were assessed. The myeloperoxidase (MPO) activity and IL-6 level in the colon mucosa were determined with the corresponding commercial kits. The expressions of the Hippo pathway components YAP1, TAZ, P-YAP, and LATS1 were detected in the colon mucosa of each group on different stages by quantitative real-time PCR (qRT-PCR) and western blotting. Immunohistochemical staining was used to evaluate the growth and apoptosis of the colon epithelium. Result. TXYF significantly improved the weight loss, colonic shortening, DAI, spleen enlargement, and histopathological score of the rats with TNBS-induced UC. TXYF also reduced the MPO activity and expression of IL-6 in the colon mucosa. Furthermore, treatment with TXYF significantly increased YAP1 expression in the early stage (3–7 days) and significantly decreased YAP1 expression in the late stage (14–28 days). In the early stage, TXYF inhibited Hippo pathway activity, which promoted proliferation and regeneration of the intestinal mucosa. In the late stage, the Hippo pathway was activated, thereby inhibiting apoptosis and promoting intestinal mucosal differentiation. Conclusion. TXYF alleviated the inflammatory response and promoted mucosal healing in rats with UC, which was probably achieved through the Hippo pathway. These results indicated that TXYF was a potential therapy for treating UC.