Grossman Joyce (milkwind1)
All target compounds significantly inhibited hTS enzyme activity and demonstrated significant antitumor activity against five cancer cell lines. Notably, 7 had a high selectivity index (SI) and unique inhibitory effects on eight NSCLC cells. In-depth research indicated that 7 could induce apoptosis by the mitochondrial pathway in A549 and PC-9 cells through the upregulation of wild-type P53 protein expression. Additionally, 7 was shown to inhibit angiogenesis and . studies, compared to PTX, 7 significantly inhibited tumor growth in A549 cell xenografts and had a higher therapeutic index (TGI). Moreover, 7 could prolong the survival of the orthotopic lung cancer murine model more effectively than PTX. The anti-angiogenic effect of 7 provides a new reference for the development of TS inhibitors and the clinical treatment of NSCLC. The anti-angiogenic effect of 7f provides a new reference for the development of TS inhibitors and the clinical treatment of NSCLC. Epithelial-mesenchymal transition (EMT) is a process of transdifferentiation where epithelial cells attain mesenchymal phenotype to gain invasive properties and thus, can contribute to metastasis of tumor cells. The antimetastatic and antitumor efficacy of brusatol (BT) was investigated in a hepatocellular carcinoma (HCC) model. We evaluated the action of BT on EMT process using various biological assays in HCC cell lines and its effect on tumorigenesis in an orthotopic mouse model. We found that BT treatment restored the expression of Occludin, E-cadherin (epithelial markers) while suppressing the levels of different mesenchymal markers in HCC cells and tumor tissues. Moreover, we observed a decline in the expression of transcription factors (Snail, Twist). Since the expression of these two factors can be regulated by STAT3 signaling, we deciphered the influence of BT on modulation of this pathway. BT suppressed the phosphorylation of STAT3 and STAT3 depletion using siRNA resulted in the restoration of epithelial markers. Importantly, BT (1mg/kg) reduced the tumor burden in orthotopic mouse model with a concurrent decline in lung metastasis. Overall, our results demonstrate that BT interferes with STAT3 induced metastasis by altering the expression of EMT-related proteins in HCC model. Overall, our results demonstrate that BT interferes with STAT3 induced metastasis by altering the expression of EMT-related proteins in HCC model. The collective impact of climate change and soil salinity is continuously increasing the degraded lands across the globe, bringing agricultural productivity and food security under stress. The high concentration of salts in saline soils impose osmotic, ionic, oxidative and water stress in plants. Biological solutions can be the most reliable and sustainable approach to ensure food security and limit the use of agro-chemicals. Halo-tolerant plant growth promoting rhizobacteria (HT-PGPR) are emerging as efficient biological tools to mitigate the toxic effects of high salt concentrations and improve the growth of plants, simultaneously remediating the degraded saline soils. The review explains the role of HT-PGPR in mitigating the salinity stress in plants through diverse mechanisms and concurrently leading to improvement of soil quality. HT-PGPR are involved in alleviating the salinity stress in plants through a number of mechanisms evoking multipronged physiological, biochemical and molecular responses. exopolysaccharides synthesis, activation of antioxidant machinery, accumulation of osmolytes, maintaining the Na+ kinetics and improving the levels of phytohormones and nutrient uptake in plants. The modification of signaling by HT-PGPR inoculation under stress conditions elicits induced systemic resistance in plants which