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Moreover, GhAP1.7 may negatively regulated by GhLFY in the regulatory pathways. This work laid the foundation for subsequent functional studies of GhAP1.7.The soil adsorption coefficient (Koc) is an environmental fate parameter that is essential for environmental risk assessment. However, obtaining Koc requires a significant amount of time and enormous expenditure. Thus, it is necessary to efficiently estimate Koc in the early stages of a chemical's development. In this study, a quantitative structure-property relationship (QSPR) model was developed using calculated physicochemical properties and molecular descriptors with the OPEn structure-activity/property Relationship App (OPERA) and Mordred software using the largest available Koc dataset. Specifically, we compared the accuracies of the model using the light gradient boosted machine (LightGBM), a gradient boosting decision tree (GBDT) algorithm, with those of previous models. The experimental results suggested the potential to develop a QSPR model that will produce highly accurate Koc values using molecular descriptors and physicochemical properties. Unlike previous studies, the use of a combination of LightGBM, OPERA and Mordred enables the prediction of Koc for many chemicals with high accuracy. In this study, OPERA was used to calculate the physicochemical properties, and Mordred was used to calculate molecular descriptors. The wide range of chemicals covered by OPERA and Mordred enables the analysis of a diverse range of chemical compounds. We also report a method to tune the LightBGM program. The use of fast-processing software, such as LightGBM, enables parameter tuning of a method required to obtain best performance. Our research represents one of the few studies in the field of environmental chemistry to use LightGBM. Purmorphamine solubility dmso Using physicochemical properties as well as molecular descriptors, we could develop highly accurate Koc prediction models when compared to prior studies. In addition, our QSPR models may be useful for preliminary environmental risk assessment without incurring significant costs during the early chemical developmental stage.
Hepatocellular carcinoma (HCC) is an aggressive solid tumor with restricted therapeutics. Lenvatinib is the second approved frontline drug for advanced HCC, however lenvatinib-resistant cases have been reported in clinical. Overexpression of fibroblast growth factor receptor (FGFR1) has been found to be associated with advanced HCC. This study was aimed to investigate the relationship between FGFR1 overexpression and lenvatinib resistance, and explore the potential candidate that can sensitize lenvatinib against FGFR1-overexpressed HCC.

Development of FGFR1 overexpression was accomplished in Hep3B and HepG2 cell lines by pCDH-FGFR1 lentiviral vector. In vitro, cell proliferation, colony formation, cell migration and cell apoptosis assays were used to explore the effect of lenvatinib and Oxysophocarpine. In vivo, BALB/c nude mice were burdened with subcutaneous FGFR1-overexpressed Hep3B tumor to assess the therapeutic effect of lenvatinib and Oxysophocarpine. qRT-PCR and western blotting were further used to identify the underlying mechanism.

Here, we revealed that overexpressed FGFR1 and its downstream AKT/mTOR and ERK signaling activation could induce lenvatinib resistance in HCC. In vivo and in vitro results showed Oxysophocarpine inhibited the proliferation and induced the apoptosis of FGFR1-overexpressed HCC cells. Oxysophocarpine could further sensitize FGFR1-overexpressed HCC cells to lenvatinib treatment. Mechanism studies revealed that Oxysophocarpine downregulated FGFR1 expression along with downstream AKT/mTOR and ERK signaling to sensitize lenvatinib against FGFR1-overexpressed HCC.

These data collectively provided evidence that FGFR1 overexpression could be a potential cause of lenvatinib resistance and Oxysophocarpine could be an ideal combined therapy with lenvatinib in HCC treatment.
These data collectively provided evidence that FGFR1 overexpression could be a potential cause of lenvatinib resistance and Oxysophocarpine could be an ideal combined therapy with lenvatinib in HCC treatment.
Indomethacin [IND] is reported to treat colon cancer. However, continuous exposure to IND causes gastric ulceration, an adverse side effect in humans. This study implies the therapeutic effect of IND and juglone [JUG] against colon carcinogenesis, without gastric ulceration - an adverse side effect of IND.

Adult male Balb/C mice were divided into six groups randomly control, AOM/DSS-induced, IND-treated, JUG-treated, IND+JUG-treated and drug-control. Levels of serum markers, haematoxylin & eosin staining to observe tissue architecture, toluidine blue staining to detect mast cells expression, Masson's trichrome and sirius-red staining were used to detect the collagen deposition. RT-PCR and western blot analysis were carried out to detect inflammation and apoptosis.

IND+JUG effectively decreased the levels of serum markers CEA, AFP, LDH, AST and ALT. Although, IND restored colonic architecture by regulating the accumulation of mast cell and collagen content, it causes gastric ulceration. To address this adverse effect of IND, JUG was given along with IND and was shown to alleviate IND-induced gastric ulceration. AOM/DSS induced animals showed increased expression of inflammatory molecules - TNFα, NFκB and Cox-2, apoptosis regulator - Bcl-2 and decreased expression of pro-apoptotic molecules - Bad, Bax and caspase3; whereas, IND and JUG treated groups showed decreased inflammatory expression with increased expression of pro-apoptotic molecules.

IND and JUG reduce the inflammatory activity and induce apoptotic cell death, while JUG effectively prevents IND induced gastric ulceration. These findings establish that a combination of IND+JUG may serve as a promising treatment regimen for colon cancer.
IND and JUG reduce the inflammatory activity and induce apoptotic cell death, while JUG effectively prevents IND induced gastric ulceration. These findings establish that a combination of IND + JUG may serve as a promising treatment regimen for colon cancer.
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