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Antimony selenide film doped with Zn2+ was deposited on ultra-white glass by hydrothermal method. The photocatalytic activity was evaluated by photocatalytic decolorization reaction with methylene blue (MB) solution. According to the free radical capture experiment, photogenerated holes (h+) and superoxide radicals (·O2−) are the decisive active substances in the photocatalytic process. [Display omitted] • Zn-doped Sb 2 Se 3 thin films prepared by hydrothermal deposition. • The amount of zinc doping is the key to the enhancement of photocatalytic activity. • The doping of Zn2+ increases the visible light absorbance of the Sb 2 Se 3 thin film. • Metal ion doping provides a simple method for metal selenide photocatalysts. Sb 2 Se 3 is a promising light-absorbing material with low cost and good photocatalytic activity. In this paper, Sb 2 Se 3 thin films doped with zinc (Zn) were deposited on ultra-white glass by hydrothermal method, using ZnCl 2 , sodium selenate and antimony potassium tartrate as raw materials. And the photocatalytic activity was evaluated by photocatalytic decolorization reaction with methylene blue (MB) solution. The results showed that the highest photocatalytic activity was displayed when Zn2+ was doped with 0.10 mmol, and its degradation rate of methylene blue was 1.66 times higher than that of pure Sb 2 Se 3. Zn2+ doped Sb 2 Se 3 film can effectively inhibit the recombination of electron-hole pairs, thereby improving the optical activity. According to the free radical capture experiment, photogenerated holes (h+) and superoxide radicals (·O2−) are the decisive active substances in the photocatalytic process. This method provides a reliable way for transition metal ions doped metal selenides to degrade organic dyes. [ABSTRACT FROM AUTHOR]

Oxaliplatin chemoresistance is a major challenge in the clinical treatment of colorectal cancer (CRC), which is one of the most common malignancies worldwide. In this study, we identified the tryptophan-aspartate repeat domain 43 (WDR43) as a potentially critical oncogenic factor in CRC pathogenesis through bioinformatics analysis. It was found that WDR43 is highly expressed in CRC tissues, and WDR43 overexpression is associated with poor prognosis of CRC patients. WDR43 knockdown significantly inhibits cell growth by arresting cell cycle and enhancing the effect of oxaliplatin chemotherapy both in vitro and in vivo. Mechanistically, upon oxaliplatin stimulation, c-MYC promotes the transcriptional regulation and expression of WDR43. WDR43 enhances the ubiquitination of p53 by MDM2 through binding to RPL11, thereby reducing the stability of the p53 protein, which induces proliferation and chemoresistance of CRC cells. Thus, the overexpression of WDR43 promotes CRC progression, and could be a potential therapeutic target of chemoresistance in CRC. [ABSTRACT FROM AUTHOR]

The role of lncRNAs in the regulation of glutamate metabolism and metabolic reprogramming of pancreatic cancer (PC) during nutrient deprivation is largely unknown. Our study found that alpha-ketoglutarate (aKG) levels were significantly reduced in the absence of XLOC_006390. We subsequently confirmed that the decrease in aKG was mainly due to the downregulation of glutamate dehydrogenase 1 (GDH1) at the mRNA level. Therefore, we first screened transcription factors targeting the GDH1 gene promoter and confirmed that c-Myc regulates GDH1 transcription. c-Myc binds to the promoter of GDH1 and activates its transcription. Downregulation of GDH1 mRNA levels by XLOC_006390 deletion could be rescued by overexpression of c-Myc. Overexpression of XLOC_006390 promoted the protein stability of c-Myc by blocking its ubiquitination. Clinically, XLOC_006390 was positively correlated with the mRNA level of GDH1, and c-Myc positively regulated GDH1 gene expression, which was tightly associated with PC patient prognosis. The dysregulated lncRNA/c-Myc axis increased glutamate metabolism, promoting PC progression to a higher stage. Therefore, XLOC_006390/c-Myc may be a potential target for PC, and its abnormal activation also indicates the progression of PC. [ABSTRACT FROM AUTHOR]

Prostate cancer (PCa) is the most common solid organ malignancy among men, outnumbering both lung and colorectal cancer, and it is the second leading cause of male tumor-related death in the United States due to high metastasis. Recently, leukemia inhibitory factor receptor (LIFR) has been found to play roles in multiple types of cancer. However, the roles of LIFR in the progression of PCa remain to be revealed. In this study, we found that LIFR plays an oncogenic role in PCa. The phosphorylation of LIFR at S1044 contributes to subsequent activation of the AKT pathway, inducing the expression of a series of proliferation and metastatic genes. Additionally, LIFR-S1044 is phosphorylated by ERK2 but not ERK1. The signal intensity of pLIFR-S1044 and pAKT S473 in PCa tissue displays a tight positive correlation. The ERK2/LIFR/AKT axis modulates PCa progression and offers a promising therapeutic and diagnostic target for PCa. [ABSTRACT FROM AUTHOR]

Apatinib, a novel tyrosine kinase inhibitor (TKI), has been confirmed for its efficacy and safety in the treatment of advanced gastric carcinoma and some other solid tumors. However, the direct functional mechanisms of tumor lethality mediated by apatinib have not yet been fully characterized, and the precise mechanisms of drug resistance are largely unknown. Here, in this study, we demonstrated that apatinib could induce both apoptosis and autophagy in human colorectal cancer (CRC) via a mechanism that involved endoplasmic reticulum (ER) stress. Moreover, activation of the IRE1α pathway from apatinib-induced ER stress is responsible for the induction of autophagy; however, blocking autophagy could enhance the apoptosis in apatinib-treated human CRC cell lines. Furthermore, the combination of apatinib with autophagy inhibitor chloroquine (CQ) tends to have the most significant anti-tumor effect of CRC both in vitro and in vivo. Overall, our data show that because apatinib treatment could induce ER stress-related apoptosis and protective autophagy in human CRC cell lines, targeting autophagy is a promising therapeutic strategy to relieve apatinib drug resistance in CRC. [ABSTRACT FROM AUTHOR]