Search

Objective To investigate the expression of CK2α' in hepatocellular carcinoma (HCC) tissues and its prognosis value. Methods Tissue microarray was made from tumor and adjacent normal tissues of 83 patients with HCC. Immunohistochemical was used to stain the microarray for semi-quantitative analysis, and the expression of CK2α' in HCC tissues and adjacent normal tissues was compared. The associations between CK2α' expression and clinicopathologic features of HCC patients were analyzed with χ2 text. The prognostic value of CK2α' was estimated using Kaplan-Meier approach. Results The average positive expression rate of CK2α' was 47.8% in HCC and 65.4% in adjacent normal tissues. The positive expression rate of CK2α' in HCC tissues was lower than that in adjacent normal tissues (P < 0.01). The expression level of CK2α' in the cancer tissues of 74.7% cases was significantly lower than that in the adjacent tissues. HCC patients with low CK2α' expression had higher risk of recurrence and shorter overall survival time (P < 0.05). The expression of CK2α' was significantly correlated with CK19 (P < 0.05). Conclusion CK2α' is down-regulated in HCC tissues and correlated with the prognosis of patients. It could be a potential prognostic marker for HCC.

BN-embedded anthracenes with chiral 3,7-dimethyloctyl side chains (namely (S,S)- and (R,R)-DPBNA) have been synthesized as novel visible-blind ultraviolet-absorbing chiral materials for ultraviolet circularly polarized light (CPL) detection. Phototransistors with a p–n heterojunction configuration have been fabricated with (S,S)/(R,R)-DPBNA serving as the p-type photoactive layer and an achiral n-type polymer as the electron transport layer. Significant discrimination between left and right CPL has been observed under 365 nm CPL irradiation with an average photocurrent dissymmetry factor of 0.033, highlighting the potential of BN-embedded semiconductors for ultraviolet CPL detection. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is one of the most common malignancies worldwide. In the clinical realm, platinum‐based drugs hold an important role in the chemotherapy of CRC. Nonetheless, a multitude of patients, due to tumor protein 53 (TP53) gene mutations, experience the emergence of drug resistance. This phenomenon gravely impairs the effectiveness of therapy and long‐term prognosis. Gallium, a metallic element akin to iron, has been reported that has the potential to be used to develop new metal anticancer drugs. In this study, we screened and established the gallium complex K6 as a potent antitumor agent in both in vitro and in vivo. K6 exhibited superior efficacy in impeding the growth, proliferation, and viability of CRC cells carrying TP53 mutations compared to oxaliplatin. Mechanistically, K6 escalated reactive oxygen species levels and led deoxyribonucleic acid (DNA) damage. Furthermore, K6 effectively suppressed the phosphoinositide 3‐kinase (PI3K)/protein kinase B (PKB)/glycogen synthase kinase 3 beta (GSK3β) pathway, leading to the degradation of its downstream effectors myelocytomatosis (c‐Myc) and Krueppel‐like factor 5 (KLF5). Conversely, K6 diminished the protein expression of WW domain‐containing protein 1 (WWP1) while activating phosphatase and tensin homolog (PTEN) through c‐Myc degradation. This dual action further demonstrated the potential of K6 as a promising therapeutic compound for TP53‐mutated CRC. [ABSTRACT FROM AUTHOR]

Simple Summary: Avian pathogenic Escherichia coli (APEC) constitutes a notable etiological agent of colibacillosis, an inflammatory disease in birds that leads to considerable economic losses within the poultry industry. In this study, we probed into the impact of the quorum sensing regulator SdiA on the transcriptional profiling of an APEC strain and proved the potential regulatory role of SdiA in biofilm formation, motility, and drug resistance. The discoveries disclose the involvement of SdiA in the pathogenesis of APEC and will furnish some novel insights into the prevention and control of colibacillosis induced by APEC. Avian pathogenic Escherichia coli (APEC) constitutes a significant cause of colibacillosis, a localized or systemic inflammatory disorder in avian species, resulting in considerable economic losses within the global poultry industry. SdiA (suppressor of division inhibitor) is a transcription factor recognized as a LuxR homolog in Escherichia coli, regulating various behaviors, including biofilm formation, multidrug resistance, and the secretion of virulence factors. However, the function of SdiA in APEC strains and its correlation with virulence and multidrug resistance remains unknown. This study probed into the function of SdiA by analyzing the effect of sdiA deletion on the transcription profile of an APEC strain. The microarray data revealed that SdiA upregulates 160 genes and downregulates 59 genes, exerting a particularly remarkable influence on the transcription of multiple virulence genes. A series of antibiotic sensitivity tests, biofilm formation assays, motility assays, and transcriptome analyses were performed, while a Normality test and t-test were conducted on the datasets. This research confirmed that SdiA inhibits biofilm formation by 1.9-fold (p-value < 0.01) and motility by 1.5-fold (p-value < 0.01). RT-qPCR revealed that SdiA positively regulates multidrug resistance by upregulating the expression of yafP, cbrA, and eamB. Collectively, the results of this study indicate the role of SdiA in the pathogenesis of APEC by controlling biofilm formation, motility, and multidrug resistance. [ABSTRACT FROM AUTHOR]