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Breast cancer (BC) is considered the second leading cause of cancer-related death in women. Accurate diagnosis is thus of utmost importance to avoid the burden of BC. Ankyrin 2 (ANK2) encodes the structural membrane adapter protein ankyrin-B, which is ubiquitously expressed in the human body. In this study, bioinformatics tools were used to determine whether ANK2 could be used as a diagnostic and prognostic biomarker in BC. ANK2 expression was analyzed using ONCOMINE, UALCAN, GEPIA2, and GENT2. Data from these servers showed the downregulated expression of ANK2 in BC relative to that in normal tissue. Further, downregulated ANK2 expression was found in such conditions as estrogen receptor-negative, human epidermal growth factor receptor 2-positive, positive nodal status, basal-like tumor, and triple-negative breast cancer, according to the data from the bc-GenExMiner v4.5 server. Analysis of 18 BC studies retrieved from the cBioPortal database revealed 88 missense mutations with 0.46%–5.09% copy number alterations in the ANK2 gene sequence. Additionally, a positive correlation between downregulated ANK2 expression and reduced survival probability of BC patients was revealed by a Kaplan–Meier plotter. Moreover, chordin-like 1, a tumor suppressor, was highly co-expressed with ANK2, as shown by the ONCOMINE, UCSC Xena, and GEPIA2 tools. The signaling pathways and gene ontologies of ANK2 and its co-expressed genes were identified using the Enrichr platform. The present results suggest that the ANK2 may serve as a biomarker for diagnosis, prognosis, and therapeutic purposes in BC.

Background: Occupational exposure is a significant factor for having respiratory symptoms and impairment of lung function in the working population. Construction workers impose a great risk of respiratory diseases since they continuously expose to construction hazards at their working place. The objective of this study was to explore the status of respiratory health of construction workers as well as correlation of blood parameters with it.Methods: This cross-sectional study was conducted among construction workers along with the control group (university staffs) by randomly selecting 50 individuals in each group from September 2019 to February 2020 in Tangail, Bangladesh. Questionaries’ survey was executed followed by spirometry and oximetry. After confirming abnormalities of lung function, blood was drawn for further IgE, ESR, and CRP analysis.Results: Significantly (p

In this study, we investigated whether wogonin significantly affects MUC5AC mucin gene expression and production in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with wogonin for 30 min and then stimulated with tumor necrosis factor-α (TNF-α) for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA, respectively. We found that incubation of NCI-H292 cells with wogonin significantly inhibited mucin production and down-regulated MUC5AC gene expression induced by TNF-α in a dose-dependent fashion. To elucidate the action mechanism of wogonin, effect of wogonin on TNF-α-induced NF-κB signaling pathway was investigated by western blot analysis. Wogonin inhibited NF-κB activation induced by TNF-α. Inhibition of IKK by wogonin led to the suppression of IκB phosphorylation and degradation, p65 nuclear translocation and NF-κB-regulated gene expression. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. Wogonin also inhibited the gene products involved in cell survival (Bcl-2) and proliferation (cyclooxygenase-2). These results suggest that wogonin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production.

ber of reports, Coptis japonica Makino and its components, berberine, have been used to control airway allergic or in fl am-matory diseases and reported to have anti-infl ammatory and anti-cancer effects (Yoo et al. , 2008; Sun et al. , 2009; Tang et al. , 2009). On the other hand, it was previously reported that berberine stimulated basal mucin release from airway goblet cells, by our group (Lee et al. , 2003; 2004). However, to the best of our knowledge, there are no reports about the effect of berberine on MUC5AC mucin gene expression and mucin production induced by epidermal growth factor (EGF), phor-bol 12-myristate 13-acetate (PMA) or tumor necrosis factor-α (TNF-α), from human airway epithelial cells. Therefore, in this study, we investigated whether berberine affects the expres-sion of MUC5AC mucin gene and the production of mucin protein induced by EGF, PMA or TNF-α, from the NCI-H292 human pulmonary mucoepidermoid cell line. MATERIALS AND METHODS Materials All chemicals and reagents used in this study, including ber

Background We investigated whether wogonin and apigenin significantly affect the epidermal growth factor receptor (EGFR) signaling pathway involved in MUC5AC mucin gene expression, and production from cultured airway epithelial cells; this was based on our previous report that apigenin and wogonin suppressed MUC5AC mucin gene expression and production from human airway epithelial cells. Methods Confluent NCI-H292 cells were pretreated with wogonin or apigenin for 15 minutes or 24 hours and then stimulated with epidermal growth factor (EGF) for 24 hours or the indicated periods. Results We found that incubation of NCI-H292 cells with wogonin or apigenin inhibited the phosphorylation of EGFR. The downstream signals of EGFR such as phosphorylation of MEK1/2 and ERK1/2 were also inhibited by wogonin or apigenin. Conclusion The results suggest that wogonin and apigenin inhibits EGFR signaling pathway, which may explain how they inhibit MUC5AC mucin gene expression and production induced by EGF.

Background We investigated whether prunetin significantly affects tumor necrosis factor-α (TNF-α)-induced MUC5AC mucin gene expression, production, inhibitory kappa B (IκB) degradation and nuclear factor kappa B (NF-κB) p65 translocation in human airway epithelial cells. Methods Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-α for 24 hours or the indicated periods. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The effect of prunetin on TNF-α-induced degradation of IκB and translocation of NF-κB p65 was investigated by western blot analysis. Results We found that incubation of NCI-H292 cells with prunetin significantly inhibited mucin production and down-regulated the MUC5AC gene expression induced by TNF-α. Prunetin inhibited TNF-α-induced degradation of IκB and translocation of NF-κB p65. Conclusion This result suggests that prunetin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-κB signaling pathway.