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The outbreak of COVID-19 has raised a global concern and calls for an urgent response. During this perpetual time of epidemic crisis, philosophy has to stand on trial and provide a responsible justification for how it is still relevant and can be of used during this global crisis. In such a time of crisis like that of COVID-19, this paper offers a philosophical reflection from within the possibility/impossibility of community thinking in India, and the demand for an ethical responsivity and response-ability to act ethically towards the Other (autrui) to show that philosophy always already emerges from within the context of crisis. As an alternative outlook to the thinking of totalitarian singularity and individualism, community-in its possible and impossible making-can offer more meaningful engagement with the other human being by being responsible and extending care towards the Other. The thinking of a shared community life is the facticity of one's own being-together-in-common without the dismissal of individual differences as can be seen in the works of Jean-Luc Nancy, and there is an ethical demand that comes from the face-to-face ethical relationship with the Other as argued by Emmanuel Levinas.Cutaneous malignant melanoma is a malignancy with one of the fastest increasing incidence rates worldwide; however, the mechanism underlying the occurrence and development of melanoma remains unclear. The aim of the present study was to identify novel biomarkers for the occurrence and development of melanoma. The results of the present study demonstrated that the expression levels of microRNA (miR)-27b were decreased in melanoma tissue samples compared with those in adjacent noncancerous tissue samples and cells according to online and experimental data. By contrast, MYC expression levels were upregulated in melanoma compared with those in adjacent noncancerous tissue samples. miR-27b overexpression significantly inhibited A375 and A2085 melanoma cell DNA synthesis, viability and invasive ability. Dual-luciferase reporter assay results demonstrated that miR-27b inhibited MYC expression through binding to the 3'-untranslated region of MYC mRNA. MYC knockdown in melanoma cells exerted similar effects to those of miR-27b overexpression on DNA synthesis, cell viability and invasive ability; the effects of miR-27b inhibition were significantly reversed by MYC knockdown. In conclusion, the miR-27b/MYC axis may modulate malignant melanoma cell biological behaviors and may be a potential target for melanoma treatment.Cancer cells undergo metabolic reprogramming, including increased glucose metabolism, fatty acid synthesis and glutamine metabolic rates. These enhancements to three major metabolic pathways are closely associated with glycolysis, which is considered the central component of cancer cell metabolism. Increasing evidence suggests that dysfunctional glycolysis is commonly associated with drug resistance in cancer treatment, and aberrant glycolysis plays a significant role in drug-resistant cancer cells. Studies on the development of drugs targeting these abnormalities have led to improvements in the efficacy of tumor treatment. The present review discusses the changes in glycolysis targets that cause drug resistance in cancer cells, including hexokinase, pyruvate kinase, pyruvate dehydrogenase complex, glucose transporters, and lactate, as well the underlying molecular mechanisms and corresponding novel therapeutic strategies. In addition, the association between increased oxidative phosphorylation and drug resistance is introduced, which is caused by metabolic plasticity. Given that aberrant glycolysis has been identified as a common metabolic feature of drug-resistant tumor cells, targeting glycolysis may be a novel strategy to develop new drugs to benefit patients with drug-resistance.MicroRNAs (miRNAs/miRs) play key roles in cancer progression. Extensive research has revealed that miR-26a is abnormally expressed and functions as a tumor suppressor in numerous types of cancer. Thus, the present study was undertaken to investigate the regulatory role and potential mechanism of action of miR-26a in breast cancer. Furthermore, the present study aimed to examine the alterations in miR-26a expression and its effects on human breast cancer cells. Reverse transcription-quantitative PCR was conducted to assess the differences in miR-26a expression between human breast cancer and normal breast specimens. A Cell Counting Kit-8 assay and cloning experiments were used to detect cell proliferation and clone formation. Wound healing and Transwell assays were performed to examine cell migration and invasion. A luciferase activity experiment was utilized to validate the association between miR-26a and family with sequence similarity 98 member A (FAM98A). Western blotting was conducted to detect the protein expression levels of FAM98A, sonic hedgehog signaling molecule (SHH), smoothened, frizzled class receptor (SMO) and GLI family zinc finger 1 (GLI1). The results indicated that miR-26a expression was decreased in breast carcinoma tissues and cell lines. Moreover, overexpression of miR-26a significantly suppressed cell proliferation, clone formation ability and metastasis, and it sensitized breast cancer cells to docetaxel. It was demonstrated that miR-26a directly targeted FAM98A, and that FAM98A, SHH, SMO and GLI1 expression levels were decreased in cells transfected with miR-26a mimics. Collectively, the results of the present study suggested that miR-26a negatively regulated the expression of FAM98A, indicating that it may play a key role in the suppression of breast carcinogenesis.Determining the spatial distribution of human papillomavirus (HPV) and performing accurate public health analyses helps to distinguish areas of healthcare that require further research, and enables therapeutic techniques and approaches in healthcare to be focused more accurately. A total of 4,560 women were enrolled in the present study. Flow-through hybridization and gene chip assays were used to detect the genotypes of HPV infection. Heat maps were then generated to present the spatial distribution of HPV infections in Zhejiang Province according to genotype. Of the exfoliated cervical cell samples from the 4,560 women, HPV was detected in 1,886 samples. HPV-16, -58, -52 and -18 were the most prevalently identified genotypes in the population included in the present study. HPV-16 and -58 infections were mainly distributed in the northern and central regions of Zhejiang Province, such as in Hangzhou and Shaoxing, where the prevalence was higher than that in the southern regions (P less then 0.05). HPV-18 infection was widespread throughout Zhejiang Province, but had a much lower infection rate in Ningbo and Huzhou (P less then 0.05). High infection rates of HPV-52 were mainly detected in Hangzhou and the eastern coastal areas of Wenzhou, with a relatively low rate of infection in the center of the province (P less then 0.05). In conclusion, HPV-16, -58, -52 and -18 were the four most prevalent HPV genotypes observed in Zhejiang Province. Heat maps were created to display the spatial distribution of HPV infection according to genotype, which varied by geographical regions. The results indicate that for individuals in Ningbo or Wenzhou, bivalent or quadrivalent vaccines may be suitable, but for those in Hangzhou and Shaoxing, nonavalent vaccines are strongly recommended.Non-small cell lung cancer (NSCLC) is a common malignant tumor. ERCC excision repair 1 endonuclease non-catalytic subunit (ERCC1) is a key mediator of nucleotide excision repair. The present study aimed to explore the synergistic effects of the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib combined with ERCC1 on the sensitivity of NSCLC cells to cisplatin. Preliminary experiments were performed to identify the optimal concentrations of cisplatin and olaparib for cellular treatment and subsequently NCI-H1299 and SK-MES-1 cells were treated with 20 µg/ml cisplatin combined with 50 µg/ml olaparib and 50 µg/ml cisplatin combined with 70 µg/ml olaparib, respectively. Subsequently, transfections were carried out to overexpress or knockdown the expression of ERCC1 in NSCLC cell lines, including NCI-H1299 and SK-MES-1. The transfection efficiency was evaluated using reverse transcription-quantitative PCR and western blotting. The results demonstrated that cells with ERCC1 overexpression and ERCC1 knockdown were successfully constructed. Finally, the cell viability and apoptosis were determined using the Cell Counting Kit-8 and Annexin V-FITC cell apoptosis assays, respectively. In NCI-H1299 or SK-MES-1 cells treated with cisplatin combined with olaparib for 24 h, the cell viability significantly increased following ERCC1 overexpression compared with the GV230 group (P less then 0.05), but significantly inhibited following ERCC1 knockdown compared with the siRNA-NC group (P less then 0.05). However, ERCC1 overexpression or knockdown had the opposite effect on apoptosis. In conclusion, olaparib combined with ERCC1 expression may enhance the sensitivity of cisplatin in NSCLC. These findings may provide novel insight for the improvement of platinum drug sensitivity and treatment of NSCLC.Drug resistance is one of the main factors limiting the efficacy of chemotherapy in patients with laryngeal cancer; thus, it is important to investigate the drug resistance of laryngeal cancer. In the present study, the mechanism of the regulation of drug resistance in laryngeal cancer cells by ATP-binding transporter G2 (ABCG2) that is present in the extracellular vesicles (EVs) released by drug-resistant cells was studied in vivo and in vitro. A cisplatin (CDDP)-resistant cell line (AMC-HN-8/CDDP) was established from AMC-HN-8 cells by continuous exposure to increasing concentrations of CDDP. The EVs extracted from the culture medium of AMC-HN-8/CDDP and AMC-HN-8 cells were termed EVs1 and EVs2, respectively. Following 48-h treatment of AMC-HN-8 cells with EVs1 or EVs2, the cells were designated as AMC-HN-8-EVs1 or AMC-HN-8-EVs2. Nude mice bearing AMC-HN-8-EVs1 and AMC-HN-8 cell-derived xenograft tumors were established to detect the effects of EVs on drug resistance. The resistance index of AMC-HN-8/CDDP cer compared with those in the blank (inoculated with AMC-HN-8 cells and was intraperitoneally injected with normal saline) and control groups (P less then 0.01). The high expression levels of ABCG2 in laryngeal carcinoma cells affected the drug resistance of the cells. The EVs released by drug-resistant cells upregulated the expression of ABCG2 and induced drug resistance in laryngeal carcinoma cells, which may be dependent on the ABCG2 gene carried by the EVs.Triple-negative breast cancer (TNBC) is a subtype with high rates of metastasis, poor prognosis and limited therapeutic options. see more The present study aimed to identify the potential pivotal genes for prognosis and treatment in TNBC. A total of two microarray expression datasets, GSE38959 and GSE65212, were downloaded from the Gene Expression Omnibus database, and RNA-sequencing data of breast cancer from The Cancer Genome Atlas database were analyzed to screen out differentially expressed genes (DEGs) between TNBC tissues and normal tissues. The intersection of DEGs was submitted to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. A protein-protein interaction (PPI) network was constructed and visualized using Cytoscape software. Furthermore, module, centrality and survival analyses were performed to identify the potential hub genes. Reverse transcription-quantitative (RT-q)PCR analysis was performed to detect the expression levels of key genes in TNBC samples, and 377 DEGs were identified.
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