The aim of the present study was to determine the effect of the long non-coding RNA (lncRNA) bladder cancer-associated transcript 1 (BLACAT1) in chemoresistance of non-small cell lung cancer (NSCLC) cells. Expression of lncRNA BLACAT1, microRNA (miR)-17, autophagy-related protein 7 (ATG7), multidrug-resistance protein 1 (MRP1), and the autophagy-associated proteins light chain 3 (LC3)-II/LC3-I and Beclin 1 were detected using the reverse transcription-quantitative polymerase chain reaction and western blot analysis. Cell viability was determined using an MTT assay. The interaction between BLACAT1 and miR-17 was determined using RNA immunoprecipitation and RNA pull-down assays. A cisplatin (DDP)-resistant NSCLC cell A549/DDP xenograft model in nude mice was established to investigate the effect of BLACAT1 on the chemoresistance of NSCLC cells. Compared with in DDP-sensitive NSCLC cells, expression of BLACAT1, ATG7, MRP1, LC3-II/LC3-I and Beclin 1 was significantly upregulated in DDP-resistant NSCLC cells, whereas miR-17 was downregulated in DDP-resistant NSCLC cells. Short interfering RNA against BLACAT1 decreased the viability of DDP-resistant NSCLC cells. In addition, BLACAT1 interacted with miR-17, and negatively regulated miR-17. BLACAT1 promoted ATG7 expression through miR-17, and facilitated autophagy and promoted chemoresistance of NSCLC cells through miR-17/ATG7. Finally, in vivo experiments indicated that inhibition of BLACAT1 ameliorated the chemoresistance of NSCLC. BLACAT1 was upregulated in DDP-resistant NSCLC cells, and promoted autophagy and chemoresistance of NSCLC cells through the miR-17/ATG7 signaling pathway.

MicroRNAs (miRNA) play an important role in tumorigenesis, proliferation, and differentiation. Altered miRNA expression in cancer indicates that miRNAs can function as tumor suppressors or oncogenes. MiR-449c downregulation in non-small cell lung cancer (NSCLC) compared with normal lung tissues was investigated in this study. NSCLC cell proliferation and invasion assays indicate that transfection of miR-449c expression plasmid inhibits the proliferation and invasion ability of NCI-H23 and NCI-H838 cells. In addition, miR-449c overexpression could suppress tumor growth in vivo. Morever, c-Myc was identified as a direct target gene of miR-449c. These findings clearly suggest that miR-449c downregulation and c-Myc amplification may be involved in the development of NSCLC.

Objectives: This study was designed to assess the awareness and knowledge of antibiotic usage and antibiotic resistance among the general public in the Cape Coast metropolis of Ghana. It also tries to decipher whether the level of education and the professional status of an individual has a positive association with the level of knowledge on antibiotic resistance. Methods: A population-base survey involving members of the public was conducted from August to November 2019. A structured questionnaire was developed to collect data from 632 respondents. Data were analyzed through SPSS v.21 using Chi square statistics and multivariate regression. Differences in knowledge were evaluated using ANOVA and the assumption of equal variance was tested with Levene statistics. Results: The response rate was 74.3%. Lower educational status group had a greater knowledge level (39.7%) on antibiotic resistance. Despite the high score, the lowest educational status group, (M = 1.82, SD = 0.769), middle educational status group (M = 1.98, SD = 0.748), and the high educational status group (M = 1.88, SD = 0.773) were not significantly different from each other with regard to their general knowledge level on antibiotic resistance (P < 0.05). The study revealed that, working in the healthcare sector is a major contributor to the level of knowledge on antibiotic resistance. Conclusion: Given the scale of the issue on antibiotic resistance and the fact that attempts to resolve it will involve efforts on the part of all, it is important that the public is aware of the importance of the issue of antibiotic resistance, its implications and what they can do to address it. The level of knowledge among respondents with lower educational status should be enough evidence to introduce more educational campaigns on antibiotic resistance.

Recent studies have shown that Beclin 1, a key regulator of autophagic process, is frequently downregulated and may serve as an independent prognostic biomarker for nonsmall cell lung cancer. However, the molecular mechanisms underlying its downregulation remain poorly understood. The signal transducer and activator of transcription 3 (Stat3) is a transcription factor which plays a crucial role for multiple tumor growth and progression. Here, we demonstrate that Beclin 1 is a direct transcriptional target of Stat3 in lung cancer cells. Interleukin-6 (IL-6) treatment or transfection of a constitutively activated Stat3 in AGS and NCI-H1650 cells inhibited Beclin 1 expression. At the molecular level, we further revealed that Stat3 could directly bind to the promoter region of Beclin 1 and repressed its transcription through recruiting histone deacetylase 3 (HDAC3). Collectively, our results suggest that the activated Stat3 may represent an important mechanism for Beclin 1 downregulation in nonsmall cell lung cancer development.

Formation of cancer stem cells (CSCs) and increased cells proliferation are involved in tumorigenesis, tumour recurrence and therapy resistance and microRNA is essential for the development of the biological traits of CSCs and the increased cells proliferation. Studying molecular mechanism of tumorigenesis, tumour recurrence and therapy resistance of lung cancer will help us to further understand the pathogenesis and progression of the disease and offer new targets for effective therapies. In the present study, we found that miR-520a-3p expression is downregulated in NSCLC (non-small cell lung cancer) and SCLC (small cell lung cancer). miR-520a-3p can inhibit proliferation and cancer stem cell phenotype in NSCLC and SCLC cells. Overexpressing miR-520a-3p can degrade HOXD8 mRNA in NSCLC cells, but its overexpression cannot suppress HOXD8 in SCLC cells. HOXD8 protein is upregulated in NSCLC tissues and its overexpression can promote proliferation, formation of cancer stem cells, migration and invasion in NSCLC cells. MET amplification plays a pivotal role in gefitinib resistance in lung cancer. We found that miR-520a-3p can downregulate MET protein expression and HOXD8 can upregulate MET protein expression. Thus, we concluded that microRNA-520a-3p inhibits proliferation and cancer stem cell phenotype by targeting HOXD8 in NSCLC cells and restoration of microRNA-520a-3p might be a therapeutic strategy to reverse gefitinib resistance.