Introduction: Particulate matter (PM) has various systemic effects. We researched the effects of PM on lung epithelial cells with next generation sequencing (NGS) and validated this with quantitative real-time polymerase chain reaction (qRT-PCR). Methods: We cultured the group exposed to PM₁₀ (Particulate matter less than 10 μm)-like fine dust (ERM^® CZ120 fine dust) at a concentration of 50 μg/mL and the untreated group for seven days in one normal lung epithelial cell line (BEAS-2B) and four lung cancer epithelial cell lines (NCI-H358, HCC-827, A549, NCI-H292). Then, we extracted the RNA from the sample and performed NGS. As a result of NGS, various gene expressions were upregulated or downregulated. Among them, we selected the gene whose mean fold change was more than doubled and changed in the same direction in all five cell lines. Based on these genes, we selected the top 10 genes, either upregulated or downregulated, to validate with the qRT-PCR. Results: There were the four genes that matched the NGS and qRT-PCR results, all of which were upregulated genes. The four genes are CYP1A1, CYP1B1, LINC01816, and BPIFA2. All four genes that matched the two results were upregulated genes and none of the downregulated genes matched. Conclusion: CYP1A1 and CYP1B1 are known to cause lung cancer by metabolizing polycyclic aromatic hydrocarbons, and long noncoding RNA is also known to play an important role in lung cancer. Considering this, we thought PM₁₀ might be associated with lung cancer by activating CYP1A1, CYP1B1, and LINC01816.

O-GlcNAc Transferase (OGT) is a complementary enzyme that regulates O-linked N-acetylglucosaminylation(O-GlcNAcylation) and plays a critical role in various cancer phenotypes, including invasion, migration, and metabolic reprogramming. In our previous study we found that miR-7-5p was downregulated at lung cancer cells with highly metastatic capacity. In the in-silico approach, OGT is the predicted target of miR-7-5p. To identify miR-7-5p′s role in cell growth and metabolism, we transfected various lung cancer cell lines with miR-7-5p. The expression level of miR-7-5p was confirmed by qRT-PCR in lung cancer cell lines. Western blot assays and qRT-PCR were performed to demonstrate miR-7-5p′s effect. Bioinformatic analysis indicated that OGT is a direct target of miR-7-5p. The binding sites of miR-7-5p in the OGT 3′ UTR were verified by luciferase reporter assay. To investigate the role of miR-7-5p in the cancer metabolism of non-small cell lung cancer (NSCLC) cells, mimic of miR-7-5p was transfected into NSCLC cells, and the effect of miR-7-5p on cancer metabolism was analyzed by LDH assays, glucose uptake, and mitochondrial ATP synthase inhibitor assay. O-GlcNAcylated protein level was determined by Western blot. The role of miR-7-5p in lung cancer growth was measured by MTS assays. To identify the delivery of miR-7-5p via PLGA, an in vitro release assay of PLGA-miR-7-5p was done. miR-7-5p was highly expressed whereas OGT showed low expression in H358, H827. However, miR-7-5p exhibited low expression while OGT had high expression in H522, H460, and H1299 cell lines. OGT were repressed by binding of miR-7a-5p to the 3′-UTR. Overexpression of miR-7-5p also diminished anaerobic glycolysis. miR-181a-5p transfection induced expression levels of OGT were diminished compared to those in the control group. O-GlcNAcylation was suppressed by miR-7-5p. Moreover, the overexpression of miR-7-5a suppressed lung cancer cell growth. miR-7-5p was released via PLGA for up to 10 days. In the present study, inhibition of OGT by miR-7-5p decreased the growth and cancer metabolism of lung cancer.

Background: Percutaneous dilatational tracheostomy (PDT) is widely used in intensive care units, but this conventional method has some disadvantages, such as requirement of a lot of equipment and experts at the site. Especially, in situations where the patient is isolated due to an infectious disease, difficulties in using the equipment may occur, and the number of exposed persons may increase. In this paper, we introduce hybrid tracheostomy that combines the advantages of surgical tracheostomy and PDT and describe our experiences.Methods: Data from 55 patients who received hybrid tracheostomy without bronchoscopy from January 2020 to February 2021 were collected and reviewed retrospectively. Hybrid tracheostomy was performed at the bedside by a single thoracic surgeon. The hybrid tracheostomy method was as follows: after the skin was incised and the trachea was exposed, only the extent of the endotracheal tube that could not be removed was withdrawn, and then tracheostomy was performed by the Seldinger method using a PDT kit.Results: The average age was 66.5 years, and the proportion of men was 69.1%. Among the patients, 21.8% were taking antiplatelet drugs and 14.5% were taking anticoagulants. The average duration of the procedure was 13.3 minutes. There was no major bleeding, and there was one case of paratracheal placement of the tracheostomy tube.Conclusions: In most patients, the procedure can be safely performed without any major complications. However, patients with a short neck, a neck burn or patients who have received radiation therapy to the neck should be treated with conventional methods.

Park SJ, et al. J Korean Med Sci. 2024 Jan;39(2):e28. https://doi.org/10.3346/jkms.2024.39.e28

There are many epidemiological studies asserting that fine dust causes lung cancer, but the biological mechanism is not clear. This study was conducted to investigate the effect of PM₁₀ (particulate matter less than 10 μm) on single nucleotide variants through whole genome sequencing in lung epithelial cancer cell lines (HCC-827, NCI-H358) that have been exposed to PM₁₀. The two cell lines were exposed to PM₁₀ for 15 days. We performed experimental and next generation sequencing analyses on experimental group that had been exposed to PM₁₀ as well as an unexposed control group. After exposure to PM₁₀, 3005 single nucleotide variants were newly identified in the NCI-H358 group, and 4402 mutations were identified in the HCC-827 group. We analyzed these single nucleotide variants with the Mutalisk program. We observed kataegis in chromosome 1 in NCI-H358 and chromosome 7 in HCC-827. In mutational signatures analysis, the COSMIC mutational signature 5 was highest in both HCC-827 and NCI-H358 groups, and each cosine similarity was 0.964 in HCC-827 and 0.979 in the NCI-H358 group. The etiology of COSMIC mutational signature 5 is unknown at present. Well-designed studies are needed to determine whether environmental factors, such as PM₁₀, cause COSMIC mutational signature 5.

Lung cancer remains one of the most common and lethal malignancies worldwide, with poor prognosis largely due to late-stage diagnosis and resistance to therapy. Emerging evidence indicates that long non-coding RNAs (lncRNAs) play critical roles in cancer development, metastasis, and treatment resistance. Particulate matter (PM), a major environmental pollutant and recognized Group 1 carcinogen, has been linked to lung cancer through mechanisms that may involve dysregulation of lncRNA expression. This study aimed to identify PM-responsive lncRNAs in lung cancer, and investigate their potential functional roles. Microarray analysis of lung cancer cell lines A549, H358, H292, and HCC827, exposed to PM10, revealed significant up-regulation of lnc-MTPAP-1. TUNEL staining confirmed that silencing of lnc-MTPAP-1 via siRNA resulted in increased apoptosis across all tested lines. Transcriptome analysis using next-generation sequencing showed that knockdown of lnc-MTPAP-1 altered the expression of apoptosis-related genes, with up-regulation of TNS4, MyD88, and IL6R, and down-regulation of CLPTM1L and EI24. These findings suggest that lnc-MTPAP-1 may exert anti-apoptotic effects in lung cancer cells, and be involved in pollution-induced cancer progression. Further research should explore the therapeutic potential of targeting lnc-MTPAP-1, and better understand the molecular impact of PM exposure on lung cancer pathogenesis.