The purpose of this study was to identify potential molecular markers of lung squamous cell carcinoma (LUSC). Three datasets containing LUSC mRNA sequencing data were downloaded from the Gene Expression Omnibus, The Cancer Genome Atlas and the Gene Expression Profiling Interactive Analysis databases. These datasets were used to identify significantly differentially expressed genes (DEGs) in LUSC. A protein-protein interaction network of the DEGs was constructed followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genomes and overall survival analyses of the DEGs. A total of 37 DEGs between LUSC and normal tissues were identified, including 26 downregulated genes and 11 upregulated genes. Biological Process enrichment analysis revealed that the DEGs were mainly enriched in ‘cell adhesion’, ‘cell-matrix adhesion’, ‘anatomical structure morphogenesis’, ‘ECM-receptor interaction’ and ‘focal adhesion’. Overall survival analysis demonstrated that transcription factor 21, α-2-macroglobulin, acyl-CoA synthetase long chain family member 5, integrin subunit β8, meiotic nuclear divisions 1 and secretoglobin family 1A member 1 were significantly associated with the occurrence and development of lung cancer, and these genes were selected as hub genes. The results obtained in the present study may aid the elucidation of the molecular mechanisms involved in the development of LUSC and may provide potential targets for LUSC treatment.

/pdf/identification-of-potential-diagnostic-and-therapeutic-ja5lvvh6el.pdf

Identification of potential diagnostic and therapeutic target genes for lung squamous cell carcinoma

Lack of glutathione peroxidase-8 in the ER impacts on lipid composition of HeLa cells microsomal membranes

BACKGROUND & AIM Accumulated evidence indicates that the elevation of lipid metabolism is an essential step in colorectal cancer (CRC) development, and analysis of the key lipogenic mediators may lead to identifying the new clinically useful prognostic gene signatures. METHODS The expression pattern of 61 lipogenic genes was assessed between CRC tumors and matched adjacent normal tissues in a training set (n = 257) with the Mann-Whitney U test. Cox's proportional hazards model and the Kaplan-Meier method were used to identifying a lipogenic-biomarkers signature associated with the prognosis of CRC. The biomarkers signature was then confirmed in two independent validation groups, including a set of 223 CRC samples and an additional set of 203 COAD profiles retrieving from the Cancer Genome Atlas (TCGA). RESULTS Five genes, including ACOT8, ACSL5, FASN, HMGCS2, and SCD1, were significantly enhanced in CRC tumors. Using the cutoff value 0.493, the samples were classified into high risk and low risk. The AUC of panel for discriminating of all, early (I-II stages), and advanced CRC (III-IV stages) were 0.8922, 0.8446, and 0.9162 (Training set), along with 0.8800, 0.8205, and 0.7351 (validation set I), and 0.9071, 0.8946, and 0.9107 (Validation set II), respectively. There was a reverse correlation between the high predicted point of panel and worse OS of CRC patients in training set (HR (95% CI): 0.1096 (0.07089-0.1694), P < 0.001), validation set I (HR (95% CI): 0.3350 (0.2116-0.5304), P < 0.001), and validation set II (HR (95% CI): 0.1568 (0.1090-0.2257), P < 0.001). CONCLUSION Our study showed that the panel of ACOT8/ACSL5/FASN/HMGBCS2/SCD1 genes had a better prognostic performance than validated clinical risk scales and is applicable for early detection of CRC and tumor recurrence.

/pdf/development-and-validation-of-a-lipogenic-genes-panel-for-234khm8tc0.pdf

Development and validation of a lipogenic genes panel for diagnosis and recurrence of colorectal cancer.

Glycolysis is the fundamental cellular process that permits cancer cells to convert energy and grow anaerobically. Recent developments in molecular biology have made it evident that mitochondrial respiration is critical to tumor growth and treatment response. As the principal organelle of cellular energy conversion, mitochondria can rapidly alter cellular metabolic processes, thereby fueling malignancies and contributing to treatment resistance. This review emphasizes the significance of mitochondrial biogenesis, turnover, DNA copy number, and mutations in bioenergetic system regulation. Tumorigenesis requires an intricate cascade of metabolic pathways that includes rewiring of the tricarboxylic acid (TCA) cycle, electron transport chain and oxidative phosphorylation, supply of intermediate metabolites of the TCA cycle through amino acids, and the interaction between mitochondria and lipid metabolism. Cancer recurrence or resistance to therapy often results from the cooperation of several cellular defense mechanisms, most of which are connected to mitochondria. Many clinical trials are underway to assess the effectiveness of inhibiting mitochondrial respiration as a potential cancer therapeutic. We aim to summarize innovative strategies and therapeutic targets by conducting a comprehensive review of recent studies on the relationship between mitochondrial metabolism, tumor development and therapeutic resistance. 

Mitochondrial metabolism as a dynamic regulatory hub to malignant transformation and anti-cancer drug resistance.

Fatty acid metabolism has attracted extensive attention for its key role in the occurrence and development of tumors. Fatty acids not only participate in the biosynthesis of phospholipids in the membrane to overcome the demand for rapidly proliferating membrane lipids but also provide ATP, signaling molecules, and NADPH through β-oxidation to maintain tumor survival and growth. However, the specific role of fatty acid β-oxidation in tumors and the description of multiple potential targets in this process are not comprehensive and systematic. Therefore, this review summarizes the function of fatty acid β-oxidation in tumors and studies of key enzymes that catalyze related reactions in various stages to improve the overall understanding of fatty acid β-oxidation and search for novel tumor treatment strategies and ideas.

/pdf/targeting-the-key-enzymes-of-abnormal-fatty-acid-b-oxidation-3enc4k3b.pdf

Targeting the Key Enzymes of Abnormal Fatty Acid β-oxidation as a Potential Strategy for Tumor Therapy.

Background and Aims. Acyl-CoA synthetase 5 (ACS5) has been reported to be associated with the development of various cancers, but the role of it in colorectal cancer (CRC) is not well understood. The present study aimed to explore the potential role of ACS5 in the development and progression of CRC. Methods. ACS5 expression in CRC tissues and CRC cell lines was examined, and its clinical significance was analyzed. The role of ACS5 in cell proliferation, apoptosis, and invasion was examined in vitro. Results. We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation. Furthermore, knockdown of ACS5 in HT29 and SW480 cells significantly dampened cell proliferation, induced cell apoptosis, and reduced cell migration and invasion. In contrast, the ectopic overexpression of ACS5 in LOVO and SW620 cells remarkably promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion. Enhanced cell growth and invasion ability mediated by the gain of ACS5 expression were associated with downregulation of caspase-3 and E-cadherin and upregulation of survivin and CD44. Conclusions. Our data demonstrate that ACS5 can promote the growth and invasion of CRC cells and provide a potential target for CRC gene therapy.

/pdf/acyl-coa-synthetase-5-promotes-the-growth-and-invasion-of-49bjc2fnzy.pdf

Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells.

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Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells.