Long non‑coding RNAs (lncRNAs) have been consistently demonstrated to be involved in oral squamous cell carcinoma (OSCC) as either tumor oncogenes or tumor suppressors. However, the underlying mechanisms of OSCC tumorigenesis and development have not yet been fully elucidated. The expression profiles of mRNAs and lncRNAs in OSCC were analyzed by a microarray assay. To verify the results of the microarray, 10 differentially expressed lncRNAs were randomly selected and measured by quantitative RT‑PCR (qRT‑PCR). Gene Ontology (GO) and metabolic pathway analyses were performed to analyze gene function and identify enriched pathways. Subsequently, two independent algorithms were used to predict the target genes of the lncRNAs. We identified 2,294 lncRNAs and 1,938 mRNAs that were differentially expressed in all three OSCC tissues by a microarray assay. Through the construction of co‑expression networks of differentially expressed genes, 4 critical lncRNAs nodes were identified as potential key factors in the pathogenesis of OSCC. Expression of the 4 critical lncRNA nodes was not associated with age, sex, smoking or tumor location (P>0.05) but was positively correlated with clinical stage, lymphatic metastasis, distant metastasis and survival status (P<0.05). Kaplan‑Meier analysis demonstrated that low expression levels of these 4 critical lncRNA nodes contributed to poor median progression‑free survival (PFS) and overall survival (OS) (P<0.05). GO and pathway analyses indicated that the functions and enriched pathways of many dysregulated genes are associated with cancer. Potential target genes of dysregulated lncRNAs were enriched in 43 metabolic pathways, with cancer pathways being the primary enrichment pathways. In summary, we analyzed the profile of lncRNAs in OSCC and identified the functions and enriched metabolic pathways of both dysregulated mRNAs and the target genes of dysregulated lncRNAs, providing new insights into molecular markers and therapeutic targets for OSCC.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6312939 | PMC |
http://dx.doi.org/10.3892/or.2018.6870 | DOI Listing |
BMC Cancer
January 2025
Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Background: Rectal cancer is a highly heterogeneous gastrointestinal tumor, and the prognosis for patients with treatment-resistant and metastatic rectal cancer remains poor. Mitophagy, a type of selective autophagy that targets mitochondria, plays a role in promoting or inhibiting tumors; however, the importance of mitophagy-related genes (MRGs) in the prognosis and treatment of rectal cancer is unclear.
Methods: In this study, we used the differentially expressed genes (DEGs) and MRGs from the TCGA-READ dataset to identify differentially expressed mitophagy-related genes (MRDEGs).
BMC Genomics
January 2025
Gansu Key Laboratory of Herbivorous Animal Biotechnology, College of Animal Science and Technology, Gansu Agricultural University, Lanzhou, 730070, China.
Wool growth and fineness regulation is influenced by some factors such as genetics and environment. At the same time, lncRNA participates in numerous biological processes in animal production. In this research, we conducted a thorough analysis and characterization of the microstructure of wool, along with long non-coding RNAs (lncRNAs), their target genes, associated pathways, and Gene Ontology terms pertinent to the wool fineness development.
View Article and Find Full Text PDFBull Exp Biol Med
January 2025
Department of Laboratory Medicine, Putian University, Putian, China.
The mechanism of Hespintor (a protein of serpin family) inhibitory action on the growth of inoculated hepatocellular carcinoma was studied in a model of human hepatoma in nude mice by using on long-noncoding RNA (lncRNA) sequencing. Two days after tumor transplantation, Hespintor or normal saline was injected into the caudal vein at a dose of 15 μg/kg (2 times a week over 4 weeks). The tumors were isolated in 4 weeks after subcutaneous injection of human hepatoma MHCC97-H cells.
View Article and Find Full Text PDFNat Neurosci
January 2025
Department of Neurobiology & Behavior, University of California, Irvine, Irvine, CA, USA.
Huntington's disease (HD) is caused by a CAG repeat expansion in the HTT gene, leading to altered gene expression. However, the mechanisms leading to disrupted RNA processing in HD remain unclear. Here we identify TDP-43 and the N6-methyladenosine (m6A) writer protein METTL3 to be upstream regulators of exon skipping in multiple HD systems.
View Article and Find Full Text PDFEMBO J
January 2025
Telethon Institute of Genetics and Medicine (TIGEM), 80078, Pozzuoli, Italy.
Endoplasmic reticulum (ER) plasticity and ER-phagy are intertwined processes essential for maintaining ER dynamics. We investigated the interplay between two isoforms of the ER-phagy receptor FAM134B in regulating ER remodeling in differentiating myoblasts. During myogenesis, the canonical FAM134B1 is degraded, while its isoform FAM134B2 is transcriptionally upregulated.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!