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Background: Lung cancer continues to be the primary cause of cancer-related deaths globally, with the majority of cases identified at advanced stages. Genetic alterations, including mutations and gene fusions, are central to its molecular pathogenesis. The discovery of therapeutically targetable gene fusions, such as ALK, RET, ROS1, and NTRK1, has significantly advanced lung cancer management.
View Article and Find Full Text PDFThe multifaceted roles of aldolase A in cancer: glycolysis, cytoskeleton, translation and beyond.
Hum Cell
January 2025
Institute of Translational Medicine, Medical College, Yangzhou University, No. 136 Jiangyangzhonglu, Yangzhou, 225009, Jiangsu, China.
Cancer, a complicated disease characterized by aberrant cellular metabolism, has emerged as a formidable global health challenge. Since the discovery of abnormal aldolase A (ALDOA) expression in liver cancer for the first time, its overexpression has been identified in numerous cancers, including colorectal cancer (CRC), breast cancer (BC), cervical adenocarcinoma (CAC), non-small cell lung cancer (NSCLC), gastric cancer (GC), hepatocellular carcinoma (HCC), pancreatic cancer adenocarcinoma (PDAC), and clear cell renal cell carcinoma (ccRCC). Moreover, ALDOA overexpression promotes cancer cell proliferation, invasion, migration, and drug resistance, and is closely related to poor prognosis of patients with cancer.
View Article and Find Full Text PDFRNA splicing variants of the novel long non-coding RNA, CyKILR, possess divergent biological functions in non-small cell lung cancer.
Mol Ther Nucleic Acids
March 2025
Department of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA 22903, USA.
The CDKN2A gene, responsible for encoding the tumor suppressors p16(INK4A) and p14(ARF), is frequently inactivated in non-small cell lung cancer (NSCLC). Herein, an uncharacterized long non-coding RNA (lncRNA) (ENSG00000267053) on chromosome 19p13.12 was found to be overexpressed in NSCLC cells with an active, wild-type CDKN2A gene.
View Article and Find Full Text PDFDNMT3A loss drives a HIF-1-dependent synthetic lethality to HDAC6 inhibition in non-small cell lung cancer.
Acta Pharm Sin B
December 2024
Department of Pharmacology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, Shenyang 110016, China.
encodes a DNA methyltransferase involved in development, cell differentiation, and gene transcription, which is mutated and aberrant-expressed in cancers. Here, we revealed that loss of promotes malignant phenotypes in lung cancer. Based on the epigenetic inhibitor library synthetic lethal screening, we found that small-molecule HDAC6 inhibitors selectively killed -defective NSCLC cells.
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