Background: RNA splicing, a fundamental step in gene expression, is aimed at intron removal and ordering of exons to form the protein's reading frame.
Objective: This review is focused on the role of RNA splicing in cancer biology; the splicing abnormalities that lead to tumor progression emerge as targets for therapeutic intervention.
Methods: We discuss the role of aberrant mRNA splicing in carcinogenesis and drug response.
Results And Conclusion: Pharmacological modulation of RNA splicing sets the stage for treatment approaches in situations where mRNA splicing is a clinically meaningful mechanism of the disease.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2174/1574892815666200908122402 | DOI Listing |
Open Biol
January 2025
School of Life Sciences, University of Dundee, Dundee, UK.
The established consensus sequence for human 5' splice sites masks the presence of two major splice site classes defined by preferential base-pairing potentials with either U5 snRNA loop 1 or the U6 snRNA ACAGA box. The two 5' splice site classes are separable in genome sequences, sensitized by specific genotypes and associated with splicing complexity. The two classes reflect the commitment to 5' splice site usage occurring primarily during 5' splice site transfer to U6 snRNA.
View Article and Find Full Text PDFMol Cell
January 2025
European Molecular Biology Laboratory (EMBL), EMBL Grenoble, 71 Avenue des Martyrs, 38042 Grenoble, France. Electronic address:
The minor spliceosome catalyzes excision of U12-dependent introns from precursors of eukaryotic messenger RNAs (pre-mRNAs). This process is critical for many cellular functions, but the underlying molecular mechanisms remain elusive. Here, we report a cryoelectron microscopy (cryo-EM) reconstruction of the 13-subunit human U11 small nuclear ribonucleoprotein particle (snRNP) complex in apo and substrate-bound forms, revealing the architecture of the U11 small nuclear RNA (snRNA), five minor spliceosome-specific factors, and the mechanism of the U12-type 5' splice site (5'SS) recognition.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Department of Pharmacology, Republic of Korea; Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, 440-746, Republic of Korea; Samsung Biomedical Research Institute, Samsung Medical Center, Seoul, 06351, Republic of Korea. Electronic address:
ZNF398/ZER6 belongs to the Krüppel-associated box (KRAB) domain-containing zinc finger proteins (K-ZNFs), the largest family of transcriptional repressors in higher organisms. ZER6 exists in two isoforms, p52 and p71, generated through alternative splicing. Our investigation revealed that p71-ZER6 is abundantly expressed in the stomach, kidney, liver, heart, and brown adipose tissue, while p52-ZER6 is predominantly found in the stomach and brain.
View Article and Find Full Text PDFHum Mol Genet
January 2025
Department of Thoracic Surgery, Huaihe Hospital of Henan University, No. 8, Baobei Road, Gulou District, Kaifeng City, Henan Province, China.
Adenocarcinoma of the esophagogastric junction (AEG) is a common and deadly cancer, and an in-depth investigation of its molecular mechanisms of metastasis is crucial for discovering new therapeutic targets. This study explores the role of the long non-coding RNA (lncRNA) LINC00115 in AEG metastasis and its underlying mechanisms. Through the analysis of 108 pairs of AEG cancer tissues and matched adjacent tissues, we found a significant upregulation of LINC00115 in AEG tissues, closely associated with TNM staging and lymph node metastasis.
View Article and Find Full Text PDFMol 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 PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!