A novel lncRNA associated with the prognosis of patients with colorectal cancer resists apoptosis through the LYN/BCL-2 pathway.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2104 (Electronic) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
    • Publication Information:
      Publication: <2002- >: San Diego, CA : Elsevier
      Original Publication: New York, Academic Press.
    • Subject Terms:
      RNA, Long Noncoding*/genetics ; RNA, Long Noncoding*/metabolism ; Colorectal Neoplasms*/genetics ; Colorectal Neoplasms*/pathology ; Colorectal Neoplasms*/metabolism ; Apoptosis*/genetics ; Proto-Oncogene Proteins c-bcl-2*/metabolism ; Proto-Oncogene Proteins c-bcl-2*/genetics ; Signal Transduction* ; Gene Expression Regulation, Neoplastic* ; src-Family Kinases*/metabolism ; src-Family Kinases*/genetics; Humans ; Prognosis ; Cell Line, Tumor ; Cell Proliferation/genetics ; Female ; Male ; Cell Movement/genetics
    • Abstract:
      Purpose: We found a novel lncRNA named lncAC138150.2 related to the overall survival and staging of patients with colorectal cancer (CRC) by bioinformatic analysis using data from the Cancer Genome Atlas (TCGA), and the study aimed to elucidate the function of lncAC138150.2 and underlying mechanisms.
      Methods: Target molecules were knocked down by transfection with antisense oligonucleotides (ASOs), siRNAs, or lentiviruses and overexpressed by transfection with plasmids. The function of lncAC138150.2 was determined using histological, cytological, and molecular biology methods. The underlying mechanism of lncAC138150.2 function was investigated using RNA-seq, bioinformatics analysis, and molecular biology methods.
      Results: The expression of lncAC138150.2 was increased in colorectal tissues compared with paired normal tissues. The lncAC138150.2 knockdown increased apoptosis but did not change the cell proliferation, cell cycle distribution, or cell migration ability of CRC cells, while lncAC138150.2 overexpression decreased CRC apoptosis. lncAC138150.2 was mainly located in the cell nucleus, and each lncAC138150.2 transcript knockdown increased CRC apoptosis. BCL-2 pathway was significantly altered in apoptosis induced by lncAC138150.2 knockdown, which was alleviated by BAX knockdown. The expression of LYN was significantly decreased with lncAC138150.2 knockdown, LYN knockdown increased CRC apoptosis, and its overexpression completely alleviated CRC apoptosis induced by lncAC138150.2 knockdown.
      Conclusion: lncAC138150.2 significantly inhibited CRC apoptosis and affected the prognosis of patients with CRC, through the LYN/BCL-2 pathway.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
      (Copyright © 2024 Elsevier Inc. All rights reserved.)
    • Contributed Indexing:
      Keywords: Apoptosis; Colorectal cancer; LYN/BCL-2 pathway; lncAC138150.2; lncRNA
    • Accession Number:
      0 (RNA, Long Noncoding)
      0 (Proto-Oncogene Proteins c-bcl-2)
      EC 2.7.10.2 (lyn protein-tyrosine kinase)
      EC 2.7.10.2 (src-Family Kinases)
      0 (BCL2 protein, human)
    • Publication Date:
      Date Created: 20240529 Date Completed: 20240622 Latest Revision: 20240711
    • Publication Date:
      20240711
    • Accession Number:
      10.1016/j.bbrc.2024.150177
    • Accession Number:
      38810320