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Analysis of copy number alterations reveals the lncRNA ALAL-1 as a regulator of lung cancer immune evasion

Data de publicació:

Autors de IIS La Fe

Autors aliens a IIS La Fe

  • Athie, A
  • Marchese, FP
  • Gonzalez, J
  • Lozano, T
  • Raimondi, I
  • Juvvuna, PK
  • Abad, A
  • Marin-Bejar, O
  • Serizay, J
  • Martinez, D
  • Ajona, D
  • Pajares, MJ
  • Montuenga, LM
  • Kanduri, C
  • Lasarte, JJ
  • Huarte, M

Grups d'Investigació

Abstract

Cancer is characterized by genomic instability leading to deletion or amplification of oncogenes or tumor suppressors. However, most of the altered regions are devoid of known cancer drivers. Here, we identify lncRNAs frequently lost or amplified in cancer. Among them, we found amplified IncRNA associated with lung cancer-1 (ALAL-1) as frequently amplified in lung adenocarcinomas. ALAL-1 is also overexpressed in additional tumor types, such as lung squamous carcinoma. The RNA product of ALAL-1 is able to promote the proliferation and tumorigenicity of lung cancer cells. ALAL-1 is a TNF alpha- and NF-kappa B-induced cytoplasmic lncRNA that specifically interacts with SART3, regulating the subcellular localization of the protein deubiquitinase USP4 and, in turn, its function in the cell. Interestingly, ALAL-1 expression inversely correlates with the immune infiltration of lung squamous tumors, while tumors with ALAL-1 amplification show lower infiltration of several types of immune cells. We have thus unveiled a pro-oncogenic lncRNA that mediates cancer immune evasion, pointing to a new target for immune potentiation.

Dades de la publicació

ISSN/ISSNe:
0021-9525, 1540-8140

JOURNAL OF CELL BIOLOGY  Rockefeller University Press

Tipus:
Article
Pàgines:
-
PubMed:
32858747
Factor d'Impacte:
5,414 SCImago ℠
Quartil:
Q1 SCImago ℠

Cites Rebudes en Web of Science: 27

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Keywords

  • LONG NONCODING RNAS; NF-KAPPA-B; USP4 INHIBITS P53; PROTEASE 4 USP4; STRUCTURAL BASIS; DNA METHYLATION; EXPRESSION; PHOSPHORYLATION; TRANSCRIPTION; LANDSCAPE

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