Faculty, Staff and Student Publications
Publication Date
5-1-2022
Journal
Genes Development
DOI
10.1101/gad.349321.121
PMID
35654454
PMCID
PMC9186390
PubMedCentral® Posted Date
5-1-2022
PubMedCentral® Full Text Version
Post-print
Abstract
Here, Kundu et al. investigated the role of the microRNA-183/96/182 cluster (m96cl) in lung cancer and used a novel conditional m96cl mouse to establish that loss of m96cl accelerated the growth of K-Ras mutant autochthonous lung adenocarcinomas. Overall, the authors identified a novel mechanistic role of the m96cl in the suppression of lung cancer growth and metastasis by inducing an IL2-mediated systemic CD8+ CTL immune response.
Keywords
Animals, CD8-Positive T-Lymphocytes, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Interleukin-2, Lung Neoplasms, Mice, MicroRNAs, T-Lymphocytes, Cytotoxic, Tumor Microenvironment, CD8+ T lymphocytes, CTL, tumor immune microenvironment, microRNA-183/96/182, antitumor immune response, interleukin-2, EMT, Zeb1, Foxf2, lung cancer
Published Open-Access
yes
Recommended Citation
Kundu, Samrat T; Rodriguez, B Leticia; Gibson, Laura A; et al., "The microRNA-183/96/182 Cluster Inhibits Lung Cancer Progression and Metastasis by Inducing an Interleukin-2-Mediated Antitumor CD8+ Cytotoxic T-Cell Response" (2022). Faculty, Staff and Student Publications. 3093.
https://digitalcommons.library.tmc.edu/uthgsbs_docs/3093
Included in
Bioinformatics Commons, Biomedical Informatics Commons, Genetic Phenomena Commons, Medical Genetics Commons, Oncology Commons