AI Article Synopsis
- The study aims to explore the genomic profiles and potential treatments for lung cancer patients with idiopathic pulmonary fibrosis (IPF-LC) by analyzing tumor and non-tumor lung tissues.
- Researchers found that two genes, CADM1 and SPC25, had high mutation rates in IPF-LC cases, with implications for cell growth and transformation associated with lung cancer.
- The mutations in CADM1 and SPC25 could serve as new diagnostic markers and therapeutic targets for addressing lung cancer in patients with IPF.
Article Abstract
Introduction: To investigate the genomic profiles of patients with lung cancer with idiopathic pulmonary fibrosis (IPF-LC), mechanism of carcinogenesis, and potential therapeutic targets.
Methods: We analyzed 29 matched, surgically resected, cancerous and noncancerous lung tissues (19 IPF-LC and 10 non-IPF-LC) by whole-exome sequencing and bioinformatics analysis and established a medical-engineering collaboration with the Department of Engineering of the Tokyo University of Science.
Results: In IPF-LC, CADM1 and SPC25 were mutated at a frequency of 47% (9 of 19) and 53% (10 of 19), respectively. Approximately one-third of the IPF-LC cases (7 of 19; 36%) had both mutations. Pathway analysis revealed that these two genes are involved in transforming growth factor-β1 signaling. CADM1 and SPC25 gene mutations decreased the expression of CADM1 and increased that of SPC25 revealing transforming growth factor-β1-induced epithelial-to-mesenchymal transition and cell proliferation in lung cancer cells. Furthermore, treatment with paclitaxel and DNMT1 inhibitor suppressed SPC25 expression.
Conclusions: CADM1 and SPC25 gene mutations may be novel diagnostic markers and therapeutic targets for IPF-LC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8551854 | PMC |
| http://dx.doi.org/10.1016/j.jtocrr.2021.100232 | DOI Listing |
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