J Cancer 2022; 13(8):2620-2630. doi:10.7150/jca.63256 This issue
1. Clinical Genetics Laboratory, Affiliated Hospital & Clinical Medical College of Chengdu University, Chengdu 610081, P.R. China.
2. Department of Respiratory and Critical Care Medicine, Affiliated Hospital & Clinical Medical College of Chengdu University, Chengdu 610081, P.R. China.
3. Department of Pathology, Affiliated Hospital & Clinical Medical College of Chengdu University, Chengdu 610081, P.R. China.
4. Institute of Blood Transfusion, Chinese Academy of Medical Sciences, Chengdu 610052, P.R. China.
#These authors are regarded as co-first authors.
Background: Long noncoding RNAs (LncRNAs) possess crucial roles in carcinogenesis. The current study aims to evaluate the effects of interleukin-1β (IL-1β)-mediated lncRNA cardiac hypertrophy-related factor (CHRF)/microRNA-489 (miR-489)/myeloid differentiation factor 88 (Myd88) on non-small-cell lung cancer (NSCLC).
Methods: Initially, the expression of IL-1β and lncRNA CHRF in NSCLC cells and tissues was determined, respectively. H460 cell line with highest lncRNA CHRF expression was selected for in vitro experimentations. Afterward, the interaction among lncRNA CHRF, miR-489, and Myd88 was verified with their significance in cell functions and tumorigenicity and lung metastasis analyzed following.
Results: IL-1β and lncRNA CHRF was remarkably upregulated in NSCLC. IL-1β was able to elevate lncRNA CHRF expression. Additionally, lncRNA CHRF targeted miR-489 and miR-489 targeted Myd88. Moreover, functional assay results suggested that under IL-1β treatment, lncRNA CHRF induced NSCLC cell malignant properties and tumorigenicity and lung metastasis through modulation of miR-489/Myd88 axis.
Conclusion: Taken together, our findings revealed that IL-1β-induced elevation of lncRNA CHRF aggravated NSCLC through modulation of miR-489/Myd88 axis, which provides a novel direction for NSCLC therapy development.
Keywords: Long noncoding RNA cardiac hypertrophy-related factor, microRNA-489, Myeloid differentiation factor 88, Interleukin-1β, Non-small cell lung cancer, Proliferation, Migration, Invasion, Apoptosis