PM2.5 promotes non-small cell lung cancer tumorigenesis by miR-21-5p targeting accumulated.
1/5 보강
[BACKGROUND] Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide.
APA
Lin YJ, Wu YH, et al. (2025). PM2.5 promotes non-small cell lung cancer tumorigenesis by miR-21-5p targeting accumulated.. Translational cancer research, 14(11), 7580-7597. https://doi.org/10.21037/tcr-2025-626
MLA
Lin YJ, et al.. "PM2.5 promotes non-small cell lung cancer tumorigenesis by miR-21-5p targeting accumulated.." Translational cancer research, vol. 14, no. 11, 2025, pp. 7580-7597.
PMID
41378000
Abstract
[BACKGROUND] Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. Fine particulate matter (PM2.5) is associated with increased risk of lung cancer. microRNAs (miRNAs) play an important role in a variety of cancers, including NSCLC. In NSCLC, existing literature has revealed upregulation of miR-21-5p. Nonetheless, the molecular mechanism of miR-21-5p in NSCLC development after PM2.5 exposure is not clear. This study aimed to investigate the role of miR-21-5p in NSCLC development after PM2.5 exposure and to elucidate the underlying molecular mechanisms.
[METHODS] Expression of miR-21-5p, , and was determined in NSCLC cell lines and tumor tissues. To measure proliferation, migration/invasion of NSCLC cells, 3-(4, 5-dimethyl-thiazolyl-2)-2, 5-diphenyl-tetrazolium bromide (MTT), colony formation, transwell and wound healing assays were accordingly performed. A tumor xenograft model was established to evaluate the effects of miR-21-5p, , and modification on tumor growth .
[RESULTS] miR-21-5p was up-regulated in NSCLC tumor tissues and cell lines. Also, PM2.5 exposure led to a higher level of miR-21-5p. The miR-21-5p mimic and inhibitor respectively promoted and decreased proliferation and migration/invasion of NSCLC cells. Tumor growth was reduced in miR-21-5p KO mice . Luciferase reporter assay indicated that was a target of miR-21-5p. Moreover, miR-21-5p regulated cell proliferation and migration/invasion by inhibiting expression after PM2.5 exposure. knockdown promoted tumor growth . P and were down-regulated in NSCLC tumor tissues and cell lines. inhibited NSCLC cell proliferation and invasion/migration and tumor growth after PM2.5 exposure by regulating miR-21-5p/PDE4DIP signaling pathway.
[CONCLUSIONS] miR-21-5p could target and promote tumor growth of NSCLC. suppressed NSCLC tumorigenesis by regulating miR-21-5p/PDE4DIP signaling pathway.
[METHODS] Expression of miR-21-5p, , and was determined in NSCLC cell lines and tumor tissues. To measure proliferation, migration/invasion of NSCLC cells, 3-(4, 5-dimethyl-thiazolyl-2)-2, 5-diphenyl-tetrazolium bromide (MTT), colony formation, transwell and wound healing assays were accordingly performed. A tumor xenograft model was established to evaluate the effects of miR-21-5p, , and modification on tumor growth .
[RESULTS] miR-21-5p was up-regulated in NSCLC tumor tissues and cell lines. Also, PM2.5 exposure led to a higher level of miR-21-5p. The miR-21-5p mimic and inhibitor respectively promoted and decreased proliferation and migration/invasion of NSCLC cells. Tumor growth was reduced in miR-21-5p KO mice . Luciferase reporter assay indicated that was a target of miR-21-5p. Moreover, miR-21-5p regulated cell proliferation and migration/invasion by inhibiting expression after PM2.5 exposure. knockdown promoted tumor growth . P and were down-regulated in NSCLC tumor tissues and cell lines. inhibited NSCLC cell proliferation and invasion/migration and tumor growth after PM2.5 exposure by regulating miR-21-5p/PDE4DIP signaling pathway.
[CONCLUSIONS] miR-21-5p could target and promote tumor growth of NSCLC. suppressed NSCLC tumorigenesis by regulating miR-21-5p/PDE4DIP signaling pathway.