Abstract:
:Effects of different levels of PM2.5 on invasion and proliferation of HeLa cells and the expression levels of inflammatory cytokines IL-1 and IL-6 under 10 µg/ml PM2.5 were investigated. Different groups of HeLa cells were treated with PM2.5 at 0, 10, 25, 50, 100 and 200 µg/ml for 36 h, respectively. Cell proliferation was detected by MTT assay. Transwell assay was performed to detect the invasion of HeLa cells. Enzyme-linked immunosorbent assay (ELISA), RT-qPCR and western blotting were used to detect the expression levels of inflammatory cytokines IL-1 and IL-6 in PM2.5-stimulated HeLa cells. It was observed that proliferation of cells treated with PM2.5 at a concentration of 10 µg/ml was basically the same as that of untreated cells, while high concentration of PM2.5 inhibited the proliferation of HeLa cells in a dose-dependent manner in the range from 25 to 200 µg/ml (P<0.05). Transwell invasion assay showed that the number of migrating HeLa cells stimulated by 10 µg/ml PM2.5 was significantly greater than that of NC group cells (P<0.05). Western blotting showed that IL-1 and IL-6 protein expression levels in HeLa cells after stimulation with 10 µg/ml PM2.5 were significantly higher than that in NC group (P<0.05). RT-qPCR results also showed that IL-1 mRNA and IL-6 mRNA expression levels in HeLa cells stimulated by 10 µg/ml PM2.5 were significantly higher than those in the NC group (P<0.05). Additionally, ELISA results showed that IL-1 and IL-6 levels in HeLa cells stimulated by 10 µg/ml PM2.5 were significantly higher than those in NC group (P<0.05). We conclude that high concentrations of PM2.5 can inhibit the proliferation of HeLa cells to a certain extent. Stimulation with 10 µg/ml PM2.5 increases the invasion ability of HeLa cells and promotes the expression of inflammatory cytokines IL-1 and IL-6.
journal_name
Oncol Lettjournal_title
Oncology lettersauthors
Huang K,Li W,Chen Y,Zhu Jdoi
10.3892/ol.2018.9516subject
Has Abstractpub_date
2018-12-01 00:00:00pages
7068-7073issue
6eissn
1792-1074issn
1792-1082pii
OL-0-0-9516journal_volume
16pub_type
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