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eIF4E is a critical regulator of human papillomavirus (HPV)-immortalized cervical epithelial (H8) cell growth induced by nicotine.
Abstract Tobacco smoke is known as a cofactor in the development of cervical precancer and cancer caused by human papillomavirus (HPV). The main component in cigarette smoke, nicotine, can be concentrated more strongly in cervical mucus than in blood and it has been implicated as a cocarcinogen that promotes a serial of cancers development through multiple prosurvival pathways. Although the mechanisms of nicotine-induced cell proliferation have been well studied in some epithelial cells, the molecular mechanism of its action in cervical epithelial cells is still unclear. The aims of this study were to investigate ...
Source: Toxicology - March 1, 2019 Category: Toxicology Authors: Chen L, Wang H Tags: Toxicology Source Type: research

Attenuated cholesterol metabolism pathway suppresses regulatory T cell development in prenatal nicotine exposed female mice.
In conclusion, this study showed that PNE could suppress Tregs development in female mice by up-regulating ABCG1-dependent cholesterol efflux, and suggested that PNE-induced thymic Tregs recession of offspring at early life was the developmental origin mechanism of immune dysfunction in later life. PMID: 31629012 [PubMed - as supplied by publisher]
Source: Toxicology - October 15, 2019 Category: Toxicology Authors: Wen X, Zhao WH, Chen LZ, Qu W, Liu HX, Yan HY, Hou LF, Ping J Tags: Toxicology Source Type: research

Snail/HDAC1/2 mediate skeletal growth retardation in fetuses caused by prenatal nicotine exposure
This study intends to clarify the specific molecular mechanism of fetal osteochondral retardation caused by PNE through animal and cellular experiments. The present study demonstrated that in male offspring of the PNE group (the pregnant rats were subcutaneously administered nicotine 1.0 mg/kg twice per day (2.0 mg/kg.d) at GD11-20), the cartilage matrix of the fetal growth plate was lightly stained, the collagen was reduced, and expression of the matrix phenotype genes, ACAN and Col2A1, was significantly decreased. It was further found that PNE decreased histone acetylation (H3K9/H3K14) levels in the ACAN and Col2A1 promo...
Source: Toxicology - July 10, 2021 Category: Toxicology Authors: Yu Deng Hui Gao Hui Wang Liaobin Chen Source Type: research