RNA binding protein YTHDF1 mediates bisphenol S-induced Leydig cell damage by regulating the mitochondrial pathway of BCL2 and the expression of CDK2-CyclinE1

Li, Jing-zhi; Zhou, Shimeng; Yuan, Wenwen; Chen, Hongqiang; Zeng, Yong; Fan, Jun; Zhang, Zhe; Wang, Na; Cao, Jun; Liu, Wen-bin

doi:10.1016/j.envpol.2023.121144

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2023

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Cited by 3 publications

References 65 publications

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Mechanistic illustration on lipid-metabolism disorders induced by triclosan exposure from the viewpoint of m6A-RNA epigenetic modification

Chen,

Wang,

Yan

et al. 2023

Science of The Total Environment

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Mechanistic illustration on lipid-metabolism disorders induced by triclosan exposure from the viewpoint of m6A-RNA epigenetic modification

Chen,

Wang,

Yan

et al. 2023

Science of The Total Environment

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YTHDF1 shapes “cold” tumor and inhibits CD8+ T cells infiltration and function in breast cancer

Jing,

Zhou,

Wang

et al. 2023

Experimental Cell Research

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Breast cancer intrinsic YTHDF1 forms “cold” tumor and inhibits CD8+ T cells infiltration and function

Jing¹,

Zhou²,

Wang³

et al. 2023

Preprint

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Backgrounds While YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) was recognized as a crucial contributor in the development and immune-related regulation of various types of tumors, its function in the immune response of breast cancer has largely remained uninvestigated. Methods Through analysis of public databases, we found YTHDF1 as a highly expressed gene in breast cancers and confirmed this finding in breast cancer cells and clinical specimens from our center. Subsequently, we examined the link between YTHDF1 expression and immune cells and molecules by utilizing immune-related public databases. We further validated our findings through cellular and animal experiments, as well as RNA sequencing. Results We observed YTHDF1 highly expressed in tumor tissues of breast cancer, which negatively correlated with patient survival. The downregulation of YTHDF1 promoted the expression of pro-inflammatory markers and improved the anti-cancer ability of immune cells in breast cancer. RNA sequencing analysis revealed that YTHDF1 knockdown resulted in enrichment of differential genes in signal transduction pathways. Additionally, in vitro experiments showed that immune cells had higher cytotoxicity against breast cancer cells with decreased YTHDF1 expression. Moreover, in vivo studies indicated that YTHDF1 promoted breast cancer growth while inhibiting CD8+ T cell infiltration and function. Conclusion We demonstrated that YTHDF1 plays a crucial role in establishing a "cold" tumor microenvironment in breast cancer by inhibiting the release of pro-inflammatory cytokines from cancer cells. As a result, the infiltration and functional differentiation of anti-tumor CD8+ T cells are hindered, ultimately resulting in the immune evasion of breast cancer.

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RNA binding protein YTHDF1 mediates bisphenol S-induced Leydig cell damage by regulating the mitochondrial pathway of BCL2 and the expression of CDK2-CyclinE1

Cited by 3 publications

References 65 publications

Mechanistic illustration on lipid-metabolism disorders induced by triclosan exposure from the viewpoint of m6A-RNA epigenetic modification

Mechanistic illustration on lipid-metabolism disorders induced by triclosan exposure from the viewpoint of m6A-RNA epigenetic modification

YTHDF1 shapes “cold” tumor and inhibits CD8+ T cells infiltration and function in breast cancer

Breast cancer intrinsic YTHDF1 forms “cold” tumor and inhibits CD8+ T cells infiltration and function

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