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Jia Cao

Researcher at Third Military Medical University

Publications -  174
Citations -  5068

Jia Cao is an academic researcher from Third Military Medical University. The author has contributed to research in topics: DNA methylation & Semen quality. The author has an hindex of 34, co-authored 169 publications receiving 3961 citations. Previous affiliations of Jia Cao include Chinese Ministry of Education & Xinxiang Medical University.

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ALX4, an epigenetically down regulated tumor suppressor, inhibits breast cancer progression by interfering Wnt/β-catenin pathway.

TL;DR: It is revealed for the first time that ALX4 acts as a novel functional tumor suppressor inactivated by DNA methylation and is an independent prognostic factor in breast cancer patients.
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Aberrant methylation accounts for cell adhesion-related gene silencing during 3-methylcholanthrene and diethylnitrosamine induced multistep rat lung carcinogenesis associated with overexpression of DNA methyltransferases 1 and 3a.

TL;DR: It is suggested that DNMT1 and DNMT3a protein overexpression may be responsible for this aberrant DNA methylation and an accumulation of hypermethylation accounts for cell adhesion-related gene silencing is associated with dynamic changes in the progression of MCA/DEN-induced rat lung carcinogenesis.
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Epigenetic inactivation of LHX6 mediated microcystin-LR induced hepatocarcinogenesis via the Wnt/β-catenin and P53 signaling pathways

TL;DR: It is demonstrated for the first time that LHX6 gene expression is regulated by DNA methylation and can inhibit the proliferation, invasion and migration through Wnt/β-catenin and P53 signaling pathways during the MC-LR-induced hepatocarcinogenesis.
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Extremely Low-Frequency Electromagnetic Fields Affect the miRNA-Mediated Regulation of Signaling Pathways in the GC-2 Cell Line.

TL;DR: Go term and KEGG pathway annotation based on the miRNA expression profiling results showed that miRNAs may regulate circadian rhythms, cytokine-cytokine receptor interactions and the p53 signaling pathway.
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BPDE and B[a]P induce mitochondrial compromise by ROS-mediated suppression of the SIRT1/TERT/PGC-1α pathway in spermatogenic cells both in vitro and in vivo.

TL;DR: The results of the present study demonstrate that B[a]P and BPDE induce mitochondrial damage through ROS production that suppresses SIRT1/TERT/PGC-1a signaling and mediate B[ a]P- and B PDE-mediated reproductive toxicity.