Effect of ovariectomy and LCAT overexpression on gene expression of mouse liver cancer
To unravel the molecular mechanisms behind estrogen-mediated alleviation of liver cancer, we initially established a liver cancer model in ovariectomized mice. Through cross-species comparison of differentially expressed genes under estrogen dominance in human and murine liver cancers, we identified LCAT as a crucial downstream molecule mediating estrogen-induced gender disparities in liver cancer. Subsequent transcriptome sequencing of mouse liver tissues overexpressing the LCAT gene revealed that LCAT plays a pivotal role in inhibiting the cholesterol synthesis pathway, potentially serving as a key molecular mechanism through which it suppresses the occurrence and progression of liver cancer. Overall design: To elucidate the molecular mechanisms underlying estrogen-mediated mitigation of liver cancer, we initially induced primary liver cancer in ovariectomized female mice and those subjected to sham surgery. To uncover the molecular mechanisms by which LCAT alleviates liver cancer, we induced primary liver cancer in mice through overexpression of LCAT in the liver, comparing it with a control group. We then obtained mouse liver tissues at the terminal sampling time point for transcriptome sequencing analysis Comparative gene expression profiling analysis of RNA-seq data between the group Sham and OVX, or Vec and LCAT.