C. Gynecological Cancer & Reproductive Health
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J Biol Chem (2010) 285:38260-9. (IF: 5.157; Rank: 86/313 = 27.48 % in Biochemistry & Molecular Biology; Citation = 67) Cancer Res (2008) 68:4050-7. (IF: 12.701; Rank: 17/313 = 5.43 % in Oncology; Citation = 67)
RSF1 amplification/overexpression has been identified as a cancerpromoting signal for aggressive types of ovarian cancer. In these two studies, we confirmed that Rsf-1 can cause chromosome instability (CIN), and the activated DDR signals act as a selection pressure for clonal evolution and selection. Cells with genetic defects/silencing in p53 signaling pathway can bypass the barrier and allow additional genetic alterations for advanced malignancy.
Oncotarget (2016) 7:76713-25. (IF: 5.168 in 2016; Citation = 14)
Biomedicines (2022) 10:185. (IF: 6.081; Rank: 33/236 = 14.0% in Pharmacy)
Ribosome biogenesis is upregulated in endometriosis and even over-activated in the associated ovarian cancer. Our finding suggested that active ribosome synthesis may function as a driving force to promote malignant transition in deeply-infiltrated endometriosis (DIE) which already harbors driver mutations but presents in normal endothelium morphology. Therapeutic strategy based on anti- RNA polymerase 1 showed promising results to trigger apoptosis in related ovarian cancer cells. This study was highly recommended by F1000Prime as a breakthrough discovery that may find the solution to actively treat endometriosis as well as to prevent the related malignancies. The therapeutic efficacy was recently confirmed in a human-like endometriosis mouse model.
Cancer Res (2009) 69:2568-76. (IF: 12.701; Rank: 17/313 = 5.43 % in Oncology; Citation = 171)
Mucins are high-molecular-weight glycoproteins that protect and
lubricate the epithelial surface of mucosa including reproductive
tracts. Emerging evidence reveal that mucin variants caused by
SNPs in the VNTR domain can influence local immunity and
trigger cell proliferation via HER2-mediated signaling. In these
serial studies, we discovered that genetic variations in mucin
genes (MUC2, MUC4, MUC17) can determine the susceptibility
to endometriosis development and the associated infertility.
Those studies provide solid evidence to indicate the involvement
of mucins in reproductive health, e.g. infertility.
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