Differential expression of mannan binding lectin serine peptidase 1 in human epithelial ovarian cancer.

Epithelial ovarian cancer (EOC) is the most lethal gynecologic cancer (1). We performed discovery of genes associated with epithelial ovarian cancer and of the high-grade serous ovarian cancer (HGSC) subtype, using published microarray data (2, 3) to compare global gene expression profiles of normal ovary or fallopian tube with that of primary tumors from women diagnosed with epithelial ovarian cancer or HGSC. We identified the gene encoding mannan binding lectin serine peptidase 1, MASP1, as among the genes whose expression was most different in epithelial ovarian cancer as compared to the normal fallopian tube. MASP1 expression was significantly lower in high-grade serous ovarian tumors relative to normal fallopian tube. MASP1 expression correlated with overall survival in patients with ovarian cancer. These data indicate that expression of MASP1 is perturbed in epithelial ovarian cancers broadly and in ovarian cancers of the HGSC subtype. MASP1 may be relevant to pathways underlying ovarian cancer initiation (transformation) or progression.

Could Kallikrein-Related Serine Peptidase 3 Be an Early Biomarker of Environmental Exposure in Young Women?

Bisphenols and phthalates affect androgen receptor-mediated signaling that directly regulates Kallikrein-Related serine Peptidase 3 (KLK3) secretion, indicating that environmental factors may play a role in KLK3 secretion. With the aim of obtaining preliminary data on whether KLK3 could serve as an early marker of environmental pollution effects, in 61 and 58 healthy women living in a high environmental impact (HEI) and low environmental impact (LEI) area, respectively, serum KLK3 levels at different phases of menstrual cycle were measured. KLK3 values resulted in always being higher in the HEI group with respect to the LEI group. These differences were particularly relevant in the ovulatory phase (cycle day 12°–13°) of the menstrual cycle. The differences in KLK3 values during the three phases of the menstrual cycle were significant in the LEI group differently from the HEI group. In addition, higher progesterone levels were observed in the LEI group with respect to the HEI group in the luteal phase, indicating an opposite trend of KLK3 and progesterone in this phase of the menstrual cycle. Although changes in KLK3 could also depend on other factors, these preliminary data could be an early indication of an expanding study of the role of biomarkers in assessing early environmental effects for female reproductive health.

The nasal symbiont Staphylococcus epidermidis shapes the cellular environment to decrease expression of SARS-CoV-2 entry factors in nasal epithelium

Background Emerging evidence indicates that severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2) targets the human nasal epithelium via the principal entry factors angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), which are highly expressed in the nasal epithelium. However, little is known about suppressive biologics against SARS-CoV-2 entry factors. Here, we report that the nasal commensal Staphylococcus epidermidis altered the host transcriptional response against SARS-CoV-2 in the nasal epithelium by reducing ACE2 and TMPRSS2 gene expression in concert with an increase in serine-peptidase inhibitors. Results Our data reveal that ACE2 was more abundantly expressed in nasal epithelial (NHNE) cells than bronchial epithelial cells, and inoculation with S. epidermidis reduced ACE2 transcription in NHNE cells. Our data also show that TMPRSS2 mRNA was significantly decreased in NHNE cells and that S. epidermidis colony number in human nasal mucus was inversely correlated with ACE2 and TMPRSS2 gene expression in the nasal mucosa. In addition, levels of the serine-peptidase inhibitors SERPINE1 and SERPINE2 were significantly increased by S. epidermidis, and this accompanied reduction of TMPRSS2 transcription in nasal epithelial cells. Conclusion These results characterize the S. epidermidis-regulated host transcriptional response restricting SARS-CoV-2 entry to the nasal epithelium via downregulation of receptors and host protease for SARS-CoV-2 cellular invasion coupled with SERPINE1 and SERPINE2 induction.