S100A7 promotes the development of human endometriosis by activating NF-κB signaling pathway in endometrial stromal cells.

Endometriosis (EM) is a chronic inflammatory disease affecting women aged between 23 and 42 years with a prevalence of 6%-10%. S100A7, a member of the S100 protein family, has been implicated in promoting inflammation. However, the role of S100A7 in EM and its underlying mechanism remain to be elucidated. S100A7 was silenced or overexpressed in primary endometrial stromal cells (ESCs). Cell proliferation was determined using a Cell Counting Kit-8. Cell cycle/apoptosis was monitored using a flow cytometer. Cell invasion was studied by a Transwell assay. Quantitative RT-PCR and Western blot analyses were used to evaluate gene expression. S100A7 and NF-κB expression is increased in both endometriotic tissue and ESCs from women with EM. The expression of S100A7 is correlated with the expression of NF-κB. S100A7 knockdown inhibits ESCs proliferation, cell cycle progression, cell invasion, and inflammation, but promotes cell apoptosis in an NF-κB dependent manner. In contrast, S100A7 overexpression demonstrated an inverse effect. S100A7 is increased in both endometriotic tissue and ESCs from women with EM. S100A7 overexpression contributes to EM through increasing ESCs proliferation, cell cycle progression, cell invasion, and inflammation, and inhibiting cell apoptosis in the NF-κB dependent manner. These findings highlight the importance of S100A7/NF-κB signaling in EM and provide new insights into therapeutic strategies for EM.

S100A7 Regulates Ovarian Cancer Cell Metastasis and Chemoresistance Through MAPK Signaling and Is Targeted by miR-330-5p.

Epithelial ovarian cancer (EOC) is the most common cause of gynecological cancer-associated death. The high mortality rate is largely due to early stage metastasis and posttreatment recurrence. Identifying crucial regulators of EOC cells as well as ways to target them promises to improve the disease's prognosis. The S100 calcium-binding protein A7 (S100A7) has been shown to promote cell proliferation, migration, invasion, and tumor metastasis. In this study, we have investigated the role that S100A7 plays in regulating EOC cells. We have also identified the microRNA protein miR-330-5p, a known suppressor of oncogenesis and chemoresistance, as an inhibitor of S100A7 activity. We employed both fresh EOC tissue specimens as well as EOC cell lines Caov3 and SKOV3. S100A7 levels were analyzed using quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry. siRNA was used to knockdown S100A7. Cell proliferation, colony formation, and Transwell migration and invasion assays were performed on EOC cell lines with and without cisplatin treatment. TargetScan was used to identify miR-330-5p as a regulator of S100A7. Luciferase reporter plasmids were constructed with either the wild-type or mutant S100A7 3'UTR to determine the effect of miR-330-5p on S100A7. S100A7 was significantly overexpressed in human EOC tissue specimens and EOC cell lines Caov3 and SKOV3. Knocking down S100A7 reduced EOC cell proliferation, migration, and invasion. Furthermore, S100A7 knockdown cells demonstrated increased sensitivity to the chemotherapeutic cisplatin. Finally, miR-330-5p was shown to target the S100A7 3'UTR and to reduce EOC cell growth by inhibiting S100A7 expression. As a regulator of EOC cell proliferation, metastasis, and chemoresistance, S100A7 represents a potential prognostic biomarker for EOC as well as a treatment target. Because miR-330-5p functions as an inhibitor of EOC cell growth and S100A7 expression, it promises to improve EOC outcomes. Further research into the clinical significance of both S100A7 and miR-300-5p is warranted.

S100A7 has an oncogenic role in oral squamous cell carcinoma by activating p38/MAPK and RAB2A signaling pathway.

Oral cancer consists of squamous cell carcinoma within the oral cavity or on the lip. The clinical prognosis of this cancer is mostly poor owing to delayed diagnosis and a lack of appropriate early detection biomarkers to identify the disease. In the current study, we investigated the role of the S100A7 calcium-binding protein in oral squamous cell carcinoma as an activator of the p38/MAPK and RAB2A signaling pathway. The aim of the present study was to determine whether S100A7 and RAB2A have a role in tumor progression and to assess their potential as early detection biomarkers for oral cancer. This study elucidated the functional and molecular mechanisms of S100A7 and RAB2A activity in oral cancer, leading us to conclude that S100A7 is the major contributing factor in the occurrence of oral cancer and promotes local tumor progression by activating the MAPK signaling pathway via the RAB2A pathway. We hypothesize that S100A7 affects cell motility and invasion by regulating the RAB2A-associated MAPK signaling cascades. Also, the downregulation of S100A7 expression by RNA interference-mediated silencing inhibits oral cancer cell growth, migration and invasion.