BACKGROUND AND IMPORTANCE A pituitary adenoma patient who underwent surgery in our department was diagnosed with COVID-19 and 14 medical staff were confirmed infected later. This case has been cited several times but without accuracy or entirety, we feel obligated to report it and share our thoughts on the epidemic among medical staff and performing endonasal endoscopic surgery during COVID-19 pandemic. CLINICAL PRESENTATION The patient developed a fever 3 d post endonasal endoscopic surgery during which cerebrospinal leak occurred, and was confirmed with SARS-CoV-2 infection later. Several medical staff outside the operating room were diagnosed with COVID-19, while the ones who participated in the surgery were not. CONCLUSION The deceptive nature of COVID-19 results from its most frequent onset symptom, fever, a cliché in neurosurgery, which makes it hard for surgeons to differentiate. The COVID-19 epidemic among medical staff in our department was deemed as postoperative rather than intraoperative transmission, and attributed to not applying sufficient personal airway protection. Proper personal protective equipment and social distancing between medical staff contributed to limiting epidemic since the initial outbreak. Emergency endonasal endoscopic surgeries are feasible since COVID-19 is still supposed to be containable when the surgeries are performed in negative pressure operating rooms with personal protective equipment and the patients are kept under quarantine postoperatively. However, we do not encourage elective surgeries during this pandemic, which might put patients in conditions vulnerable to COVID-19.
Signal transducer and activator of transcription-3 (STAT3) is critical for cancer progression by regulating tumor cell survival, proliferation, and angiogenesis. Herein, we investigated the regulation of STAT3 activation and the therapeutic effects of Icaritin, a prenyl flavonoid derivative from Epimedium Genus, in renal cell carcinoma (RCC). Icaritin showed significant anti-tumor activity in the human and mouse RCC cell lines, 786-O and Renca, respectively. Icaritin inhibited both constitutive and IL-6-induced phospho-STAT3 (STAT3Y705) and reduced the level of STAT3-regulated proteins Bcl-xL, Mcl-1, Survivin, and CyclinD1 in a dose-dependent manner. Icaritin also inhibited activation of Janus-activated kinase-2 (JAK2), while it showed minimal effects on the activation of other key signaling pathways, including AKT and MAPK. Expression of the constitutively active form of STAT3 blocked Icaritin-induced apoptosis, while siRNA directed against STAT3 potentiated apoptosis. Finally, Icaritin significantly blunted RCC tumor growth in vivo, reduced STAT3 activation, and inhibited Bcl-xL and Cyclin E, as well as VEGF expression in tumors, which was associated with reduced tumor angiogenesis. Overall, these results suggest that Icaritin strongly inhibits STAT3 activation and is a potentially effective therapeutic option for the treatment of renal cell carcinoma.
Icaritin, a prenylflavonoid derivative from Epimedium Genus, has been shown to exhibit many pharmacological and biological activities. However, the function and the underlying mechanisms of icaritin in human non-small cell lung cancer have not been fully elucidated. The purpose of this study was to investigate the anticancer effects of icaritin on A549 cells and explore the underlying molecular mechanism. The cell viability after icaritin treatment was tested by MTT assay. The cell cycle distribution, apoptosis and reactive oxygen species (ROS) levels were analyzed by flow cytometry. The mRNA and protein expression levels of the genes involved in proliferation and apoptosis were respectively detected by RT-PCR and Western blotting. The results demonstrated that icaritin induced cell cycle arrest at S phase, and down-regulated the expression levels of S regulatory proteins such as Cyclin A and CDK2. Icaritin also induced cell apoptosis characterized by positive Hoechst 33258 staining, accumulation of the Annexin V-positive cells, increased ROS level and alteration in Bcl-2 family proteins expression. Moreover, icaritin induced sustained phosphorylation of ERK and p38 MAPK. These findings suggested that icaritin might be a new potent inhibitor by inducing S phase arrest and apoptosis in human lung carcinoma A549 cells.
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