Objective: To investigate the mechanism by which icariin ( ICA) inhibits the invasion and metastasis of human triple-negative breast cancer ( TNBC) cells via downregulation of the transforming growth factor-β/ Smad ( TGF-β/ Smad) signaling pathway． Methods: TNBC cells ( MDA-MB-231 and MDA-MB-468) were cultured in vitro and divided into four groups: an experimental group treated with 15 μmol / L ICA; a model group treated with 10 μmol / L TGF-β receptor inhibitor LY2109761; a combination group ( LY2109761 + ICA) treated with both 15 μmol / L ICA and 10 μmol / L LY2109761; and a control group．Cell proliferation，migration，and invasion were as- sessed using CCK-8，colony formation，5-ethynyl-2 '-deoxyuridine ( EdU) ，wound healing，and Transwell assays． The expression levels of epithelial-mesenchymal transition ( EMT) -related proteins，as well as TGF-β1，Smad2， and phosphorylated Smad2 ( P-Smad2) were detected by immunofluorescence and Western blot． Results: CCK-8 results showed that cell proliferation decreased gradually with increasing concentrations of ICA ( P＜0. 05) ．Colony formation and EdU assays indicated significantly inhibited proliferation in the ICA-treated group compared to the control ( P＜0. 05) ．Wound healing and Transwell assays demonstrated reduced migration and invasion capabilities in the experimental group relative to the control ( P＜0. 05) ．Compared to the model group，the LY2109761 + ICA group exhibited further suppression of invasion ( P＜0. 05) ．Immunofluorescence revealed decreased Vimentin ex- pression in the experimental group ( P＜0. 05) ，with an even more pronounced reduction in the LY2109761 + ICA group ( P＜0. 01) ．Western blot analysis showed that the protein levels of N-cadherin，matrix metalloproteinase-9( MMP9) ，Vimentin，TGF-β1，Smad2，and P-Smad2 were downregulated in the experimental group compared to the control ( P＜0. 05) ．These proteins were further suppressed in the LY2109761 + ICA group compared to the model group ( P＜0. 05) ． Conclusion ICA inhibits TNBC cells proliferation，invasion，metastasis，and EMT by downregulating the TGF-β/ Smad signaling pathway．

Objective To investigate the role of bufalin(BU)in inhibiting M2-type macrophage-mediated colorec-tal cancer metastasis.Methods Human acute leukemia mononuclear cells(THP-1)were differentiated into M0 macrophages using phorbol ester induction(PMA)for 48 hours.The M0 macrophages were then treated with IL-4 and IL-13 medium.Surface markers and morphological changes were observed through ELISA,morphology,and RT-qPCR experiments.RT-PCR and ELISA experiments were conducted to detect the surface markers TGF-β and IL-10 of M2 macrophages.The secretion level of IL-6 in the supernatant of M2 macrophages and colorectal cancer cells HCT116 was compared using ELISA.Additionally,the effect of conditioned medium on colorectal cancer cell HCT116 was assessed through Transwell,Wound healing,RT-qPCR,and Western blot experiments.Subsequent-ly,bufalin was added to the conditioned medium and the changes in AKT/PI3K protein,migration,and epithelial-mesenchymal transition ability in HCT116 were observed using Western blot,Transwell,Wound healing and RT-qPCR experiments.Results THP-1 were successfully differentiated into M2 macrophages.The activation of AKT/PI3K protein in HCT116 cells was induced by the secretion of IL-6 from M2 macrophages,which in turn promoted the migration and epithelial-mesenchymal transition ability of the HCT116 cells.The migration and epithelial-mes-enchymal transition mediated by M2 macrophages in HCT116 cells were effectively inhibited by Bufalin.Conclu-sion The release of IL-6 from M2 macrophages activates the AKT/PI3K signaling pathway in colorectal cancer cells,thereby promoting their migration and epithelial-mesenchymal transition capacity.Moreover,bufalin exhibits inhibitory effects on this effect.

Pregnancy is a physiological state that predisposes women to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, a disease that can cause adverse maternal and perinatal outcomes. The severity of coronavirus disease 2019 (COVID-19) disease is known to vary by viral strain; however, evidence for the effects of this virus in pregnant women has yet to be fully elucidated. In this review, we describe maternal and perinatal outcomes, vaccination, and vertical transmission, among pregnant women infected with the different SARS-CoV-2 variants identified to date. We also summarize existing evidence for maternal and perinatal outcomes in pregnant women with specific information relating to SARS-CoV-2 variants. Our analysis showed that Omicron infection was associated with fewer severe maternal and perinatal adverse outcomes while the Delta variant was associated with worse pregnancy outcomes. Maternal deaths arising from COVID-19 were found to be rare (<1.0%), irrespective of whether the virus was a wild-type strain or a variant. Severe maternal morbidity was more frequent for the Delta variant (10.3%), followed by the Alpha (4.7%), wild-type (4.5%), and Omicron (2.9%) variants. The rates of stillbirth were 0.8%, 4.1%, 3.1%, and 2.3%, respectively, in pregnancies infected with the wild-type strain, Alpha, Delta, and Omicron variants, respectively. Preterm birth and admission to neonatal intensive care units were more common for cases with the Delta infection (19.0% and 18.62%, respectively), while risks were similar for those infected with the wild-type (14.7% and 11.2%, respectively), Alpha (14.9% and 13.1%), and Omicron variants (13.2% and 13.8%, respectively). As COVID-19 remains a global pandemic, and new SARS-CoV-2 variants continue to emerge, research relating to the specific impact of new variants on pregnant women needs to be expanded.

Pregnancy is a physiological state that predisposes women to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, a disease that can cause adverse maternal and perinatal outcomes. The severity of coronavirus disease 2019 (COVID-19) disease is known to vary by viral strain; however, evidence for the effects of this virus in pregnant women has yet to be fully elucidated. In this review, we describe maternal and perinatal outcomes, vaccination, and vertical transmission, among pregnant women infected with the different SARS-CoV-2 variants identified to date. We also summarize existing evidence for maternal and perinatal outcomes in pregnant women with specific information relating to SARS-CoV-2 variants. Our analysis showed that Omicron infection was associated with fewer severe maternal and perinatal adverse outcomes while the Delta variant was associated with worse pregnancy outcomes. Maternal deaths arising from COVID-19 were found to be rare (<1.0%), irrespective of whether the virus was a wild-type strain or a variant. Severe maternal morbidity was more frequent for the Delta variant (10.3%), followed by the Alpha (4.7%), wild-type (4.5%), and Omicron (2.9%) variants. The rates of stillbirth were 0.8%, 4.1%, 3.1%, and 2.3%, respectively, in pregnancies infected with the wild-type strain, Alpha, Delta, and Omicron variants, respectively. Preterm birth and admission to neonatal intensive care units were more common for cases with the Delta infection (19.0% and 18.62%, respectively), while risks were similar for those infected with the wild-type (14.7% and 11.2%, respectively), Alpha (14.9% and 13.1%), and Omicron variants (13.2% and 13.8%, respectively). As COVID-19 remains a global pandemic, and new SARS-CoV-2 variants continue to emerge, research relating to the specific impact of new variants on pregnant women needs to be expanded.