The anti-tumor capacities of HANPs with different morphologies and particle sizes against two kinds of OS cells, human OS 143B cells and rat OS UMR106 cells.
Background Glioma is a lethal primary tumor of central nervous system. Ferroptosis is a newly identified form of necrotic cell death. Triggering ferroptosis has shown potential to eliminate aggressive tumors. GPX7, a member of glutathione peroxidase family (GPXs), has been described to participate in oxidative stress and tumorigenesis. However, the biological functions of GPX7 in glioma are still unknown. Methods Bioinformatics method was used to assess the prognostic role of GPX7 in glioma. CCK8, wound healing, transwell and cell apoptosis assays were performed to explore the functions of GPX7 in glioma cells. In vivo experiment was also conducted to confirm in vitro findings. Ferroptosis-related assays were carried out to investigate the association between GPX7 and ferroptosis in glioma. Results GPX7 was aberrantly expressed in glioma and higher expression of GPX7 was correlated with adverse outcomes. GPX7 silencing enhanced ferroptosis-related oxidative stress in glioma cells and t
15 Basal epithelial cells are a blood–prostate barrier between luminal cells and basement membrane
16 but are absent in prostate carcinoma.
17–19 Loss of basal epithelial cells is a characteristic of prostate carcinoma
20,21 and one of the diagnostic criteria of prostate cancer,
19 suggesting that some essential connections might exist between basal epithelial cells and prostate cancer cells. So, we put out a question regarding whether basal epithelial cells could suppress migration or invasion of prostate cancer cells when basal epithelial cells are artificially added into a cultured system of prostate cancer cells. Through extensive reading of the medical literature, we found that the effects of basal epithelial cells on prostate cancer cells are still limited. One previous study reported that extracellular matrix of basal epithelial cell inhibited the proliferation of prostate cancer cell LNCaP by secreting TGF-β1.