Rabbit Anti-Human STEAP3 (a.a. 1-100) Polyclonal antibody

Glioblastoma (GBM) is the most common, malignant, and deadly primary glioma. Six-transmembrane epithelial antigen of prostate (STEAP) family is involved in tumorigenesis; here, we have explored the biological function and the prognostic value of the STEAP family in GBM. Differentially expressed STEAP genes in tumor and normal samples were screened by using The Cancer Genome Atlas (TCGA) database. Univariate and multivariate Cox regression identified the prognosis-related genes: STEAP2 and STEAP3, which were involved in the regulation of immune response and cell cycle. Finally, a prognostic nomogram combining age, gender, chemotherapy, radiotherapy, IDH1 status, and the risk score model based on STEAP2 and STEAP3 was built and further validated in TCGA and Chinese Glioma Genome Atlas (CGGA) cohorts via concordance index and calibration plot, which suggested a favorable value for prognosis prediction. In conclusion, our results provided a comprehensive analysis of the STEAP family and a model for the prognosis prediction of GBM.

Bone marrow injury remains a serious concern in traditional cancer treatment. Ferroptosis is an iron- and oxidative-dependent form of regulated cell death that has become part of an emerging strategy for chemotherapy. However, the key regulator of ferroptosis in bone marrow injury remains unknown. Here, we show that Fanconi anemia complementation group D2 (FANCD2), a nuclear protein involved in DNA damage repair, protects against ferroptosis-mediated injury in bone marrow stromal cells (BMSCs). The classical ferroptosis inducer erastin remarkably increased the levels of monoubiquitinated FANCD2, which in turn limited DNA damage in BMSCs. FANCD2-deficient BMSCs were more sensitive to erastin-induced ferroptosis (but not autophagy) than FANCD2 wild-type cells. Knockout of FANCD2 increased ferroptosis-associated biochemical events (e.g., ferrous iron accumulation, glutathione depletion, and malondialdehyde production). Mechanically, FANCD2 regulated genes and/or expression of proteins involved in iron metabolism (e.g., FfH1, TF, TFRC, HAMP, HSPB1, SLC40A1, and STEAP3) and lipid per oxidation (e.g., GPX4). Collectively, these findings indicate that FANCD2 plays a novel role in the negative regulation of ferroptosis. FANCD2 could represent an amenable target for the development of novel anticancer therapies aiming to reduce the side effects of ferroptosis inducers. (C) 2016 Elsevier Inc. All rights reserved.