Rabbit Anti-Human SLC7A11 Polyclonal antibody

Objective: Pancreatic carcinoma (PANC) is one of the important aggressive cancers, with deficiency in effective therapeutics. The study aimed to investigate the effects and molecular mechanism of miR-139-5p/SLC7A11 on the proliferation and metastasis of PANC. Methods: Bioinformatics was used to analyze the differentially expressed genes in the TCGA database. PANC cell lines with overexpressed miR-139-5p and Solute Carrier Family 7, Member 11 (SLC7A11) was established, and have been used to detect cell proliferation, invasion and metastasis of PANC Subsequently, bioinformatic analysis and dual luciferase reporter assay were performed to confirm that SLC7A11 was a target gene of miR-1395p. Xenograft mice model was used to explore the functions of miR-139-5p in PANC tumorigenicity. Results: MiR-139-5p could regulate and affect the protein expression of P13K and Akt associated with phosphatidylinositol signaling pathway by inhibiting SLC7A11. MiR-139-5p was found to be lowly expressed in PANC tissues, while SLC7A11 was highly expressed. Low expression of miR-139-5p and high expression of SLC7A11 were positively associated with poor clinical outcomes. PANC cell proliferation, invasion and metastasis could be inhibited by miR-139-5p overexpression and be promoted by SLC7A11 overexpression. MiR-1395p overexpression could suppress PANC tumor growth and the expressions of SLC7A11, p-PI3K, p-Akt in tumor tissues. Therefore, the inhibitory of miR-139-5p to PANC cell proliferation, invasion and metastasis was partly due to its inhibiting effect on SLC7A11 expression. Conclusion: Our study proves that miR-139-5p/SLC7A11 has important functions on PANC, suggesting that miR139-5p can be used as a biomarker for PANC patients.

Ferroptosis, a form of iron-dependent, nonapoptotic cell death that is induced by excessive lipid peroxidation, has been recently identified as a new tumor suppression mechanism. In this issue of Cancer Research, Liu and colleagues demonstrate that the deubiquitinase (DUB) OTUB1 is frequently overexpressed in human cancers, and functions to "dub" (trim) the ferroptosis process in cancer cells and promotes tumor development by stabilizing the cystine transporter, SLC7A11. This study not only reveals a hitherto unappreciated regulatory mechanism of ferroptosis but also identifies potential therapeutic targets for cancer treatment.