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Fucosyltransferase 11 Inhibits Ferroptosis in Gastric Cancer
- The study explores the role of Fucosyltransferase 11 (FUT11) in regulating ferroptosis in gastric cancer by modulating the antioxidative enzyme GPX4.
- Ferroptosis, an iron-dependent cell death pathway, plays a crucial role in cancer cell proliferation and survival, with FUT11 identified as a key player in gastric cancer progression.
- FUT11 overexpression in gastric cancer cells correlates with advanced disease stage and poor patient outcomes, making it a potential biomarker for aggressive gastric cancer.
- Knockdown of FUT11 led to decreased cell proliferation in gastric cancer cell lines, highlighting its role in sustaining tumor growth.
- FUT11 inhibition resulted in reduced GPX4 levels, a defender against ferroptosis, leading to increased lipid peroxidation and ferroptotic cell death in gastric cancer cells.
- Overexpressing GPX4 in FUT11-deficient cells rescued cells from ferroptosis, demonstrating the link between FUT11, GPX4 expression, and ferroptotic pathways.
- In mouse xenograft models, FUT11 knockdown impaired tumor growth, whereas GPX4 overexpression counteracted this effect, underscoring the therapeutic potential of targeting this pathway.
- The study highlights FUT11 as a promising target to sensitize gastric cancer cells to ferroptosis, offering new avenues for cancer treatment beyond conventional therapies.
- Inhibiting FUT11 or modulating its downstream effectors could potentially overcome therapeutic resistance in advanced gastric tumors through ferroptotic cell death induction.
- The research underscores the intricate interplay between glycosylation enzymes like FUT11, ferroptosis regulation, and cancer cell survival, paving the way for innovative therapeutic strategies.
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