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GENE:
MOCS2 (Molybdenum Cofactor Synthesis 2)
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Other names: MOCS2, Molybdenum Cofactor Synthesis 2, MOCO1, Molybdopterin Synthase Catalytic Subunit, MOCS2A, MOCS2B, Molybdopterin Synthase Sulfur Carrier Subunit, MCBPE, Molybdenum Cofactor Synthesis Protein 2 Small Subunit, Molybdenum Cofactor Synthesis Protein 2 Large Subunit, Molybdenum Cofactor Biosynthesis Protein E, Molybdenum Cofactor Synthesis Protein 2A, Molybdenum Cofactor Synthesis Protein 2B, Molybdopterin Synthase Large Subunit, Molybdopterin Synthase Small Subunit, Molybdopterin-Synthase Small Subunit, Molybdopterin-Synthase Large Subunit, Sulfur Carrier Protein MOCS2A, MPT Synthase Large Subunit, MOCO1-A, MOCO1-B, MOCODB, MPTS
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Our study established a robust metabolism-based prognostic model for SCLC that effectively stratifies patients into risk groups with distinct survival outcomes, immune profiles, and drug sensitivity patterns. Functional validation experiments confirmed MOCS2 as an important regulator of SCLC cell proliferation and migration, providing valuable insights for treatment selection and prognosis prediction in SCLC.
9 months ago
Journal
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MOCS2 (Molybdenum Cofactor Synthesis 2) • SMYD2 (SET And MYND Domain Containing 2)
When combined with high-throughput drug sensitivity testing, UAMOCS can accurately predict sensitivity to azacitidine (AZA) and venetoclax. The UAMOCS system is available as an R package. The UAMOCS system has the potential to redefine AML subtypes, enhance prognostic predictions, and guide treatment strategies based on patients' immune status and expected responses to therapies.
These data suggest that many of the miR-365 targets are expressed in the oral cancers screened, with the differential expression of UBR3, ZCCHC14, HOMEZ, and NUDT12, which may be correlated with chemoresistance among two specific oral cancer cell lines (SCC25, SCC9). These results suggest this differential expression may signal potential targets for patient treatment with tumors exhibiting miR-365 and chemotherapeutic resistance.
MOCS classification could stably predict prognosis of SKCM; patients with a high cancer stemness index combined with genomic instability may be predisposed to an immune exhaustion state.Communicated by Ramaswamy H. Sarma.
Receptor tyrosine kinase signaling inhibitors (SB505124 and EphB4) might be sensitive to UAMOCS1. Taken together, UAMOCS model was generated that can classify AML patients independently and help develop precise chemotherapeutic strategy for patients with AML in the future.