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    GENE:

    SKP2 (S-phase kinase-associated protein 2)

    i
    Other names: SKP2, S-phase kinase-associated protein 2, F-Box/LRR-Repeat Protein 1, P45skp2, FBXL1, CDK2/Cyclin A-Associated Protein P45, Cyclin-A/CDK2-Associated Protein P45, FBL1
    Associations

    News

    Trials
    13d
    Natural Product-Inspired PROTACs for Leukemia Therapy: Hederagenin-Driven Targeted Degradation of SKP2. (PubMed, J Med Chem)
    Mechanistically, HD15 effectively degraded SKP2 (DC50 = 0.29 μM), stabilizing SOCS1 expression and modulating immunoproteasome expression via the JAK/STAT pathway, thereby suppressing tumor cell proliferation. The discovery of HD15 demonstrates the promise of PROTAC technology in enhancing the efficacy of natural products and identifying therapeutic targets, offering a novel strategy for developing therapeutics from natural products.
    Journal
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    SOCS1 (Suppressor Of Cytokine Signaling 1) • SKP2 (S-phase kinase-associated protein 2)
    14d
    ECRG4 suppressed the progression of breast cancer via modulating NFIC/PTEN and SHP2/PI3K/SP1 signaling. (PubMed, Eur J Med Res)
    ECRG4 inhibits breast cancer progression by positively regulating NFIC/PTEN to suppress the SHP2/PI3K/SP1 signaling pathway. Targeting this signaling axis may provide a new strategy for breast cancer treatment.
    Journal
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    PTEN (Phosphatase and tensin homolog) • DNMT1 (DNA methyltransferase 1) • NFIC (Nuclear Factor I C) • SKP2 (S-phase kinase-associated protein 2) • SP1 (Sp1 Transcription Factor)
    17d
    The ubiquitination-autophagy axis in cancer therapy resistance: mechanistic insights and therapeutic opportunities. (PubMed, Front Pharmacol)
    Finally, we discuss potential therapeutic strategies, including Proteolysis Targeting Chimeras (PROTACs), dual E3 ligase/autophagy inhibitors, and autophagy flux modulators, to overcome resistance and enhance treatment efficacy across multiple cancer types. These insights establish the foundation for targeting the ubiquitin-autophagy network as a cohesive strategy to combat refractory cancer.
    Review • Journal
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    ATG7 (Autophagy Related 7) • IL17RB (Interleukin 17 Receptor B) • MIR138 (MicroRNA 138) • SKP2 (S-phase kinase-associated protein 2) • USP1 (Ubiquitin Specific Peptidase 1) • USP14 (Ubiquitin Specific Peptidase 14)
    19d
    Discovery of SKP2-Recruiting PROTACs for Target Protein Degradation. (PubMed, Adv Sci (Weinh))
    We designed and synthesized SKP2-recruiting degraders by linking SL1 to the BRD4 inhibitor JQ1...We further demonstrate that SKP2-directed PROTACs effectively degrade Androgen receptor (AR) in 22RV1 cells. These findings emphasize that SKP2, frequently overexpressed in various tumor cells, can be successfully exploited for TPD through non-covalent PROTACs, expanding the pool of E3 ligases available for potential therapeutic applications.
    Journal
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    AR (Androgen receptor) • BRD4 (Bromodomain Containing 4) • SKP2 (S-phase kinase-associated protein 2)
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    JQ-1
    1m
    The Establishment of Prostate-specific, SKP2 Humanized Mice by CRISPR Knock-in Method Reveals Neoplastic Initiation and Microenvironmental Reprogramming. (PubMed, Res Sq)
    Both of which selectively decreased viability and altered the morphologies of organoids of hSKP2 knock-in rather than wild-type mice. Our studies provide a well-characterized prostate-specific hSKP2 knock-in mouse model and offer new mechanistic insights for understanding the oncogenic role of SKP2 in shaping the prostatic microenvironment during early carcinogenesis.
    Preclinical • Journal
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    CD8 (cluster of differentiation 8) • SKP2 (S-phase kinase-associated protein 2)
    1m
    Exploring the characteristics of the SKP2-CDK6 axis in pancreatic cancer cell metastasis and its clinical significance. (PubMed, Exp Mol Pathol)
    The SKP2-CDK6 axis may drive PDAC progression and chemoresistance. Co-targeting SKP2 and CDK6 in combination with gemcitabine may represent a promising therapeutic approach, warranting further preclinical and clinical evaluation to improve outcomes for patients with PDAC.
    Journal
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    CDK6 (Cyclin-dependent kinase 6) • SKP2 (S-phase kinase-associated protein 2)
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    gemcitabine
    2ms
    Targeting FOXM1 regulates metabolic signatures through ROS-dependent JNK/Bmi1/Skp2 axis in human cutaneous T-cell lymphoma. (PubMed, Cell Death Dis)
    Moreover, thiostrepton treatment sensitized the CTCL cells to proteasome inhibitor bortezomib, promoting apoptosis and autophagy. Collectively, these findings demonstrate that FOXM1 targeting disrupts the metabolic status and stemness features of CTCL cells via JNK activation, thereby offering novel insights into potential therapeutic strategies for overcoming therapeutic challenges in CTCL.
    Journal
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    KLF4 (Kruppel-like factor 4) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • FOXM1 (Forkhead Box M1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • SKP2 (S-phase kinase-associated protein 2)
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    bortezomib • thiostrepton (RSO-021)
    2ms
    Guaianolide dimer KGA-1002 targets GRP94 and triggers unfolded protein response-associated degradation of SKP2/AKT axis as a novel antihepatoma agent. (PubMed, J Adv Res)
    KGA-1002 was identified as a highly promising lead compound for antiHCC. Its mechanism involved triggering UPR-associated degradation and disrupting the GRP94-AKT interaction. KGA-1002 simultaneously induced apoptosis and ferroptosis in HCC cells through the GRP94/AKT/SKP2/P21 signaling axis.
    Journal
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    CDKN1A (Cyclin-dependent kinase inhibitor 1A) • SKP2 (S-phase kinase-associated protein 2)
    2ms
    Network toxicology and Mendelian randomization reveal pathogenic factors of monoethyl phthalate-induced thyroid cancer. (PubMed, Eur Thyroid J)
    Molecular docking simulations suggested potential direct interactions between monoethyl phthalate and their protein products. Our findings propose 10 genes as potential mediators of monoethyl phthalate-induced thyroid cancer, with ESR1, SKP2, CASP8, ARNT, and CDKN1B highlighted as core factors potentially involved in thyroid cancer pathogenesis.
    Journal
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    ER (Estrogen receptor) • CASP8 (Caspase 8) • CDKN1B (Cyclin dependent kinase inhibitor 1B) • SKP2 (S-phase kinase-associated protein 2)
    2ms
    DDX11/SKP2 Inhibits Cisplatin Sensitivity in Liver Cancer Cells by Regulating DNA Damage Repair and ER Stress. (PubMed, Appl Biochem Biotechnol)
    Mechanistically, DDX11 inhibited cisplatin-induced DNA damage and ER stress by upregulating SKP2 expression, ultimately reducing the sensitivity of HCC cells to cisplatin. This study revealed that the DDX11/SKP2 axis may be a promising therapeutic target for improving resistance to cisplatin in patients with HCC.
    Journal
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    SKP2 (S-phase kinase-associated protein 2)
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    cisplatin
    2ms
    Network-based insights into miR-30a-5p-mediated regulation and EGCG targeting in triple-negative breast cancer. (PubMed, Front Bioinform)
    The results emphasizes that EGCG has strong binding affinity towards YWHAZ, revealing that miR-30a-EGCG targets TNBC synergistically through cell-cycle-mediated pathways. The findings give rational support for miRNA-guided phytochemical-based TNBC therapeutic development.
    Journal
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    HER-2 (Human epidermal growth factor receptor 2) • PGR (Progesterone receptor) • PCNA (Proliferating cell nuclear antigen) • RRM2 (Ribonucleotide Reductase Regulatory Subunit M2) • CDC20 (Cell Division Cycle 20) • KIF11 (Kinesin Family Member 11) • ANLN (Anillin Actin Binding Protein) • CCNA1 (Cyclin A1) • MIR30A (MicroRNA 30a) • SKP2 (S-phase kinase-associated protein 2) • YWHAZ (Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Zeta)
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    HER-2 expression
    3ms
    Fascin Drives Breast Cancer Cell Proliferation Partly by Modulating the Cell Cycle Checkpoint Regulators of the G1-S Phase. (PubMed, Cells)
    Immunohistochemistry in samples from 68 patients demonstrated significant correlations between fascin and Ki-67 expression, in addition to SKP2 overexpression and p27 downregulation. Collectively, these data demonstrate the role of fascin as a driver of the G1-S-phase transition during cell cycle proliferation, thereby revealing new opportunities for targeted therapeutic intervention.
    Journal
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    FAS (Fas cell surface death receptor) • FSCN1 (Fascin Actin-Bundling Protein 1) • SKP2 (S-phase kinase-associated protein 2)