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Showing CKS1B — CKS1 is a alias.

CKS1B

Cyclin-dependent kinases regulatory subunit 1 · UniProt P61024

Length
79 aa
Mass
9.7 kDa
Annotated
2026-06-09
40 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CKS1B is a small CDK regulatory subunit that couples cyclin-dependent kinase complexes to phosphoprotein substrates and to SCF-mediated proteolysis, functioning as a hub for cell-cycle control and proliferative signaling (PMID:8601310, PMID:17303695). Structurally it is a single compact domain with a four-stranded beta-sheet flanked by two helices, presenting an anion/phosphate-binding pocket (Lys11, Arg20, Ser51, Trp54, Arg71) and a beta-hinge region whose opening generates a domain-swapped dimer; in the monomeric state it docks via all four beta-strands onto the CDK2 C-terminal lobe—away from the cyclin and regulatory phosphorylation sites—simultaneously exposing the CDK2 ATP site and its own phosphate pocket, positioning the kinase toward phosphorylated substrates (PMID:7791211, PMID:8601310). CKS1B is a required cofactor for SCF(SKP2)-driven ubiquitination and degradation of the CDK inhibitor p27Kip1: its depletion stabilizes p27Kip1 and arrests proliferation, while its interaction with SKP2 also reciprocally modulates CKS1B availability to CDK2 (PMID:11349131, PMID:16188652). Beyond the canonical SKP2/p27 axis, CKS1B sustains tumor-cell survival, proliferation, and drug resistance through STAT3 and MEK/ERK signaling with BCL2 as a downstream effector, and SCF-coupled degradation of IRF3 suppresses type I interferon signaling and antigen presentation, promoting CD8+ T-cell exhaustion (PMID:17303695, PMID:20930946, PMID:42090485). CKS1B expression is controlled transcriptionally by GLI2 within HH signaling and by FOXM1, and its overexpression establishes a synthetic-dosage-lethal dependence on PLK1 conserved from yeast to human cancer cells (PMID:27558135, PMID:38761090).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1995 High

    Established the atomic architecture of human CKS1B, defining a phosphate-binding pocket and a conformational beta-hinge switch that would underlie its substrate-targeting and oligomerization behavior.

    Evidence X-ray crystallography of CksHs1 at 2.9 Å with conserved-residue identification

    PMID:7791211

    Open questions at the time
    • Did not show binding to any physiological phosphoprotein
    • Functional role of the phosphate pocket inferred, not demonstrated
  2. 1996 High

    Resolved how CKS1B engages CDK2, showing a beta-strand interface on the CDK2 C-terminal lobe that leaves the kinase active site free, supporting a model in which CKS1B targets CDK2 to phosphoproteins.

    Evidence X-ray crystallography of the CDK2–CksHs1 complex at 2.6 Å with site-directed mutagenesis of the interface

    PMID:8601310

    Open questions at the time
    • Specific phosphoprotein substrates engaged via the exposed pocket not identified
    • No cyclin present in the structure
  3. 1995 Medium

    Placed CKS1B downstream of TGF-beta receptor signaling, linking its transcriptional regulation to growth arrest.

    Evidence Northern blot after TGF-beta treatment plus a dominant-negative TGF-beta type 2 receptor cell line

    PMID:8845303

    Open questions at the time
    • Mechanism connecting CKS1B downregulation to arrest not defined
    • No direct transcriptional regulator identified
  4. 2001 Medium

    Showed that SKP2 directly binds CKS1B and competes with its CDK2 interaction, revealing a regulatory partition of CKS1B between CDK2 inhibition and SCF engagement.

    Evidence Co-immunoprecipitation, CDK2 kinase assays, and overexpression in cells

    PMID:11349131

    Open questions at the time
    • Single-lab biochemistry without structural mapping of the SKP2-CKS1B interface
    • Physiological balance between the two states not quantified
  5. 2002 Medium

    Characterized the marginal thermodynamic and kinetic stability of CKS1B and linked refolding to transient domain-swapped oligomerization.

    Evidence Equilibrium denaturation and folding/unfolding kinetics in vitro

    PMID:11802719

    Open questions at the time
    • Biological relevance of the dimer in cells unresolved
    • No connection to in-cell CDK2 or SKP2 binding
  6. 2007 High

    Demonstrated that CKS1B drives myeloma survival through both SKP2/p27Kip1-dependent and -independent routes, expanding its role beyond the canonical degradation pathway.

    Evidence Lentiviral shRNA, SKP2 knockdown, non-degradable p27T187A expression, and a p27-null cell line with apoptosis/cell-cycle readouts

    PMID:16188652 PMID:17303695

    Open questions at the time
    • Identity of the p27-independent survival mechanism not defined here
    • Restricted to myeloma models
  7. 2010 Medium

    Connected CKS1B to STAT3 and MEK/ERK/BCL2 signaling as a driver of proliferation and multidrug resistance, providing a candidate non-canonical effector arm.

    Evidence Overexpression, shRNA, pathway inhibitors, and viability rescue in myeloma cells

    PMID:20930946

    Open questions at the time
    • Direct molecular link between CKS1B and pathway activation not established
    • Single lineage context
  8. 2016 High

    Identified a conserved synthetic-dosage-lethal dependency: CKS1B overexpression sensitizes cells to loss of PLK1 activity, defining a targetable vulnerability.

    Evidence Yeast SDL screen with Swe1/Sic1 epistasis plus PLK1 shRNA and pharmacological inhibition in human cancer cell lines

    PMID:27558135

    Open questions at the time
    • Molecular basis of the CKS1B-PLK1 lethal interaction not resolved
    • Yeast-to-human mechanistic conservation inferred from phenotype
  9. 2024 Medium

    Placed CKS1B transcriptionally downstream of HH-GLI2 signaling controlling a proliferation-to-maturation switch, extending its role beyond cancer.

    Evidence GLI2 promoter-binding assay and CKS1B overexpression in hiPSC-cardiomyocytes with maturation and calcium readouts

    PMID:38761090

    Open questions at the time
    • Downstream effectors in cardiomyocytes not mapped
    • Single developmental model
  10. 2025 Medium

    Revealed an immune-evasion function in which the CKS1B-SKP1/SKP2 complex ubiquitinates and degrades IRF3 to suppress type I interferon signaling and drive CD8+ T-cell exhaustion, with pharmacological disruption restoring immunity.

    Evidence Spatial/single-cell proteomics, Co-IP of the CKS1B-SKP complex with IRF3, ubiquitination assay, compound 14i blockade, and checkpoint-blockade combination in vivo

    PMID:42090485

    Open questions at the time
    • Whether IRF3 is a direct SCF(SKP2) substrate via CKS1B docking not structurally shown
    • Single study

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CKS1B partitions between its CDK2-targeting, SCF-adaptor, and signaling functions to selectively destabilize specific substrates (p27Kip1, IRF3) in different tissue contexts remains unresolved.
  • No structure of CKS1B within an SCF(SKP2)-substrate complex
  • Determinants of substrate selectivity unknown
  • Direct versus indirect basis of STAT3/MEK-ERK/PI3K-AKT engagement not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 3 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2
Pathway
R-HSA-392499 Metabolism of proteins 3 R-HSA-162582 Signal Transduction 2 R-HSA-1640170 Cell Cycle 2 R-HSA-168256 Immune System 1
Partners
CDK2SKP1SKP2
Complex memberships
SCF(SKP2)

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 Crystal structure of human CksHs1 determined at 2.9 Å resolution, revealing a single polypeptide domain fold with a four-stranded beta-sheet flanked by two alpha-helices, and identifying a phosphate-binding pocket with conserved residues Lys11, Arg20, Ser51, Trp54, and Arg71 as a potential recognition site for phosphorylated CDK residues. A novel beta-hinge region (Glu61–His65) was identified that controls monomer versus domain-swapped dimer conformation. X-ray crystallography at 2.9 Å resolution Journal of molecular biology High 7791211
1996 Crystal structure of human CDK2 in complex with CksHs1 at 2.6 Å resolution revealed that CksHs1 binds via all four beta-strands to the CDK2 C-terminal lobe, far from the N-terminal lobe, cyclin, and regulatory phosphorylation sites. Mutational analysis confirmed this interface is biologically critical. The beta-hinge opening to form the domain-swapped dimer sterically precludes CDK2 binding. The complex exposes the phosphate-binding region of Cks and the ATP-binding site of CDK2 on one face, suggesting CKS1B targets CDK2 to phosphoproteins. X-ray crystallography at 2.6 Å + site-directed mutagenesis Cell High 8601310
1995 TGF-beta treatment strongly downregulates CKShs1 transcripts in mink lung cells and keratinocytes within 10 hours (prior to growth arrest), and this downregulation is abolished in cells expressing a dominant-negative TGF-beta type 2 receptor. This places CKShs1 downstream of TGF-beta receptor signaling and suggests a role in TGF-beta-mediated G1/G2 cell cycle arrest. Northern blot analysis; genetic test using stably transfected dominant-negative TGF-beta receptor cell line Cell growth & differentiation Medium 8845303
2001 The carboxyl-terminal region of p45(SKP2) directly associates with CksHs1, and this interaction negatively regulates the binding of CksHs1 to CDK2. Overexpression of CksHs1 inhibits CDK2 kinase activity, and additional expression of p45(SKP2) overcomes this inhibition and restores CDK2 kinase activity. The proposed mechanism is that SKP2 sequesters CksHs1, preventing it from binding and inhibiting CDK2. Co-immunoprecipitation, CDK2 kinase activity assay, overexpression experiments The Journal of biological chemistry Medium 11349131
2002 CksHs1 has marginal thermodynamic stability (ΔG ~3.0 kcal/mol at 25°C) and low kinetic stability (unfolding rate ~1 s⁻¹ in water). Refolding from denatured states to monomeric form is slowed by transient oligomerization via domain swapping. Interconversion between monomer and domain-swapped dimer requires unfolding and is faster in CksHs1 than in yeast suc1, reflecting faster unfolding rates. Biochemical folding/unfolding kinetics assays, equilibrium denaturation Biochemistry Medium 11802719
2005 RNA interference knockdown of CKS1B mRNA in myeloma cell lines led to reduced CKS1B protein, accumulation of p27Kip1, and profound growth inhibition, establishing that CKS1B regulates SCF(Skp2)-mediated ubiquitination and proteolysis of p27Kip1 in myeloma cells. RNAi knockdown; Western blot for p27Kip1; cell proliferation assay Hematology Medium 16188652
2007 Lentiviral shRNA knockdown of CKS1B in multiple myeloma cell lines caused stabilization of p27Kip1, cell cycle arrest, and apoptosis. Notably, CKS1B ablation induced strong apoptosis even in a cell line with biallelic deletion of p27Kip1 (CDKN1B), demonstrating that CKS1B regulates myeloma cell survival through both SKP2/p27Kip1-dependent and independent mechanisms. Lentiviral shRNA knockdown; cell cycle analysis; apoptosis assay; forced expression of non-degradable p27T187A; SKP2 knockdown Blood High 17303695
2010 Forced expression of CKS1B in multiple myeloma cells activated STAT3 and MEK/ERK signaling pathways and increased multidrug resistance. Stimulation of these pathways partially rescued cells from CKS1B-knockdown-induced death, and BCL2 was identified as a downstream target of MEK/ERK signaling in this context. Forced overexpression; shRNA knockdown; pathway inhibitors; Western blot; cell viability assay Oncotarget Medium 20930946
2015 CKS1B mechanistically connects to a miR-197/CKS1B/STAT3 axis regulating PD-L1 expression and chemoresistance in NSCLC. miR-197 targets CKS1B, and loss of miR-197 leads to CKS1B upregulation driving STAT3-mediated expression of oncogenic genes (Bcl-2, c-Myc, cyclin D1) and PD-L1. miR-197 mimic sensitized PD-L1-high drug-resistant cells to chemotherapy. In vitro and in vivo functional assays; miR-197 mimic transfection; mechanistic pathway analysis Molecular therapy Medium 25597412
2015 CKS1B-overexpressing myeloma cells are resistant to the proteasome inhibitor bortezomib but sensitive to the NEDD8 inhibitor MLN4924. MLN4924 induced stabilization of p21 (not p27), and shRNA knockdown of p21 abolished MLN4924 sensitivity, establishing that MLN4924 overcomes CKS1B-induced drug resistance via p21 stabilization rather than p27. shRNA knockdown of p21; proliferation, viability, clonogenic, and senescence assays; immunoblot analysis Clinical cancer research Medium 26156395
2016 Genetic epistasis in yeast showed that CKS1 overexpression synthetic dosage lethality (SDL) with mitotic entry checkpoint genes requires Swe1 inhibitory activity on CDK Cdc28, and SDL with mitotic exit network genes is suppressed by modulating CDK inhibitor Sic1. Mutation of polo-like kinase Cdc5 (human PLK1 ortholog) is lethal with overexpressed CKS1. In human cancer cells, CKS1B overexpression increased sensitivity to PLK1 knockdown and pharmacological PLK1 inhibition, conserving the yeast SDL interaction. High-throughput yeast SDL screen; epistasis with Swe1 and Sic1 mutants; shRNA knockdown of PLK1 in human tumor cell lines; PLK1 inhibitor treatment of CKS1B-overexpressing cells; WEE1+PLK1 double inhibition epistasis Genetics High 27558135
2017 Ectopic CKS1B overexpression in lung cancer cells induced chemoresistance to cisplatin and doxorubicin through Hsp90 and MEK1/2 pathways, independent of the canonical Skp2-p27 pathway. Inhibition of either Hsp90 or MEK1/2 alone resensitized CKS1B-overexpressing cells to chemotherapy, and 3-COA was identified as a novel Hsp90 inhibitor that mimics this resensitization. shRNA knockdown; selective pathway inhibitors (Hsp90, MEK1/2); in vitro and in vivo tumor models; overexpression of CKS1B Biochemical pharmacology Medium 28288818
2024 GLI2 directly binds the CKS1B promoter to regulate CKS1B transcription in cardiomyocytes (CMs). CKS1B overexpression in late-stage hiPSC-CMs promoted proliferation with loss of maturation, identifying CKS1B as a downstream effector of the HH-GLI2 signaling cascade that controls the proliferation-to-maturation transition in CMs. GLI2 promoter binding assay (ChIP-type); hiPSC-CM overexpression of CKS1B; maturation indices; calcium handling measurements; transcriptomic analysis Stem cells translational medicine Medium 38761090
2021 CKS1B knockdown in hepatocellular carcinoma (HCC) cell lines inhibited proliferation, induced apoptosis, suppressed migration and invasion, and decreased p-STAT3 levels and STAT3 target genes (TIMP-1, Bcl-2, VEGF). Overexpression of CKS1B had opposite effects, establishing CKS1B promotion of HCC progression via JAK/STAT3 pathway activation. shRNA knockdown; overexpression plasmid; MTT, colony formation, flow cytometry, wound healing, transwell assays; Western blot for p-STAT3 and targets Animal cells and systems Medium 34408811
2025 CKS1B forms a complex with S-phase kinase-associated protein (SKP1/SKP2) to promote ubiquitination and degradation of IRF3 (interferon regulatory factor 3), thereby suppressing type I interferon signaling and antigen presentation in tumor cells. This drives persistent CD8+ T cell stimulation and exhaustion. Pharmacological blockade of the CKS1B-IRF3 interaction with compound 14i restored CD8+ T cell function and synergized with immune checkpoint blockade. Single-cell and spatial proteomics; co-immunoprecipitation (CKS1B-SKP complex with IRF3); ubiquitination assay; pharmacological blockade with 14i; in vivo tumor models; immune checkpoint blockade combination Science advances Medium 42090485
2025 FOXM1 transcriptionally regulates CKS1B expression in pancreatic ductal adenocarcinoma (PDAC), establishing a novel FOXM1-CKS1B signaling axis. CKS1B knockdown sensitized PDAC cells to gemcitabine and oxaliplatin and reduced cancer stemness properties. Molecular biology methods (chromatin binding/promoter assays implied); in vitro and in vivo PDAC models; CKS1B knockdown with chemosensitivity assays; stemness assays International journal of biological sciences Low 39897042
2020 CKS1B knockdown in papillary thyroid carcinoma (PTC) cells inhibited cell viability and invasion, suppressed STAT3/PD-L1 signaling, and reduced Akt phosphorylation. STAT3 or PD-L1 inhibition reversed the pro-tumorigenic effects of CKS1B overexpression. siRNA knockdown; overexpression plasmid; MTT and transwell assays; Western blot for p-STAT3, p-Akt, PD-L1; pharmacological inhibitors (WP1066, Pembrolizumab) Journal of clinical laboratory analysis Low 32960462
2025 CKS1B knockdown in NSCLC cells inhibited proliferation, migration, and invasion; reduced MEK and ERK phosphorylation (MAPK/ERK signaling); and upregulated E-cadherin while downregulating N-cadherin, suppressing EMT. siRNA knockdown; Western blot for p-MEK, p-ERK, E-cadherin, N-cadherin; proliferation and invasion assays Discover oncology Low 41171587
2025 CKS1B knockdown in NSCLC cells and xenografts enhanced radiosensitivity by stimulating apoptosis, inhibiting cell cycle progression, and impairing DNA damage repair. CKS1B-induced radioresistance was mediated through the PI3K/AKT signaling pathway. shRNA knockdown; xenograft model with ionizing radiation; apoptosis, cell cycle, DNA damage repair assays; Western blot for PI3K/AKT pathway components Cellular signalling Low 40262716

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 The clinical relevance of the miR-197/CKS1B/STAT3-mediated PD-L1 network in chemoresistant non-small-cell lung cancer. Molecular therapy : the journal of the American Society of Gene Therapy 222 25597412
1996 Crystal structure and mutational analysis of the human CDK2 kinase complex with cell cycle-regulatory protein CksHs1. Cell 215 8601310
2007 CKS1B, overexpressed in aggressive disease, regulates multiple myeloma growth and survival through SKP2- and p27Kip1-dependent and -independent mechanisms. Blood 140 17303695
2005 Amplification and overexpression of CKS1B at chromosome band 1q21 is associated with reduced levels of p27Kip1 and an aggressive clinical course in multiple myeloma. Hematology (Amsterdam, Netherlands) 125 16188652
2010 Over-expression of CKS1B activates both MEK/ERK and JAK/STAT3 signaling pathways and promotes myeloma cell drug-resistance. Oncotarget 101 20930946
1995 Crystal structure of the human cell cycle protein CksHs1: single domain fold with similarity to kinase N-lobe domain. Journal of molecular biology 67 7791211
2017 Integrated MicroRNA-mRNA Analysis Reveals miR-204 Inhibits Cell Proliferation in Gastric Cancer by Targeting CKS1B, CXCL1 and GPRC5A. International journal of molecular sciences 42 29283424
2015 NEDD8 Inhibition Overcomes CKS1B-Induced Drug Resistance by Upregulation of p21 in Multiple Myeloma. Clinical cancer research : an official journal of the American Association for Cancer Research 40 26156395
2020 Circular RNA NOX4 promotes the development of colorectal cancer via the microRNA‑485‑5p/CKS1B axis. Oncology reports 34 32901890
2019 MicroRNA-1258 Inhibits the Proliferation and Migration of Human Colorectal Cancer Cells through Suppressing CKS1B Expression. Genes 30 31717435
2016 A Synthetic Dosage Lethal Genetic Interaction Between CKS1B and PLK1 Is Conserved in Yeast and Human Cancer Cells. Genetics 30 27558135
2016 Outcome of Patients with Multiple Myeloma and CKS1B Gene Amplification after Autologous Hematopoietic Stem Cell Transplantation. Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation 29 27638366
2020 CKS1B as Drug Resistance-Inducing Gene-A Potential Target to Improve Cancer Therapy. Frontiers in oncology 28 33102238
2019 Downregulation of CKS1B restrains the proliferation, migration, invasion and angiogenesis of retinoblastoma cells through the MEK/ERK signaling pathway. International journal of molecular medicine 28 31115482
2006 Significant increase of CKS1B amplification from monoclonal gammopathy of undetermined significance to multiple myeloma and plasma cell leukaemia as demonstrated by interphase fluorescence in situ hybridisation. British journal of haematology 28 16889615
2010 CKS1B nuclear expression is inversely correlated with p27Kip1 expression and is predictive of an adverse survival in patients with multiple myeloma. Haematologica 26 20421271
2002 Folding and association of the human cell cycle regulatory proteins ckshs1 and ckshs2. Biochemistry 23 11802719
2017 3-O-(Z)-coumaroyloleanolic acid overcomes Cks1b-induced chemoresistance in lung cancer by inhibiting Hsp90 and MEK pathways. Biochemical pharmacology 22 28288818
1995 Transforming growth factor beta down-regulation of CKShs1 transcripts in growth-inhibited epithelial cells. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 17 8845303
2011 CDC28 protein kinase regulatory subunit 1B (CKS1B) expression and genetic status analysis in oral squamous cell carcinoma. Histology and histopathology 16 21117028
2020 CKS1B promotes cell proliferation and invasion by activating STAT3/PD-L1 and phosphorylation of Akt signaling in papillary thyroid carcinoma. Journal of clinical laboratory analysis 14 32960462
2023 Involvement of CKS1B in the anti-inflammatory effects of cannabidiol in experimental stroke models. Experimental neurology 13 38104887
2020 The survival impact of CKS1B gains or amplification is dependent on the background karyotype and TP53 deletion status in patients with myeloma. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 13 32908255
2022 Regulation of microRNA miR-197-3p/CDC28 protein kinase regulatory subunit 1B (CKS1B) axis by Circular RNA hsa_circ_0000285 promotes glioma progression. Bioengineered 12 35174774
2017 CKS1BP7, a Pseudogene of CKS1B, is Co-Amplified with IGF1R in Breast Cancers. Pathology oncology research : POR 12 28439706
2021 CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway. Animal cells and systems 11 34408811
2010 CKS1B amplification is a frequent event in cutaneous squamous cell carcinoma with aggressive clinical behaviour. Genes, chromosomes & cancer 11 20737481
2010 Differential expression of CKS-1B in typical and blastoid variants of mantle cell lymphoma. Human pathology 10 20688354
2001 Association of the cell cycle regulatory proteins p45(SKP2) and CksHs1. Functional effect on CDK2 complex formation and kinase activity. The Journal of biological chemistry 10 11349131
2021 Knockdown of LINC00657 inhibits the viability, migration and invasion of pancreatic cancer cells by regulating the miR-520h/CKS1B axis. Experimental and therapeutic medicine 9 34504588
2014 Quantitative analysis of CKS1B mRNA expression and copy number gain in patients with plasma cell disorders. Blood cells, molecules & diseases 9 24973170
1995 Crystallization and preliminary crystallographic study of human CksHs1: a cell cycle regulatory protein. Proteins 8 7716171
2024 The HH-GLI2-CKS1B network regulates the proliferation-to-maturation transition of cardiomyocytes. Stem cells translational medicine 6 38761090
2025 FOXM1-Driven CKS1B Upregulation Promotes Pancreatic Cancer Progression and Therapeutic Resistance. International journal of biological sciences 3 39897042
2025 CKS1B regulates the radiosensitivity of lung cancer via activating the PI3K/AKT signaling pathway. Cellular signalling 2 40262716
2024 [Retracted] Downregulation of CKS1B restrains the proliferation, migration, invasion and angiogenesis of retinoblastoma cells through the MEK/ERK signaling pathway. International journal of molecular medicine 2 38757359
2023 A novel human multiple myeloma cell line with a 1q21 gain genetic abnormality and CKS1B overexpression. Annals of translational medicine 1 36819558
2026 CKS1B is a tumor-intrinsic factor driving CD8+ T cell exhaustion via maintaining persistent tumor-antigen stimulation. Science advances 0 42090485
2025 Multidimensional analysis of hsa-miR-140-3p and CKS1B correlation via the MAPK/ERK pathway in lung adenocarcinoma progression. Discover oncology 0 41171587
2024 [Retracted] Circular RNA NOX4 promotes the development of colorectal cancer via the microRNA‑485‑5p/CKS1B axis. Oncology reports 0 39054968

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