ArticleBlood2007
CKS1B, overexpressed in aggressive disease, regulates multiple myeloma growth and survival through SKP2- and p27Kip1-dependent and -independent mechanisms.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.
- Targeting Ubiquitin-Proteasome Pathway by Natural Products: Novel Therapeutic Strategy for Treatment of Neurodegenerative Diseases.Frontiers in physiology · 2020Pooled it
- Trial
- Ixazomib-Thalidomide-Dexamethasone for induction therapy followed by Ixazomib maintenance treatment in patients with relapsed/refractory multiple myeloma.British journal of cancer · 2019Trial
- Trial
- PYGO2 is overexpressed in multiple myeloma patients with 1q21 amplification, driving plasma cell proliferation and cell cycle progression.Cancer gene therapy · 2026Article
- CKS1B is a tumor-intrinsic factor driving CD8Science advances · 2026Article
- Proteomic profiling revealed unique disease biology associated with 1q abnormalities in multiple myeloma.NPJ precision oncology · 2026Article
- Integrating single-cell biophysical and transcriptomic features to resolve functional heterogeneity in mantle cell lymphoma.Science advances · 2025Article
- TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells.Nature immunology · 2025Article
- Liquid Biopsy as a Means of Assessing Prognosis and Identifying Novel Risk Factors in Multiple Myeloma.International journal of molecular sciences · 2025Article
- Multiple myeloma with 1q gain/amplification exhibits reduced CD38 expression via interleukin-6 receptor overexpression.British journal of haematology · 2025Article
- Exploring the oncogenic role and prognostic value ofFrontiers in genetics · 2025Article
- FOXM1-Driven CKS1B Upregulation Promotes Pancreatic Cancer Progression and Therapeutic Resistance.International journal of biological sciences · 2025Article
- Single-cell sequencing analysis of multiple myeloma heterogeneity and identification of new theranostic targets.Cell death & disease · 2024Article
- Multi-omic profiling of simultaneous ductal carcinoma in situ and invasive breast cancer.Breast cancer research and treatment · 2024Article
- 1q amplification and PHF19 expressing high-risk cells are associated with relapsed/refractory multiple myeloma.Nature communications · 2024Article
- The Genetic and Molecular Drivers of Multiple Myeloma: Current Insights, Clinical Implications, and the Path Forward.Pharmacogenomics and personalized medicine · 2024Review
- Amplification of Chromosome 1q Predicts Poor Overall Survival in Newly Diagnosed Multiple Myeloma Patients.Journal of hematology · 2023Article
- A novel human multiple myeloma cell line with a 1q21 gain genetic abnormality and CKS1B overexpression.Annals of translational medicine · 2023Article
- PLAGL1 is associated with prognosis and cell proliferation in pancreatic adenocarcinoma.BMC gastroenterology · 2023Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of CKS1B, a gene mapping within a minimally amplified region between 153 to 154 Mb of chromosome 1q21, is linked to a poor prognosis in multiple myeloma (MM). CKS1B binds to and activates cyclin-dependent kinases and also interacts with SKP2 to promote the ubiquitination and proteasomal degradation of p27(Kip1). Overexpression of CKS1B or SKP2 contributes to increased p27(Kip1) turnover, cell proliferation, and a poor prognosis in many tumor types. Using 4 MM cell lines harboring MAF-, FGFR3/MMSET-, or CCND1-activating translocations, we show that lentiviral delivery of shRNA directed against CKS1B resulted in ablation of CKS1B mRNA and protein with concomitant stabilization of p27(Kip1), cell cycle arrest, and apoptosis. Although shRNA-mediated knockdown of SKP2 and forced expression of a nondegradable form of p27(Kip1) (p27(T187A)) led to cell cycle arrest, apoptosis was modest. Of importance, while knockdown of SKP2 or overexpression of p27(T187A) induced cell cycle arrest in KMS28PE, an MM cell line with biallelic deletion of CDKN1B/p27(Kip1), CKS1B ablation induced strong apoptosis. These data suggest that CKS1B influences myeloma cell growth and survival through SKP2- and p27(Kip1)-dependent and -independent mechanisms and that therapeutic strategies aimed at abolishing CKS1B function may hold promise for the treatment of high-risk disease for which effective therapies are currently lacking.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.