ArticleInternational journal of hematology2013
Cell adhesion to fibronectin down-regulates the expression of Spy1 and contributes to drug resistance in multiple myeloma cells.
Article in International journal of hematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 20 citations in OpenAlex.
- Whole-exome sequencing of primary plasma cell leukemia discloses heterogeneous mutational patterns.Oncotarget · 2015Trial
- Review
- Article
- Fibronectin Promotes the Malignancy of Glioma Stem-Like Cells Via Modulation of Cell Adhesion, Differentiation, Proliferation and Chemoresistance.Frontiers in molecular neuroscience · 2018Article
- High Spy1 expression predicts poor prognosis in colorectal cancer.Cancer management and research · 2018Article
- Expression of vaccinia-related kinase 1 (VRK1) accelerates cell proliferation but overcomes cell adhesion mediated drug resistance (CAM-DR) in multiple myeloma.Hematology (Amsterdam, Netherlands) · 2016Article
- Spy1 participates in the proliferation and apoptosis of epithelial ovarian cancer.Journal of molecular histology · 2016Article
- Cell adhesion down-regulates the expression of vacuolar protein sorting 4B (VPS4B) and contributes to drug resistance in multiple myeloma cells.International journal of hematology · 2015Article
- Killing me softly--future challenges in apoptosis research.International journal of molecular sciences · 2014Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spy1 is a member of the Speedy/Ringo family, which regulates cell proliferation and survival. Spy1 has been demonstrated to promote the cell-cycle progress through p27(Kip1) degradation. Previous investigations have suggested cell adhesion-mediated drug resistance (CAM-DR) in multiple myeloma (MM) is a primary factor for minimal residual disease (MRD) leading to relapse after chemotherapy. However, the precise mechanism remains elusive. In this study, we used MM cell lines to determine whether Spy1 plays a role in CAM-DR. We demonstrated that adhesion of MM cells to fibronectin (FN) decreased Spy1 expression. Overexpression of Spy1 did not affect MM cells adhesion to FN, but did reverse the doxorubicin- or mitoxantrone-induced CAM-DR phenotype. Spy1 protein level was also correlated with reciprocal up-regulation of p27(Kip1) when RPMI 8226 cells bound FN. Spy1 overexpression promoted p27(Kip1) phosphorylation at T187, then induced the p27(Kip1) degradation in the adhesion model. In addition, increasing p27(Kip1) level or disturbing p27(Kip1) phosphorylation at T187 abolished the CAM-DR reversion when Spy1 was overexpressed. Collectively, our data suggest that Spy1 plays an important role in CAM-DR, which depends on the function of p27(Kip1). Our findings provide a rational framework for further development of Spy1 as a novel target for MM therapy.
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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.