ArticleJournal of experimental & clinical cancer research : CR2010
Cancer cell sensitivity to bortezomib is associated with survivin expression and p53 status but not cancer cell types.
Article in Journal of experimental & clinical cancer research : CR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
- Autophagy and oxidative stress modulation mediate Bortezomib resistance in prostate cancer.PloS one · 2024Article
- RNF4 and USP7 cooperate in ubiquitin-regulated steps of DNA replication.Open biology · 2023Article
- Article
- Severe cellular stress drives apoptosis through a dual control mechanism independently of p53.Cell death discovery · 2022Review
- Article
- Article
- The deubiquitinase USP7 stabilizes Maf proteins to promote myeloma cell survival.The Journal of biological chemistry · 2020Article
- Survivin is a prognostic marker and therapeutic target for extranodal, nasal-type natural killer/T cell lymphoma.Annals of translational medicine · 2019Article
- Aplidin (plitidepsin) is a novel anti-myeloma agent with potent anti-resorptive activity mediated by direct effects on osteoclasts.Oncotarget · 2019Article
- Predicting drug response of tumors from integrated genomic profiles by deep neural networks.BMC medical genomics · 2019Article
- Spliced XBP1 Levels Determine Sensitivity of Multiple Myeloma Cells to Proteasome Inhibitor Bortezomib Independent of the Unfolded Protein Response Mediator GRP78.Frontiers in oncology · 2019Article
- G2/M inhibitors as pharmacotherapeutic opportunities for glioblastoma: the old, the new, and the future.Cancer biology & medicine · 2018Article
- Improving anticancer activity towards colon cancer cells with a new p53-activating agent.British journal of pharmacology · 2018Article
- Combination of Proteasome and Histone Deacetylase Inhibitors Overcomes the Impact of Gain-of-Function p53 Mutations.Disease markers · 2018Article
- Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition.American journal of cancer research · 2018Article
- Article
- Signaling mechanisms of bortezomib in TRAF3-deficient mouse B lymphoma and human multiple myeloma cells.Leukemia research · 2016Article
- Article
- Recent Advances on Small-Molecule Survivin InhibitorsCurrent medicinal chemistry · 2015Article
- Synergistic effect of allyl isothiocyanate (AITC) on cisplatin efficacy in vitro and in vivo.American journal of cancer research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSurvivin is known playing a role in drug resistance. However, its role in bortezomib-mediated inhibition of growth and induction of apoptosis is unclear. There are conflicting reports for the effect of bortezomib on survivin expression, which lacks of a plausible explanation.
methodsIn this study, we tested cancer cells with both p53 wild type and mutant/null background for the relationship of bortezomib resistance with survivin expression and p53 status using MTT assay, flow cytometry, DNA fragmentation, caspase activation, western blots and RNAi technology.
resultsWe found that cancer cells with wild type p53 show a low level expression of survivin and are sensitive to treatment with bortezomib, while cancer cells with a mutant or null p53 show a high level expression of survivin and are resistant to bortezomib-mediated apoptosis induction. However, silencing of survivin expression utilizing survivin mRNA-specific siRNA/shRNA in p53 mutant or null cells sensitized cancer cells to bortezomib mediated apoptosis induction, suggesting a role for survivin in bortezomib resistance. We further noted that modulation of survivin expression by bortezomib is dependent on p53 status but independent of cancer cell types. In cancer cells with mutated p53 or p53 null, bortezomib appears to induce survivin expression, while in cancer cells with wild type p53, bortezomib downregulates or shows no significant effect on survivin expression, which is dependent on the drug concentration, cell line and exposure time.
conclusionsOur findings, for the first time, unify the current inconsistent findings for bortezomib treatment and survivin expression, and linked the effect of bortezomib on survivin expression, apoptosis induction and bortezomib resistance in the relationship with p53 status, which is independent of cancer cell types. Further mechanistic studies along with this line may impact the optimal clinical application of bortezomib in solid cancer therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
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.