ArticleJournal of molecular medicine (Berlin, Germany)2014
RelB, together with RelA, sustains cell survival and confers proteasome inhibitor sensitivity of chronic lymphocytic leukemia cells from bone marrow.
Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Long-acting nanoparticulate DNase-1 for effective suppression of SARS-CoV-2-mediated neutrophil activities and cytokine storm.Biomaterials · 2021Trial
- Tumor Cell Survival Factors and Angiogenesis in Chronic Lymphocytic Leukemia: How Hot Is the Link?Cancers · 2024Review
- RNA-Seq-Based Transcriptome Analysis of Chinese Cordyceps Aqueous Extracts Protective Effect against Adriamycin-Induced mpc5 Cell Injury.International journal of molecular sciences · 2024Article
- The TOX-RAGE axis mediates inflammatory activation and lung injury in severe pulmonary infectious diseases.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- In Silico, In Vitro, and In Vivo Evaluation of Caffeine-Coated Nanoparticles as a Promising Therapeutic Avenue for AML through NF-Kappa B and TRAIL Pathways Modulation.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Expression and Activity of the NF-κB Subunits in Chronic Lymphocytic Leukaemia: A Role for RelB and Non-Canonical Signalling.Cancers · 2023Article
- Cleavage-Responsive Biofactory T Cells Suppress Infectious Diseases-Associated Hypercytokinemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Lung-selective 25-hydroxycholesterol nanotherapeutics as a suppressor of COVID-19-associated cytokine storm.Nano today · 2021Article
- PEGylated nanoparticle albumin-bound steroidal ginsenoside derivatives ameliorate SARS-CoV-2-mediated hyper-inflammatory responses.Biomaterials · 2021Article
- Bioinspired DNase-I-Coated Melanin-Like Nanospheres for Modulation of Infection-Associated NETosis Dysregulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine storm.Signal transduction and targeted therapy · 2020Article
- Expression Of Intracellular Components of the NF-κB Alternative Pathway (NF-κB2, RelB, NIK and Bcl3) is Associated With Clinical Outcome of NSCLC Patients.Scientific reports · 2019Article
- Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling.Leukemia · 2018Article
- RelB plays an oncogenic role and conveys chemo-resistance to DLD-1 colon cancer cells.Cancer cell international · 2018Article
- The nuclear transcription factor RelB functions as an oncogene in human lung adenocarcinoma SPC-A1 cells.Cancer cell international · 2018Article
- Microenvironmental agonists generateBlood advances · 2017Article
- NF-κB signaling pathway and its potential as a target for therapy in lymphoid neoplasms.Blood reviews · 2017Review
- Stress and Non-Stress Roles of Inflammatory Signals during HSC Emergence and Maintenance.Frontiers in immunology · 2016Review
- Expression and role of RIP140/NRIP1 in chronic lymphocytic leukemia.Journal of hematology & oncology · 2015Review
- NF-κB pathways in hematological malignancies.Cellular and molecular life sciences : CMLS · 2014Review
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
No grant is acknowledged in the PubMed record.
Abstract
unlabelledAlthough the biological factors that contribute to the pathogenesis of chronic lymphocytic leukemia (CLL) remain widely unresolved, it has been suggested that dysregulated cell survival and proliferation are fundamental to this process. Constitutive classical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation protects CLL B-cells from cell death and plays a critical role in the acquisition of chemoresistance. RelB, representing the alternative NF-κB activity, functions specifically in lymphoid organogenesis and B-cell maturation. RelB indeed plays a tumor-supportive role and confers radiation resistance in tumors. However, the involvement of RelB in CLL has not been addressed. Here, we analyzed the NF-κB activation in 67 of CLL bone marrow (BM). Both the RelA and RelB activity were detected in CLL B-cells from BM, in spite of inevitable variability. Low RelB activity was linked to a favorable prognosis of CLL. The migration and adhesion abilities of CLL B-cells were not affected by the RelB activity. High RelB activity, together with the RelA activity, maintained basal survival of cells. The induction of RelA and RelB expression in the nucleus was responsible for better survival of CLL B-cells supported by bone marrow stromal cells. In addition, the presence of high RelB activity in CLL B-cells was correlated with sensitivity to proteasome inhibitor but not fludarabine. Taken together, we provided evidences that not only RelA but also RelB, subunits of NF-κB family, played an important role in the cellular behaviors of CLL cells from BM. The strength of RelB activity influenced the prognosis of CLL patients. KEY MESSAGE: RelB, with RelA activity, maintained the basal survival of CLL cells from BM. RelB, with RelA, conferred the proteasome inhibitor sensitivity of CLL cells. Induction of RelA and RelB was responsible for the better survival of CLL B-cells. The strength of RelB activity influenced the prognosis of CLL patients.
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.