ArticleBritish journal of pharmacology2011
Celastrol inhibits proliferation and induces chemosensitization through down-regulation of NF-κB and STAT3 regulated gene products in multiple myeloma cells.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 135 citations in OpenAlex.
- Ferric ion-mediated biomimetic mineralization of human serum albumin with doxorubicin and celastrol for enhanced antitumor therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mechanistic and translational insights into plant-derived natural products in preclinical multiple myeloma research: Current evidence.Translational oncology · 2026Review
- Anti-neoplastic activity of celastrol in experimentally-induced mammary adenocarcinoma in mice: targeting wnt/β-catenin signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- PNPO-Mediated Oxidation of DVL3 Promotes Multiple Myeloma Malignancy and Osteoclastogenesis by Activating the Wnt/β-Catenin Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bilayered skin equivalent mimicking psoriasis as predictive tool for preclinical treatment studies.Communications biology · 2024Article
- Prodrug-inspired adenosine triphosphate-activatable celastrol-Fe(III) chelate for cancer therapy.Science advances · 2024Article
- Terpenoid-Mediated Targeting of STAT3 Signaling in Cancer: An Overview of Preclinical Studies.Biomolecules · 2024Review
- Recent Trends in anti-tumor mechanisms and molecular targets of celastrol.International journal of biological sciences · 2024Review
- Withaferin A and Celastrol Overwhelm Proteostasis.International journal of molecular sciences · 2023Review
- Dihydrocelastrol induces antitumor activity and enhances the sensitivity of bortezomib in resistant multiple myeloma by inhibiting STAT3-dependent PSMB5 regulation.Acta biochimica et biophysica Sinica · 2023Article
- Bioactive Phytoconstituents and Their Therapeutic Potentials in the Treatment of Haematological Cancers: A Review.Life (Basel, Switzerland) · 2023Review
- Disruption of Proteostasis by Natural Products and Synthetic Compounds That Induce Pervasive Unfolding of Proteins: Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Article
- Epigenetic derepression converts PPARγ into a druggable target in triple-negative and endocrine-resistant breast cancers.Cell death discovery · 2021Article
- Celastrol attenuates the inflammatory response by inhibiting IL‑1β expression in triple‑negative breast cancer cells.Oncology reports · 2021Article
- Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy.Cells · 2020Review
- Overview of the STAT-3 signaling pathway in cancer and the development of specific inhibitors.Oncology letters · 2020Review
- Celastrol Alleviates Gamma Irradiation-Induced Damage by Modulating Diverse Inflammatory Mediators.International journal of molecular sciences · 2020Article
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeActivation of pro-inflammatory transcription factors NF-κB and signal transducer and activator of transcription 3 (STAT3) is one of the major contributors to both pathogenesis and chemoresistance in multiple myeloma (MM), which results in high mortality rate. Thus, in the present study, we investigated whether celastrol could suppress the proliferation and induce chemosensitization of MM cells by interfering with NF-κB and STAT3 activation pathways. EXPERIMENTAL APPROACH: The effects of celastrol were investigated using both a virtual predictive tumour cell system and different MM cell lines resistant to doxorubicin, melphalan and bortezomib. KEY
resultsCelastrol inhibited the proliferation of MM cell lines regardless of whether they were sensitive or resistant to bortezomib and other conventional chemotherapeutic drugs. It also synergistically enhanced the apoptotic effects of thalidomide and bortezomib. This correlated with the down-regulation of various proliferative and anti-apoptotic gene products including cyclin D1, Bcl-2, Bcl-xL, survivin, XIAP and Mcl-1. These effects of celastrol were mediated through suppression of constitutively active NF-κB induced by inhibition of IκBα kinase activation; and the phosphorylation of IκBα and of p65. Celastrol also inhibited both the constitutive and IL6-induced activation of STAT3, which induced apoptosis as indicated by an increase in the accumulation of cells in the sub-G1 phase, an increase in the expression of pro-apoptotic proteins and activation of caspase-3. CONCLUSIONS AND IMPLICATIONS: Thus, based on our experimental findings, we conclude that celastrol may have great potential as a treatment for MM and other haematological malignancies.
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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.