ArticleCellular and molecular life sciences : CMLS2015
Rapamycin inhibits BAFF-stimulated cell proliferation and survival by suppressing mTOR-mediated PP2A-Erk1/2 signaling pathway in normal and neoplastic B-lymphoid cells.
Article in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
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- An Unusual Case of Primary Sjögren's Syndrome and Lymphangioleiomyomatosis Diagnosed From Refractory Cough.Cureus · 2025Article
- Sirolimus versus mycophenolate mofetil for the treatment of lupus nephritis: Results from a real-world CSTAR cohort study.Rheumatology and immunology research · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Protein serine/threonine phosphatases in tumor microenvironment: a vital player and a promising therapeutic target.Theranostics · 2025Review
- ICAM-1 mediated cell-cell adhesion exerts dual roles on human B cell differentiation and IgG production.iScience · 2023Article
- Modelling Microglial Innate Immune Memory In Vitro: Understanding the Role of Aerobic Glycolysis in Innate Immune Memory.International journal of molecular sciences · 2023Article
- A cellular overview of immunometabolism in systemic lupus erythematosus.Oxford open immunology · 2023Review
- B cell activation via immunometabolism in systemic lupus erythematosus.Frontiers in immunology · 2023Review
- Resveratrol induces autophagy impeding BAFF-stimulated B-cell proliferation and survival by inhibiting the Akt/mTOR pathway.Biochemical pharmacology · 2022Article
- The mTOR Signaling Pathway in Multiple Sclerosis; from Animal Models to Human Data.International journal of molecular sciences · 2022Review
- Altered Germinal-Center Metabolism in B Cells in Autoimmunity.Metabolites · 2022Review
- PD-L1 blockade potentiates the antitumor effects of ALA-PDT and optimizes the tumor microenvironment in cutaneous squamous cell carcinoma.Oncoimmunology · 2022Article
- Association of Viral Infection With the Development and Pathogenesis of Systemic Lupus Erythematosus.Frontiers in medicine · 2022Review
- Metformin prevents BAFF activation of Erk1/2 from B-cell proliferation and survival by impeding mTOR-PTEN/Akt signaling pathway.International immunopharmacology · 2021Article
- Metabolic Program of Regulatory B Lymphocytes and Influence in the Control of Malignant and Autoimmune Situations.Frontiers in immunology · 2021Review
- Rapamycin Modulates the Proinflammatory Memory-Like Response of Microglia Induced by BAFF.Frontiers in immunology · 2021Article
- B Cell Metabolism and Autophagy in Autoimmunity.Frontiers in immunology · 2021Review
- Rapamycin inhibits B-cell activating factor (BAFF)-stimulated cell proliferation and survival by suppressing CaCell calcium · 2020Article
- Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases.Current opinion in rheumatology · 2020Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
B-cell activating factor (BAFF) is involved in not only physiology of normal B cells, but also pathophysiology of aggressive B cells related to malignant and autoimmune diseases. Rapamycin, a lipophilic macrolide antibiotic, has recently shown to be effective in the treatment of human lupus erythematosus. However, how rapamycin inhibits BAFF-stimulated B-cell proliferation and survival has not been fully elucidated. Here, we show that rapamycin inhibited human soluble BAFF (hsBAFF)-induced cell proliferation and survival in normal and B-lymphoid (Raji and Daudi) cells by activation of PP2A and inactivation of Erk1/2. Pretreatment with PD98059, down-regulation of Erk1/2, expression of dominant negative MKK1, or overexpression of wild-type PP2A potentiated rapamycin's suppression of hsBAFF-activated Erk1/2 and B-cell proliferation/viability, whereas expression of constitutively active MKK1, inhibition of PP2A by okadaic acid, or expression of dominant negative PP2A attenuated the inhibitory effects of rapamycin. Furthermore, expression of a rapamycin-resistant and kinase-active mTOR (mTOR-T), but not a rapamycin-resistant and kinase-dead mTOR-T (mTOR-TE), conferred resistance to rapamycin's effects on PP2A, Erk1/2 and B-cell proliferation/viability, implying mTOR-dependent mechanism involved. The findings indicate that rapamycin inhibits BAFF-stimulated cell proliferation/survival by targeting mTOR-mediated PP2A-Erk1/2 signaling pathway in normal and neoplastic B-lymphoid cells. Our data highlight that rapamycin may be exploited for preventing excessive BAFF-induced aggressive B-cell malignancies and autoimmune diseases.
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