Cytokine-Mediated Dysregulation of Signaling Pathways in the Pathogenesis of Multiple Myeloma
Open accessAbstract
Multiple myeloma (MM) is a hematologic disorder of B lymphocytes characterized by the accumulation of malignant plasma cells (PCs) in the bone marrow. The altered plasma cells overproduce abnormal monoclonal immunoglobulins and also stimulate osteoclasts. The host’s immune system and microenvironment are of paramount importance in the growth of PCs and, thus, in the pathogenesis of the disease. The interaction of MM cells with the bone marrow (BM) microenvironment through soluble factors and cell adhesion molecules causes pathogenesis of the disease through activation of multiple signaling pathways, including NF-κβ, PI3K/AKT and JAK/STAT. These activated pathways play a critical role in the inhibition of apoptosis, sustained proliferation, survival and migration of MM cells. Besides, these pathways also participate in developing resistance against the chemotherapeutic drugs in MM. The imbalance between inflammatory and anti-inflammatory cytokines in MM leads to an increased level of pro-inflammatory cytokines, which in turn play a significant role in dysregulation of signaling pathways and proliferation of MM cells; however, the association appears to be inadequate and needs more research. In this review, we are highlighting the recent findings on the roles of various cytokines and growth factors in the pathogenesis of MM and the potential therapeutic utility of aberrantly activated signaling pathways to manage the MM disease.
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The pathogenesis of multiple myeloma involves interaction between MM cells and the bone marrow microenvironment through soluble cytokines and cell adhesion molecules, activating PI3K/AKT/mTOR, RAS/MAPK, JAK/STAT, Wnt/β-catenin, and NF-κB pathways.
“The pathogenesis of MM involves the interaction between MM cells and the bone marrow microenvironment through soluble cytokines and cell adhesion molecules, which activate various signaling pathways such as PI3K/AKT/mTOR, RAS/MAPK, JAK/STAT, Wnt/β-catenin, and NF-κB pathways.”
From Multiple myeloma: signaling pathways and targeted therapy (2024) · cites this paper as [23]
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- Authors
- Akhtar, S., Ali, T. A., Faiyaz, A., Khan, O. S., Raza, S. S., Kulinski, M., Omri, H. E., Bhat, A. A., & Uddin, S.
- Affiliations
- Hamad Medical Corporation (QA)
- Midwestern University (US)
- Department of Stem Cell Biology and Regenerative Medicine, Era University, Lucknow 226003, India
- Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha 3050, Qatar
- Sidra Medical and Research Center (QA)
- ORCID
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-07-15
- Volume
- 21
- Issue
- 14
- Pages
- 5002
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7403981
- OpenAlex
- W3043754799
- Cited by
- 44
- References
- 185
- Citations by year
- 2026: 11 · 2025: 8 · 2024: 9 · 2023: 7 · 2022: 6 · 2021: 3
- FWCI
- 0.63
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Hamad Medical Corporation (MRC-01-18-120)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Health Sciences › Medicine › Genetics › Chronic Lymphocytic Leukemia Research
- Health Sciences › Medicine › Oncology › Bone health and treatments
- Keywords
- multiple myeloma, cytokines, signaling pathways, NF-κB, PI3K/Akt, JAK/STAT signaling, bone marrow microenvironment, plasma cells, inflammatory cytokines, apoptosis inhibition, drug resistance, growth factors, therapeutic target
- MeSH terms
- Animals, Bone Marrow, Humans, Inflammation, Multiple Myeloma, Neoplasm Invasiveness, Plasma Cells, Signal Transduction, Cytokines, Tumor Escape, Cell Proliferation, Tumor Microenvironment
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