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Targeting STAT3 and STAT5 in Cancer
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Every minute, 34 new patients are diagnosed with cancer globally. Although over the past 50 years treatments have improved and survival rates have increased dramatically for several types of cancers, many remain incurable. Several aggressive types of blood and solid cancers form when mutations occur in a critical cellular signaling pathway, the JAK-STAT pathway; (Janus Kinase-Signal Transducer and Activator of Transcription). Currently, there are no clinically available drugs that target the oncogenic STAT3/5 proteins in particular or their Gain of Function hyperactive mutant products. Here, we summarize targeting approaches on STAT3/5, as the field moves towards clinical applications as well as we illuminate on upstream or downstream JAK-STAT pathway interference with kinase inhibitors, heat shock protein blockers or changing nuclear import/export processes. We cover the design paradigms and medicinal chemistry approaches to illuminate progress and challenges in understanding the pleiotropic role of STAT3 and STAT5 in oncogenesis, the microenvironment, the immune system in particular, all culminating in a complex interplay towards cancer progression.
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Keywords
- ADAM17
- adoptive T cell therapy
- Akt
- androgens
- Apoptosis
- autoimmune disease
- autosomal-dominant hyper IgE syndrome
- Biology, Life Sciences
- Bone Marrow Failure Syndromes
- Breast cancer
- Cancer
- cancer models
- cancer progression
- cancer-stem cell
- CD38
- CD4+ T cells
- CD8+ T cells
- Cell Cycle
- cell hierarchy
- chaperones
- chemotherapy resistance
- cirrhosis
- colon cancer
- Companion Animals
- comparative oncology
- cytokine
- cytokine receptor signaling
- Dynamic programming
- endoplasmic reticulum (ER) stress
- epidermal growth factor receptor (EGF-R)
- Erk1/2
- escape mechanisms
- gain-of-function mutation
- Glioblastoma
- Glioma
- growth hormone insensitivity syndrome
- Heat shock proteins
- Hedging
- hematopoietic cancers
- hepatitis C virus (HCV)
- hepatocellular carcinoma (HCC)
- hepatocyte nuclear factor 4 alpha (HNF4A)
- immune check point
- immune suppression
- Immunosuppression
- Immunotherapy
- Inflammation
- inflammation associated cancer
- inflammatory hepatocellular adenomas
- interleukin-6
- JAK
- JAK family of protein tyrosine kinases
- JAK2 V617F
- knockout
- lipopolyplex
- lung cancer
- lymphocytes
- Lymphoma
- M2 macrophages
- Mathematics & science
- Melanoma
- Meta-analysis
- metalloprotease
- metastasis
- microRNA-122 (miR-122)
- Mitochondria
- MPN
- mTOR
- multiple myeloma
- Mutations
- myeloid cells
- myeloid leukemia
- n/a
- nanoparticle
- neoplastic stem cells
- NGS
- NK cells
- nuclear factor erythroid 2-related factor 2 (Nrf2)
- nuclear pore complex
- nuclear transport receptors
- nucleocytoplasmic shuttling
- ovarian cancer
- oxidative stress (OS)
- PD-L1
- PEI
- pharmacological inhibitor
- pharmacological inhibitors
- polyethylenimine
- post-decision state variable
- Prolactin
- proliferation
- prostate cancer
- Reference, information & interdisciplinary subjects
- Research & information: general
- RhoA
- Risk management
- S3I-1757
- SH2 domain
- shedding
- signal transducer and activator of transcription
- signal transducer and activator of transcription 3 (STAT3)
- siRNA delivery
- siRNA/RNAi
- small-molecule inhibitors
- solid cancers
- stabilization
- stat
- STAT transcription factors
- STAT3
- STAT3 inhibitor XIII
- STAT5
- STAT5 signaling
- STAT5B signaling
- Stem/progenitor cells
- stemness
- T-cell large granular lymphocytic leukemia
- T-cell leukemia
- T-cell prolymphocytic leukemia
- T-cells
- T-PLL
- targeted therapy
- targeting
- Therapeutic targeting
- therapy resistance
- trans-signaling
- transaction costs
- Tumor microenvironment
- tumor necrosis factor alpha (TNFα)
- tumor suppression
- tumor-associated macrophages
- tumorigenesis
- tumor–immune cell interactions
- tyrosine kinase 2
- unfolded protein response (UPR)
Links
DOI: 10.3390/books978-3-03943-037-6Editions