2022
DOI: 10.3389/fimmu.2022.903679
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Tumor Necrosis Factor α: Taking a Personalized Road in Cancer Therapy

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Cited by 26 publications
(8 citation statements)
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“…This cytokine demonstrated its ability to hinder tumor growth by inflicting damage on the tumor vasculature and directly inducing cancer cell apoptosis. These effects were particularly pronounced in cases where NF-κB and JNK activation were impaired [63][64][65][66]. Furthermore, TNF-α exhibited the potential to enhance the effectiveness of cancer treatment drugs/chemotherapy by promoting increased blood vessel permeability [67].…”
Section: Discussionmentioning
confidence: 99%
“…This cytokine demonstrated its ability to hinder tumor growth by inflicting damage on the tumor vasculature and directly inducing cancer cell apoptosis. These effects were particularly pronounced in cases where NF-κB and JNK activation were impaired [63][64][65][66]. Furthermore, TNF-α exhibited the potential to enhance the effectiveness of cancer treatment drugs/chemotherapy by promoting increased blood vessel permeability [67].…”
Section: Discussionmentioning
confidence: 99%
“…It is also known that AAW tend to have higher systemic inflammation levels and endothelial dysfunction compared with CAW [81]. This can be a consequence of TNF-α overexpression, as well as other pro-inflammatory cytokines secreted by tumor and stromal cells to recruit leukocytes with metastatic effects, to generate cancer stem cells, epithelial-mesenchymal transition (EMT), invasion, resistance to therapy and metabolic reprogramming [82]. Evidence has revealed a pro-tumorigenic role of TNF-α during BC progression and metastasis [83].…”
Section: Bc Immune Landscape and Bc Disparitiesmentioning
confidence: 99%
“…TNF-α activation improves the mesenchymality of breast cancer stem cells (BCSCs) in triple-negative breast cancer (TNBC), boosting their capacity for invasion, self-renewal, proliferation, and inducing intra-tumoral stromal invasion [ 152 , 153 ]. Additionally, TNF-α stimulates stromal cells to produce matrix metalloprotease (MMP)-2, vascular endothelial growth factor (VEGF)-A, and colony-stimulating factor (CSF)-1, which promotes colon cancer carcinogenesis [ 154 , 155 ]. Another treatment strategy to reduce angiogenic responses in the TME and stop secondary organ metastasis might be to target TNF-α [ 156 , 157 ].…”
Section: Introductionmentioning
confidence: 99%