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Duality of Interactions Between TGF-β and TNF-α During Tumor Formation

Journal

FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.810286

Keywords

TGF-beta; TNF-alpha; proliferation; apoptosis; inflammation; genomic instability; epithelial-mesenchymal transition

Categories

Funding

  1. National Natural Science Foundation of China [81973595]
  2. National Natural Science Foundation of China [82004094]
  3. Support Program for Longyuan Youth
  4. Fundamental Research Funds for the Universities of Gansu Province [GZTZ[2021]17-1]
  5. Provincial university industry support project in Gansu [2020C-15]

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The tumor microenvironment plays a crucial role in the formation and development of tumors. Cytokines, such as TGF-beta and TNF-alpha, have different effects on tumor growth, metastasis, and prognosis at different stages. Inhibiting TGF-beta can promote tumor formation, while TGF-beta can contribute to tumor malignancy. TNF-alpha, initially identified as a natural immune serum mediator for tumor hemorrhagic necrosis, has broad biological activities and can be targeted for immune diseases and tumors. However, there is limited research on the interaction between these two cytokines in the tumor microenvironment.
The tumor microenvironment is essential for the formation and development of tumors. Cytokines in the microenvironment may affect the growth, metastasis and prognosis of tumors, and play different roles in different stages of tumors, of which transforming growth factor beta (TGF-beta) and tumor necrosis factor alpha (TNF-alpha) are critical. The two have synergistic and antagonistic effect on tumor regulation. The inhibition of TGF-beta can promote the formation rate of tumor, while TGF-beta can promote the malignancy of tumor. TNF-alpha was initially determined to be a natural immune serum mediator that can induce tumor hemorrhagic necrosis, it has a wide range of biological activities and can be used clinically as a target to immune diseases as well as tumors. However, there are few reports on the interaction between the two in the tumor microenvironment. This paper combs the biological effect of the two in different aspects of different tumors. We summarized the changes and clinical medication rules of the two in different tissue cells, hoping to provide a new idea for the clinical application of the two cytokines.

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