Correlation between Oxidative Stress and Transforming Growth Factor-Beta in Cancers

The downregulation of reactive oxygen species (ROS) facilitates precancerous tumor development, even though increasing the level of ROS can promote metastasis. The transforming growth factor-beta (TGF-beta) signaling pathway plays an anti-tumorigenic role in the initial stages of cancer development but a pro-tumorigenic role in later stages that fosters cancer metastasis. TGF-beta can regulate the production of ROS unambiguously or downregulate antioxidant systems. ROS can influence TGF-beta signaling by enhancing its expression and activation. Thus, TGF-beta signaling and ROS might significantly coordinate cellular processes that cancer cells employ to expedite their malignancy. In cancer cells, interplay between oxidative stress and TGF-beta is critical for tumorigenesis and cancer progression. Thus, both TGF-beta and ROS can develop a robust relationship in cancer cells to augment their malignancy. This review focuses on the appropriate interpretation of this crosstalk between TGF-beta and oxidative stress in cancer, exposing new potential approaches in cancer biology.

Automated summary

The interaction between reactive oxygen species (ROS) and transforming growth factor-beta (TGF-beta) signaling pathway plays a critical role in tumor development and progression. While ROS can influence TGF-beta signaling, the TGF-beta pathway can regulate ROS production, leading to a complex relationship between the two in cancer cells. Understanding this crosstalk may provide new insights and potential approaches in cancer biology.