Abstract
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-β) 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-β can regulate the production of ROS unambiguously or downregulate antioxidant systems. ROS can influence TGF-β signaling by enhancing its expression and activation. Thus, TGF-β 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-β is critical for tumorigenesis and cancer progression. Thus, both TGF-β 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-β and oxidative stress in cancer, exposing new potential approaches in cancer biology.
Highlights
Transforming growth factor-beta (TGF-β) has been claimed to play a biphasic role in cancer progression, behaving as a cancer suppressor in the early stages of carcinogenesis and exercising an oncogenic function in the later stages of cancer [1]
The objective of this review is to reveal the significance of TGF-β in cancer and its molecular relationship with the oxidative stress generated by reactive oxygen species (ROS) in cancer-cell metastasis
Nox4 gene, which contributes to ROS production through a Smad3-dependent mechanism, and it might be significant for the development of TGF-β-generated epithelial-mesenchymal transition (EMT) in breast cancer [63]
Summary
Transforming growth factor-beta (TGF-β) has been claimed to play a biphasic role in cancer progression, behaving as a cancer suppressor in the early stages of carcinogenesis and exercising an oncogenic function in the later stages of cancer [1]. TGF-β initiates the epithelial-mesenchymal transition (EMT) of transformed cells, which influences a cancer aggression and metastasis and is repeatedly observed to be elevated in carcinoma cells [2,3]. Abnormal ROS production and/or antioxidant activity can lead to redox imbalances that promote cancer progression and are a characteristic of various cancer types [4,5]. TGF-β can control the level of ROS by increasing their production, as well as decreasing the activity of antioxidative/scavenging systems [7,8]. Elevated ROS levels may increase TGF-β expression and promote the release of TGF-β, making this growth factor bioavailable and effective [9]. The objective of this review is to reveal the significance of TGF-β in cancer and its molecular relationship with the oxidative stress generated by ROS in cancer-cell metastasis
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