ROS and TGF[beta]: from pancreatic tumour growth to metastasis.

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Date: May 3, 2021
Publisher: BioMed Central Ltd.
Document Type: Article
Length: 6,885 words
Lexile Measure: 1510L

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Abstract :

Transforming growth factor [beta] (TGF[beta]) signalling pathway switches between anti-tumorigenic function at early stages of cancer formation and pro-tumorigenic effects at later stages promoting cancer metastasis. A similar contrasting role has been uncovered for reactive oxygen species (ROS) in pancreatic tumorigenesis. Down-regulation of ROS favours premalignant tumour development, while increasing ROS level in pancreatic ductal adenocarcinoma (PDAC) enhances metastasis. Given the functional resemblance, we propose that ROS-mediated processes converge with the spatial and temporal activation of TGF[beta] signalling and thereby differentially impact early tumour growth versus metastatic dissemination. TGF[beta] signalling and ROS could extensively orchestrate cellular processes and this concerted function can be utilized by cancer cells to facilitate their malignancy. In this article, we revisit the interplay of canonical and non-canonical TGF[beta] signalling with ROS throughout pancreatic tumorigenesis and metastasis. We also discuss recent insight that helps to understand their conflicting effects on different stages of tumour development. These considerations open new strategies in cancer therapeutics. Keywords: TGF[beta] signalling pathway, Reactive Oxygen Species (ROS), Epithelial-to-mesenchymal transition, Pancreatic cancer, Metastasis, Cancer stem cells (CSCs)

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Gale Document Number: GALE|A661432594