LncRNA-Dependent Mechanisms of Transforming Growth Factor-β: From Tissue Fibrosis to Cancer Progression

Transforming growth factor-beta (TGF-beta) is a crucial pathogenic mediator of inflammatory diseases. In tissue fibrosis, TGF-beta regulates the pathogenic activity of infiltrated immunocytes and promotes extracellular matrix production via de novo myofibroblast generation and kidney cell activation. In cancer, TGF-beta promotes cancer invasion and metastasis by enhancing the stemness and epithelial mesenchymal transition of cancer cells. However, TGF-beta is highly pleiotropic in both tissue fibrosis and cancers, and thus, direct targeting of TGF-beta may also block its protective anti-inflammatory and tumor-suppressive effects, resulting in undesirable outcomes. Increasing evidence suggests the involvement of long non-coding RNAs (lncRNAs) in TGF-beta-driven tissue fibrosis and cancer progression with a high cell-type and disease specificity, serving as an ideal target for therapeutic development. In this review, the mechanism and translational potential of TGF-beta-associated lncRNAs in tissue fibrosis and cancer will be discussed.

Automated summary

Transforming growth factor-beta (TGF-beta) plays a crucial role in inflammatory diseases by regulating immune cell activity and promoting extracellular matrix production. In cancer, TGF-beta enhances cancer cell invasion and metastasis by affecting stemness and epithelial mesenchymal transition. However, directly targeting TGF-beta could have undesirable outcomes as it also has protective anti-inflammatory and tumor-suppressive effects. Long non-coding RNAs (lncRNAs) associated with TGF-beta are being investigated as potential therapeutic targets for tissue fibrosis and cancer progression.