Role and clinical significance of TGF‑β1 and TGF‑βR1 in malignant tumors (Review)

Abstract

The appearance and growth of malignant tumors is a complicated process that is regulated by a number of genes. In recent years, studies have revealed that the transforming growth factor-β (TGF-β) signaling pathway serves an important role in cell cycle regulation, growth and development, differentiation, extracellular matrix synthesis and immune response. Notably, two members of the TGF-β signaling pathway, TGF-β1 and TGF-β receptor 1 (TGF-βR1), are highly expressed in a variety of tumors, such as breast cancer, colon cancer, gastric cancer and hepatocellular carcinoma. Moreover, an increasing number of studies have demonstrated that TGF-β1 and TGF-βR1 promote proliferation, migration and epithelial-mesenchymal transition of tumor cells by activating other signaling pathways, signaling molecules or microRNAs (miRs), such as the NF-κB signaling pathway and miR-133b. In addition, some inhibitors targeting TGF-β1 and TGF-βR1 have exhibited positive effects in in vitro experiments. The present review discusses the association between TGF-β1 or TGF-βR1 and tumors, and the development of some inhibitors, hoping to provide more approaches to help identify novel tumor markers to restrain and cure tumors.

Integrated analysis reveals the participation of IL4I1, ITGB7, and FUT7 in reshaping the TNBC immune microenvironment by targeting glycolysis

“…Additionally, increased fucosylated activity was also reported positively relative to increased glucose uptake by the pancreatic, lung, and ovarian carcinoma cell lines [47]. According to previous studies, the upregulation of IL4I1 maybe a result of naturally occurring Single Nucleotide Polymorphisms (SNPs) [48], the DNA demethylation of FUT7 could lead to its overexpression [49], and highly expressed ITGB7 may be induced by TGF-beta1 [50,51]. However, the potential basis for upregulation of above genes remains unknown in patients with breast cancers.…”

Halophilic Carotenoids and Breast Cancer: From Salt Marshes to Biomedicine

“…High ROS levels also contribute to the invasiveness of a tumor due to the activity of transforming growth factor beta-1 (TGFß1) [62]. TGFß1 induces the epithelial-mesenchymal transition (EMT) and the secretion of various invasiveness biomarkers, such as VEGF and interleukin 6 [63]. Furthermore, ROS activates matrix metalloproteinase (MMP) synthesis via Ras and MAPK signaling pathways or via NF-kB [64].…”

Comprehensive Characterization of Transforming Growth Factor Beta Receptor 1 in Stomach Adenocarcinoma Identifies a Prognostic Signature for Predicting Clinical Outcomes and Immune Infiltrates

“…TGFBR1 participate in TGFBR1-epidermal growth factor receptor (EGFR)-CTNNB1-CDH1 axis in regulating the invasion and migration in lung cancer [18]. Additionally, the activation or overexpression of TGFBR1 is observed in different types of tumors and can serve an important role in tumor cell proliferation and migration to other tissues [8,9].Cells that lack TGFBR1 do not respond to TGF-β1, which further affects the transduction of the TGF-β signaling pathway [19,20]. It's reported that some inhibitors of TGFBR1 had been join in phase 1 study in patients with advanced cancer, such as galunisertib [21,22].…”

“…TGFBR1 mediated phosphorylation of ILK and its subsequent binding to CD103, thus initiating inside-out signaling leading to activation of the integrin and strengthening of CD103-E-cadherin adhesion [25]. The existing body of research have shown a vital role for TGF-β signals in regulation of NK cells [19,26], T-Lymphocyte Accumulation and Antitumor Activity [25] and safe-guarding speci c Treg cell functions [27]. However, the mechanisms whereby TGFβ2 governs tumor progression, immune cell in ltration and the prognosis value of TGFBR1 expression and its correlation with tumor microenvironment (TME) in STAD remains unintelligible.…”