In a mouse hepatic metastasis model, treated with AMD3100 or Cy blocked the metastatic potential of HCT116 cells and the hepatic CAFs differentiation.<b>Conclusions</b>: These results indicated that CXCR4/TGF-β1 axis plays an important role in CRC liver metastasis through mediating HSCs differentiation into CAFs, providing preclinical evidences that blockade of the axis might be beneficial for anti-metastasis therapy in CRC.
<i>In vivo</i> xenograft experiments also demonstrated that MSCs promoted differentiation into CAFs through CXCR4/TGF-β1 signaling in either primary tumor tissues or hepatic metastatic tissues of CRC.<b>Conclusion</b>: Our studies have revealed the essential role of CXCR4/TGF-β1 axis playing in the transformation of tumor microenvironment by mediating MSCs differentiation into CAFs, promoting CRCs growth and metastasis.
These findings point to a novel molecular mechanism underlying the tumor‑promoting function of TGF‑β1, which may be utilized in the development of a novel therapeutic strategy for the treatment of colorectal cancer.
Human CRC cell lines HT-29 and SW480 were treated by TPL for 24 h in the presence or absence of epithelial-to-mesenchymal transition (EMT) inducer TGF-β1.
Ginsenoside Rb2 could inhibit EMT of colorectal cancer cells through the TGF-β1/Smad signaling, and might be a potential candidate for the treatment of colorectal cancer.
In the present study, we explored the role of two single nucleotide polymorphisms (SNPs) in the promoter regions of TGFB1 and IL10 genes and their associations with infiltrating DCs in CRC.A case-control study was designed.
The results showed that the expression of miR-34a was downregulated whereas TGF-β1 and VEGF were upregulated in CRC tumor tissues and peripheral blood macrophages.
Since transforming growth factor beta 1 (TGF-β1) regulates integrin function and promotes EMT/cell motility, we were prompted to investigate whether TGF-β1 induces EMT and cell motility through Cten signalling in colorectal cancer.
This study aimed to assess the effect of statins on CRC by studying cellular infiltration of Regulatory T Lymphocytes (Tregs) into CRC tissues and their effect on Transforming growth factor beta 1 (TGF-β<sub>1</sub>) level and on angiogenesis.
OM alleviated EMT induced in colorectal cancer via inhibition of TGF-β1/Smad signaling pathway activation by reducing P38-dependent increased expression of PAI-1.
Tanshinone IIA inhibits β-catenin/VEGF-mediated angiogenesis by targeting TGF-β1 in normoxic and HIF-1α in hypoxic microenvironments in human colorectal cancer.
Upregulation of Smad7, an inhibitor of transforming growth factor-β1 (TGF-β1), occurs in sporadic colorectal cancer (CRC) and knockdown of Smad7 inhibits CRC cell growth, a phenomenon that associates with decreased expression of cell division cycle 25 homolog A and arrest of cells in the S phase of the cell cycle.
The results of the current study revealed that miR‑329 suppresses CRC cell proliferation and invasion through targeting TGF‑β1, thus suggesting that targeting miR‑329/TGF‑β1 may provide a novel effective therapeutic approach for the treatment of patients with CRC.
In this study, we simultaneously investigated the protein expression pattern of 3 regulators in the TGF-β/SMAD signaling pathway, including SMAD4, PPM1A, and TGF-β1, and their clinicopathological correlations in CRCs by immunohistochemistry.
The present study aimed to analyze the effects and mechanisms underlying TGF-β1-induced chemoresistance to oxaliplatin (LOH) in human colorectal cancer (CRC) cell lines.
Numerous studies indicate that the interaction between cancer-associated fibroblasts (CAFs) and tumors is manifested in the entire process of colorectal cancer (CRC) cell development, in which TGF-β1 plays a key role and has a significant effect on promoting the activation of CAFs.