The simultaneous expression of TNC and Twist1 in GC stromal fibroblasts was positively associated with tumor location, pT stage, lymph node metastasis and clinical stage.
CAFs-derived HGF was found to promote MET-unamplified gastric cancer (GC) proliferation, migration, and invasion through the activation of HGF/c-Met/STAT3/twist1 pathway.
Twist1 was recently reported to be a key regulator of CAFs in gastric cancer, but its role in other types of cancer remains unclear, especially for esophageal squamous cell carcinoma (ESCC).
In the present study, we detected MACC1 expression and microvessel density (MVD) by immunohistochemistry in 159 patients with stage I-III GC, and investigated the role of TWIST1 and vascular endothelial growth factor A (VEGF-A) in MACC1-induced endothelium-dependent angiogenesis using nude mice with GC xenografts, and human umbilical vein endothelial cells (HUVECs) that were co-cultured with conditioned media from overexpression and interference MACC1 GC cells.
In conclusion, miR-186 affects the proliferation, invasion and migration of human gastric cancer by inhibition of Twist1, and could be a tumor suppressor in GC development.
To study the role of Twist gene in gastric cancer by gene silencing, including the potential of induction of apoptosis, cell cycle arrest, and proliferation inhibition in human malignant gastric SGC7901 cells.
Additionally, Twist1 could induce proliferation, invasion and EMT in gastric cancer; of these, FGFR2 was required for invasion and EMT, rather than proliferation.
Our results have identified TWIST as a critical regulator of gastric cancer cell proliferation and migration, suggesting a potential therapeutic approach to inhibit the growth and metastasis of gastric cancer through inactivation of TWIST.
However, there was no correlation to upregulated TWIST mRNA levels, as we have shown previously for diffuse-type gastric cancers with abnormal N-cadherin expression.