Over-expression of HMGA2 was associated with vascular invasion (OR = 0.16, 95% CI = 0.05-0.49; P = 0.001) and lymphatic invasion (OR = 1.89, 95% CI = 1.06-3.38; P = 0.032).
CONCLUSIONS In the A20 murine DLBCL cell line, high glucose upregulated the expression of HMGA2 to induce EMT and promote cell migration and invasion through the Wnt/ß-catenin signaling pathway.
Silencing HMGA2 suppressed cell viability, migration and invasion, enhanced cell apoptosis and sensitivity to DNR, and almost restored the DNR inhibitory function that was promoted by LiCl treatment.
Mechanistically, we first discovered that HMGA2, together with GCN5, facilitated the invasion of glioma cells via inducing chromatin conformational remodeling of the MMP2 gene promoter and epigenetically activating MMP2 gene transcription.
Collectively, our study provides evidence that HMGA2 gene silencing inhibits the activation of the ATR/Chk1 signaling pathway, whereby repressing EMT, proliferation, migration and invasion of CC cells and lymph node metastasis, and promoting CC cell apoptosis.
CONCLUSIONS miR-495 acts as a tumor suppressor in gastric cancer by inhibiting cell migration and invasion, which may be associated with its direct inhibition on HMGA2.
The simultaneous interference of HMGA2 expression and the overexpression of TWIST1 in MKN-45 cells reversed the inhibitory effect of HMGA2 interference on the invasion and migration of gastric cancer cells, EMT and the expression of stemness markers.
Furthermore, high mobility group AT-hook 2 (HMGA2) was identified to be a direct target of miR-219 in NSCLC, and downregulation of HMGA2 suppressed NSCLC cell proliferation, migration and invasion in vitro.
The results of the present study indicate that higher HMGA2 levels were significantly associated with TNM stage, lymph node status, vascular invasion, and poor OS in patients with gastric cancer.
To the best of our knowledge, the present study is the first to demonstrate that propofol could downregulate the expression of HMGA2, which inhibited the Wnt/β-catenin pathway, thus leading to the inhibition of cell proliferation and invasion, as well as the apoptosis of HepG2 cells.
Univariate analysis showed that age (P = 0.041), depth of tumor invasion (P = 0.031), lymph node status (P = 0.001), and HMGA2 expression (P = 0.024) were correlated with prognosis.
By combining HMGA2 immunostaining and clinicopathological characteristics as analyzing factors, high HMGA2 expression was specifically correlated with poor survival in patients with perineural invasion and lymph node metastasis of OSCC.
HMGA2 expression was associated with numerous adverse clinicopathological parameters, including higher T- and N-stage, the presence of lymphovascular invasion and with a worse recurrence-free and overall survival.