BMI-1 mRNA and positive protein levels were correlated with the National Institutes of Health (NIH) risk grade, tumor diameter and infiltration, and metastasis.
For the first time, we provide images of human prostate carcinoma metastasis precursor cells isolated from blood and shown to overexpress both BMI1 and Ezh2 oncoproteins.
The overexpression of miR-132 could reduce the expression level of Bmi-1 in SKOV3/DDP cells, increase the sensitivity of SKOV3/DDP cells to DDP, and inhibit cell invasion and metastasis.
The results showed that CCAT1 knockdown markedly inhibited cell proliferation, migration and invasion, arrested the cell cycle at G0/G1 phase in vitro, and inhibited peritoneal metastasis in nude mice, along with the downregulation of Bmi-1.
BMI1 expression was observed to be elevated in metastatic tumors (lymph nodes, lungs, bones, liver) of Caucasian and African-American prostate cancer patients.
Thus, our findings indicate that Huaier n-butanol extract suppresses the proliferation and metastasis of GC cells via a c-Myc-Bmi1-mediated approach, providing a new perspective for our understanding of the anti-tumour effects of Huaier.
Finally, we identified that BMI-1 expression activating PI3K/AKT singing pathway by negative regulating PTEN was the main mechanism of promoting invasion and metastasis ability of pancreatic CSCs.
Additionally, CBX4 promotes proliferation and metastasis via regulating the expression of BMI-1 which is a significant regulator of proliferation and migration in lung cancer cells.
Compounding a previously described Bmi1-transgene and Pten-deficiency prostate cancer mouse model with the Ezh2 transgene did not enhance tumour progression or drive metastasis formation.
These results suggest that Bmi-1 is a key gene in regulation of EMT and migration of breast cancer cells induced by IR through activation of PI3K/AKT signaling; therefore, Bmi-1 could be a new target for inhibiting metastasis caused by IR.
These data yield key insights into melanoma biology and establish BMI1 as a compelling drug target whose inhibition would suppress both metastasis and chemoresistance of melanoma.
But high Bmi1 expression was significantly correlated with the clinical stage (pooled OR=3.04, 95%CI=1.31-7.07, P=0.010, random effect), tumor size (pooled OR=2.01, 95%CI=1.14-3.55, P=0.016, random effect), T classification (pooled OR=2.79, 95%CI=1.94-4.03, P<0.001, fixed effect), lymph node metastasis (pooled OR=2.24, 95%CI=1.47-3.39, P<0.001, random effect) and distant metastasis (pooled OR=5.05, 95%CI=1.29-19.70, P=0.020, random effect), and led to a poor overall survival (OS) in GC patients (RR=3.38, 95%CI=2.43-4.69, P<0.001, fixed effect).
These findings demonstrate the novel mechanism for BMI-1 in contributing to EC cell invasion and that repression of BMI-1 by miR-194 could have a therapeutic potential to suppress EC metastasis.
Putative cancer stem cells (CSCs) have been identified in HNSCC, and BMI1 expression has been linked to these phenotypes, but optimal treatment strategies to overcome chemotherapeutic resistance and eliminate metastases have not yet been identified.
Suppression of endogenous miR-429 promoted cell growth and metastasis. miR-429 was shown to directly target the 3' untranslated regions of B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) and E2F transcription factor 3 (E2F3) transcripts, regulating their expression, as well as that of the downstream epithelial-to-mesenchymal transition markers E-cadherin, N-cadherin, vimentin, p14, and p16.
The B-cell-specific Moloney leukemia virus inset site 1 gene (BMI-1) has attracted considerable attention in recent years because of its key role in breast cancer development and metastasis.
It is known that epithelial-mesenchymal transition and stemness transcription factors (TWIST1, SNAI2/SLUG, and BMI1) play an important role in metastasis and their dysregulation has been demonstrated in metastatic cancers.
In the current study, a relatively lower miR-452 and higher BMI1 expression levels were confirmed to be associated with advanced tumor stage and more extent of lymph nodes metastasis.
The results showed that Bmi-1 was significantly associated with tumor size (n = 7, OR = 1.79, 95% CI = 1.19-2.71, P = .005, fixed effect), poor differentiation (OR = 1.61, 95% CI = 1.11-2.33, P = .011, fixed effect), and distant metastasis (n = 4, OR = 4.69, 95% CI = 1.52-14.41, P = .007, fixed effect).
Moreover, immunohistochemical staining revealed Bmi-1 was overexpressed in 63.2% UCC tissues (Bmi-1 ++ or +++), and the overexpression of Bmi-1 protein was significantly correlated with tumor size (P = 0.046), clinical stage (P = 0.021), and regional lymph nodes metastasis (P = 0.010).