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.
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.
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.
BMI-1 mRNA and positive protein levels were correlated with the National Institutes of Health (NIH) risk grade, tumor diameter and infiltration, 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.
Doublecortin-Like Kinase 1 (DCLK1) Regulates B Cell-Specific Moloney Murine Leukemia Virus Insertion Site 1 (Bmi-1) and is Associated with Metastasis and Prognosis in Pancreatic Cancer.
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.
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.
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.
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).
(2017) show that mouse and human HNSCCs and their metastases depend on Bmi1-expressing cancer stem cells and AP1 signaling and that simultaneously inhibiting Bmi1 or AP1, combined with Cisplatin, reduces tumor growth effectively in preclinical models.
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.
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).
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.
Our study implies that detection of Bmi-1 and RKIP is valuable in predicting patient survival and therapeutic response in gastric cancer, and the inverse association between Bmi-1 and RKIP reveals the potential molecular mechanisms underlying tumor metastasis and chemotherapy resistance.
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.
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.
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.
Taken together, our findings disclose for the first time that Bmi-1 level accumulates strongly in early stage and then declines in late stage, which is potentially important for NSCLC cell invasion and metastasis during progression.