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BIOMARKER:

BMI1 expression

i
Other names: BMI1, PCGF4, RNF51, BMI1 proto-oncogene, polycomb ring finger
Entrez ID:
Related biomarkers:
9d
These effects reflected caspase 3-mediated apoptosis and could be attenuated or abolished by inhibiting ROS production with N-acetyl-L-cysteine, inhibiting autophagy with chloroquine, or silencing ATG7 with targeted siRNA...Accordingly, exposure to dorsomorphin (Compound C), an AMPK inhibitor, and AICAR, an AMPK activator, respectively inhibited and stimulated BA-induced autophagy in EJ and T24 cells. The effects of Bmi-1 overexpression in vitro and decreased Bmi-1 expression in BA-treated T24 cell xenografts in nude mice suggested that downregulation of Bmi-1 is the underlying mechanism in BA-mediated, autophagy-dependent apoptosis.
Journal
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CASP3 (Caspase 3) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • AMPK (Protein Kinase AMP-Activated Catalytic Subunit Alpha 1) • ATG7 (Autophagy Related 7)
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BMI1 expression
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chloroquine phosphate
26d
We suggest that high BMI1 expression could be a therapeutic target in breast cancer. These results could contribute to the design of future experimental research and drug development programs for breast cancer.
Journal
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CD8 (cluster of differentiation 8) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • CD4 (CD4 Molecule)
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CD8 expression • BMI1 expression
2ms
A gradient of lymphangiogenic factors over the extracellular matrix gel induced the formation of luminated sprouts. Adding mouse colon cancer organoids adjacent to the lymphatic vessel resulted in a stable long-lived coculture model in which cancer cell-induced lymphangiogenesis and cancer cell motility can be investigated. Thus, the development of a stable immortalized lymphatic endothelial cell line in a membrane-free, perfused microfluidic chip yields a highly standardized lymphangiogenesis and lymphatic vessel-tumor cell coculture assay.
Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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BMI1 expression
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Luminate (risuteganib)
2ms
Materials and Methods The effect of an mTOR inhibitor (temsirolimus) on resistance of MEC CSCs to cisplatin was evaluated in a panel of human MEC cell lines (UM-HMC-1, UM-HMC-3A, UM-HMC-3B), and using a patient-derived xenograft (PDX) model of MEC (UM-HMC-PDX-18). Nakano); Soda Toyoji Memorial Foundation (T. Nakano).
BMI1 (BMI1 proto-oncogene, polycomb ring finger) • CD44
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BMI1 expression
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cisplatin • Torisel (temsirolimus)
2ms
Exosomal circHIPK3 knockdown also suppressed tumor growth in vivo. Exosomal circHIPK3 knockdown inhibited PCa progression by regulating miR-212/BMI-1 axis, at least in part, offering a new insight into the molecular mechanism of PCa.
Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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BMI1 expression
2ms
Our study provides solid evidence for a different BMI-1 expression in EOC and NEOC, corresponding to the differences in their etiopathogeny. The reported differences in the BMI-1 expression of EOC and NEOC need to be further validated in a larger and homogenous cohort of study.
Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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BMI1 expression
2ms
In parallel, treatment with the BMI1 inhibitor PTC-209 mimicked the effects of BTF3 knockdown on stem cell-like traits and EMT of cultured HCT116 cells. Together, these results support the notion that BTF3 and BMI1 are potential therapeutic targets to limit CRC metastasis.
Journal
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CD133 • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • TCF3 (Transcription Factor 3)
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BMI1 expression
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PTC-209
2ms
Our work suggested that lncAY might elevate BMI1 expression and further activate the Wnt/β-catenin signaling. BMI1 reverses the suppressive effects of lncAY depletion in HCC cells. Collectively, our work uncovers a novel undefined regulatory signaling pathway, namely lncAY/BMI1/Wnt/β-catenin axis, involved in liver cancer progression.
Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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BMI1 expression
3ms
C-kit PLCs had the characteristics of tumor stem cells and were more sensitive to chemotherapy drugs.
Journal
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NOTCH1 (Notch 1) • ABCB1 (ATP Binding Cassette Subfamily B Member 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • ABCG2 • CDH1 (Cadherin 1) • GPC3 (Glypican 3) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • EPCAM (Epithelial cell adhesion molecule) • POU5F1 (POU Class 5 Homeobox 1) • SOX2 • NANOG (Nanog Homeobox) • NES (Nestin)
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KIT expression • CDH1 expression • NOTCH1 expression • BMI1 expression • POU5F1 expression
4ms
Moreover, sodium butyrate, a histone deacetylase and BMI-1 inhibitor, reduced HCT116 and LOVO liver metastasis in immunodeficient mice. Our results suggest that BMI-1 is a major regulator of CRCLM and provide a potent molecular target for CRCLM treatment.
Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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BMI1 expression
4ms
CD-44 and ALDH-1 may be useful in differentiating between primary SCCs and metastatic disease. BMI-1 and SOX-2 are correlated with poorer prognosis.
Retrospective data • Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger) • CD44 • SOX2 • VIM (Vimentin) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
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BMI1 expression • VIM expression
4ms
Preclinical • Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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BMI1 expression
5ms
LTC-IC experiments pinpointed that PKCδ inhibition strongly decreased the progenitors/LSCs frequency. All together, these results demonstrate that targeting of PKCδ in combination with a conventional TKI could be a new therapeutic opportunity to affect for CML cells.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • BCL2L1 (BCL2-like 1) • CD34 (CD34 molecule) • CASP3 (Caspase 3) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • CASP9 (Caspase 9)
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BCL2 expression • BMI1 expression
5ms
Finally, expression of BMI1 increased the phosphorylation of STAT3, which is important for cell proliferation, survival, migration, and invasion. Therefore, we suggest that AL plays a pivotal role in inhibiting BMI1 in the tumorigenesis of cervical cancer and is a potential therapeutic agent for cervical cancer.
Journal
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STAT3 (Signal Transducer And Activator Of Transcription 3) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • VIM (Vimentin)
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BMI1 expression • BMI1 overexpression • VIM expression
5ms
Thus, regulatory transcriptional factors are potential therapeutic targets to reduce Bmi-1 expression in cancer cells. Thus, the present review provides an up-to-date review on the regulation of BMI-1 gene expression at the transcriptional and post-transcriptional level.
Review • Journal
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CDKN2A (Cyclin-dependent kinase inhibitor 2A) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • SALL4 (Spalt Like Transcription Factor 4)
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BMI1 expression • CDKN2A expression
7ms
The HDAC inhibitor vorinostat (SAHA) prevented Sp1 binding to the BMI1 promoter, leading to a decreased expression of BMI1 and attenuating tumor growth of TMZ-resistant glioma xenografts. Importantly, we further performed survival analysis using PROGgeneV2 and found that an elevated expression of HDAC1,3/Sp1/BMI1 but not BMI1 alone showed an increased risk of death in both high- and low-grade glioma patients. Thus, HDAC-mediated Sp1 deacetylation is critical for BMI1 regulation to attenuate stress- and therapy-induced death in glioma cells, and the HDAC/Sp1 axis is more important than BMI1 and appears as a therapeutic target to prevent recurrence of malignant glioma cells persisting after primary therapy.
Journal
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BMI1 (BMI1 proto-oncogene, polycomb ring finger) • HDAC1 (Histone Deacetylase 1)
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BMI1 expression
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temozolomide • Zolinza (vorinostat)