BMI1: A Biomarker of Hematologic Malignancies

Sahasrabuddhe, Anagh A.

doi:10.4137/bic.s33376

Cited by 38 publications

(46 citation statements)

References 153 publications

(137 reference statements)

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“…In this study, we focused on the stemness factor BMI1 in lung cancer. We found that knockdown of BMI1 blocked LAC cell migration, invasion, chemo-resistance, and tumor initiation in vitro and in vivo (Figure 1 and 4E), confirming the previous recognition of BMI1 as a stemness regulator in cancer (6-9). Accordingly, targeting BMI1 with BI-44 suppressed LAC tumor formation and progression in pre-clinical model (Figure 6).…”

Section: Discussionsupporting

confidence: 87%

“…BMI1 gene amplification or protein overexpression has also been found in various cancer types (7). BMI1 expression has been linked to the promotion of stemness properties of tumor cells, including to tumor initiation, cell proliferation, epithelial-mesenchymal transition (EMT), invasion, repression of apoptosis or senescence, and drug resistance (6-9). In lung cancer, however, the role of BMI1 has not been fully characterized.…”

Section: Introductionmentioning

confidence: 99%

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Targeting BMI1 and MCL1 for Lung Adenocarcinoma Treatment

Lin

Hsu

et al. 2018

Preprint

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Lung cancer is the leading cause of cancer-associated death worldwide. Early metastasis and the recurrence remain major challenges for lung cancer treatment in clinic. Targeting the cancer stemness could be a potential strategy to restrain tumor progression. In the current study, we found that in lung adenocarcinoma (LAC), BMI1 and MCL1 play crucial roles in invasion, chemo-resistance, and tumor initiation. JNK signaling is a link between oncogenic pathway or environment stress to cancer stemness. The activation of JNK, either by EGFR or chemotherapy agent, stabilized BMI1 and MCL1 proteins through suppressing the expression of E3-ubiquitin ligase HUWE1. In lung cancer patient samples, high level of BMI1 is correlated with poor survival, and the expression of BMI1 is positively correlated with MCL1. A novel small-molecule BI-44 was synthesized, which effectively suppressed BMI1/MCL1 expression and inhibited tumor formation and progression in preclinical models. Targeting BMI1/MCL1 provides the basis for a new therapeutic approach in the treatment of LAC.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Targeting BMI1 and MCL1 for Lung Adenocarcinoma Treatment

Lin

Hsu

et al. 2018

Preprint

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“…Silencing of HOTAIR inhibited cell viability and induced G1-phase arrest by stimulating miR-218 expression. Inhibition of HOTAIR also activated expressions of P16 (INK4a) and P14 (ARF), the main downstream targets of miR-218 and 2 tumor suppressor genes, by enhancing miR-218 and suppressing B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1), a member of the polycomb-group gene family [41], resulting in the inhibition of tumorigenesis in HCC [42]. In addition, HOTAIR increased the migration and invasion of HCC cells by inhibiting the expression of RNA-binding motif protein 38 [43].…”

Section: Hotair In Hepatocellular Carcinomamentioning

confidence: 99%

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

Tang

Hann

2018

Cell Physiol Biochem

219

135

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Long non-coding RNAs (LncRNAs) represent a novel class of noncoding RNAs that are longer than 200 nucleotides without protein-coding potential and function as novel master regulators in various human diseases, including cancer. Accumulating evidence shows that lncRNAs are dysregulated and implicated in various aspects of cellular homeostasis, such as proliferation, apoptosis, mobility, invasion, metastasis, chromatin remodeling, gene transcription, and post-transcriptional processing. However, the mechanisms by which lncRNAs regulate various biological functions in human diseases have yet to be determined. HOX antisense intergenic RNA (HOTAIR) is a recently discovered lncRNA and plays a critical role in various areas of cancer, such as proliferation, survival, migration, drug resistance, and genomic stability. In this review, we briefly introduce the concept, identification, and biological functions of HOTAIR. We then describe the involvement of HOTAIR that has been associated with tumorigenesis, growth, invasion, cancer stem cell differentiation, metastasis, and drug resistance in cancer. We also discuss emerging insights into the role of HOTAIR as potential biomarkers and therapeutic targets for novel treatment paradigms in cancer.

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“…LPS-activated murine splenic B cells were transduced with pools of retroviral particles encoding genes associated with tumor transformation namely human MYC [8,9], BCLXL [10,11], hTERT [12], BMI1 [13,14], and activated HRAS (HRAS-V12) [15]. The transcription factor IRF4 [4, 6, 16,17] was also included due to its role in B-to plasma cell differentiation [18,19].…”

Section: Identification Of Gene Combinations Causing Transformation Omentioning

confidence: 99%

Transformation of mature mouse B cells into malignant plasma cells in vitro via introduction of defined genetic elements

et al. 2019

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An experimental system where defined alterations in gene function or gene expression levels in primary B cells would result in the development of transformed plasma cells in vitro would be useful in order to facilitate studies of the underlying molecular mechanisms of plasma cell malignancies. Here, such a system is described in which primary murine B cells rapidly become transformed into surface CD138+, IgM−/low, CD19− IgM‐secreting plasma cells as a result of expression of the transcription factors IRF4 and MYC together with simultaneous expression of BMI1, mutated p53 or silencing of p19Arf, and suppression of intrinsic apoptosis through expression of BCLXL. Analysis of gene expression patterns revealed that this combination of transforming genes resulted in expression of a number of genes previously associated with terminally differentiated B cells (plasma cells) and myeloma cells, whereas many genes associated with mature B cells and B‐cell lymphomas were not expressed. Upon transplantation, the transformed cells preferentially localized to the bone marrow, presenting features of a plasma cell malignancy of the IgM isotype. The present findings may also be applicable in the development of novel methods for production of monoclonal antibodies.

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BMI1: A Biomarker of Hematologic Malignancies

Cited by 38 publications

References 153 publications

Targeting BMI1 and MCL1 for Lung Adenocarcinoma Treatment

Targeting BMI1 and MCL1 for Lung Adenocarcinoma Treatment

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

Transformation of mature mouse B cells into malignant plasma cells in vitro via introduction of defined genetic elements

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