BMI-1 interacts with sMEK1 and inactivates sMEK1-induced apoptotic cell death

Kim, Boh Ram; Kwon, Young Joo; Rho, Seung Bae

doi:10.3892/or.2016.5262

Cited by 9 publications

(7 citation statements)

References 55 publications

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“…In accordance, other studies found that BMI1 was involved in inducing epithelial mesenchymal transition, leading to tumor invasion and metastasis [ 26 ]. Moreover, over-expression of BMI1 in EOC cells was found to up-regulate the expression of cyclin D1, CDK4 and Bcl-2, promoting cell growth and inhibiting cell apoptosis [ 27 ]. In contrast, silencing BMI1 in our study manifested a reverse impact on regulation of the cell cycle and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Role of BMI1 in epithelial ovarian cancer: investigated via the CRISPR/Cas9 system and RNA sequencing

et al. 2018

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BackgroundB-cell-specific Moloney murine leukemia virus integration site 1 (BMI1) might be an appropriate biomarker in the management of epithelial ovarian cancer (EOC). However, the biological role of BMI1 and its relevant molecular mechanism needs further elaboration. Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system is an excellent genome-editing tool and is scarcely used in EOC studies.MethodsWe first applied CRISPR/Cas9 technique to silence BMI1 in EOC cells; thereafter we accomplished various in vivo and in vitro experiments to detect biological behaviors of ovarian cancer cells, including MTT, flow cytometry, Transwell, real-time polymerase chain reaction and western blotting assays, etc.; eventually, we used RNA sequencing to reveal the underlying molecular traits driven by BMI1 in EOC.ResultsWe successfully shut off the expression of BMI1 in EOC cells using CRISPR/Cas9 system, providing an ideal cellular model for investigations of target gene. Silencing BMI1 could reduce cell growth and metastasis, promote cell apoptosis, and enhance the platinum sensitivity of EOC cells. BMI1 might alter extracellular matrix structure and angiogenesis of tumor cells through regulating Focal adhesion and PI3K/AKT pathways.ConclusionBMI1 is a potential biomarker in EOC management, especially for tumor progression and chemo-resistance. Molecular traits, including BMI1 and core genes in Focal adhesion and PI3K/AKT pathways, might be alternatives as therapeutic targets for EOC.Electronic supplementary materialThe online version of this article (10.1186/s13048-018-0406-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Role of BMI1 in epithelial ovarian cancer: investigated via the CRISPR/Cas9 system and RNA sequencing

et al. 2018

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“…[ 90 , 91 , 92 , 93 ]. Bmi-1 can also activate the PI3K/mTOR/4EBP1 signaling pathway in ovarian cancer cells to regulate cell proliferation [ 94 ]. N-acetylglucosamine transferase (OGT) is the only known enzyme to catalyze the O-GlcNAcylation in humans.…”

Section: Bmi-1-targeted Processes In Cancermentioning

confidence: 99%

The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies

Shi

et al. 2022

IJMS

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B-cell-specific Moloney murine leukemia virus integration region 1 (Bmi-1, also known as RNF51 or PCGF4) is one of the important members of the PcG gene family, and is involved in regulating cell proliferation, differentiation and senescence, and maintaining the self-renewal of stem cells. Many studies in recent years have emphasized the role of Bmi-1 in the occurrence and development of tumors. In fact, Bmi-1 has multiple functions in cancer biology and is closely related to many classical molecules, including Akt, c-MYC, Pten, etc. This review summarizes the regulatory mechanisms of Bmi-1 in multiple pathways, and the interaction of Bmi-1 with noncoding RNAs. In particular, we focus on the pathological processes of Bmi-1 in cancer, and explore the clinical relevance of Bmi-1 in cancer biomarkers and prognosis, as well as its implications for chemoresistance and radioresistance. In conclusion, we summarize the role of Bmi-1 in tumor progression, reveal the pathophysiological process and molecular mechanism of Bmi-1 in tumors, and provide useful information for tumor diagnosis, treatment, and prognosis.

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“…Previous studies have found the overexpression of BMI‐1 in many cancers and tumor cells and have suggested that BMI‐1 may be a new target for the treatment of many types of cancers and tumors [13–15]. Recently, the effects of BMI‐1 gene silencing on cell cycle and apoptosis rate were confirmed in cancer cells [16]. A high BMI‐1 protein expression was detected in many hematopoietic and malignant solid tumors; thus, the crucial role of BMI‐1 in the treatment of many tumors has been suggested [17].…”

Section: Introductionmentioning

confidence: 98%

ShRNA‐mediated BMI‐1 gene silencing inhibits gastrointestinal stromal tumor cell telomerase activity and enhances apoptosis

Wang

Xiao

et al. 2018

The Kaohsiung J of Med Scie

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Gastrointestinal stromal tumors (GISTs) are the most frequently occurring mesenchymal tumors of the gastrointestinal tract. Telomerase activity is well acknowledged as a critical factor in oncogenesis. The objective of the present study is to evaluate the effect of BMI gene silencing on proliferation, apoptosis and telomerase activity in human GIST882 cells. GIST882 cells were transfected with a eukaryotic expression vector of an shRNA fragment. The silencing efficiency in the GIST882 cells was determined by RT‐qPCR and a western blot analysis. After the shRNA‐BMI‐1 plasmid was transfected into the GIST882 cells and nude mice, a cell counting kit‐8 (CCK‐8) assay and flow cytometry were utilized to detect the GIST882 cell proliferation, the apoptosis rate and the cell cycle. Tumor growth was observed by tumor xenograft in nude mice. Telomerase activity and telomere length were detected by a Southern blot and a target region amplified polymorphism. The shRNA‐BMI‐1 recombinant plasmid was successfully constructed. The mRNA and protein expression of the BMI‐1 gene in GIST882 cells was suppressed by the shRNA‐BMI‐1 recombinant plasmid. Meanwhile, BMI‐1 gene silencing inhibited the cell proliferation, tumor growth, and cell cycle in the GIST882 cells. However, cell apoptosis was increased and telomerase activity was decreased with the silencing of the BMI‐1 gene. Collectively, the results of this study suggest that silencing the BMI‐1 gene may provide a new target for the treatment of GISTs.

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BMI-1 interacts with sMEK1 and inactivates sMEK1-induced apoptotic cell death

Cited by 9 publications

References 55 publications

Role of BMI1 in epithelial ovarian cancer: investigated via the CRISPR/Cas9 system and RNA sequencing

Role of BMI1 in epithelial ovarian cancer: investigated via the CRISPR/Cas9 system and RNA sequencing

The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies

ShRNA‐mediated BMI‐1 gene silencing inhibits gastrointestinal stromal tumor cell telomerase activity and enhances apoptosis

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