Overexpression of <scp>BMI</scp>‐1 is associated with poor prognosis in cervical cancer

Tong, Yongqing; Liu, Bei; Zheng, Hongyun; He, Ying; Gu, Jian; Li, Feng

doi:10.1111/j.1743-7563.2012.01564.x

Cited by 32 publications

(29 citation statements)

References 25 publications

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“…Consistent with our results, research on ovarian cancer [35], breast cancer [36, 37], clear cell renal cancer [38], laryngeal carcinoma [39], cervical cancer [40], and esophageal adenocarcinoma [41] have reported an association between high Bmi-1 expression and an unfavorable prognosis. It has also been reported that high expression of Bmi-1 in AML cells is associated with an unfavorable prognosis [42].…”

Section: Discussionsupporting

confidence: 92%

Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia

et al. 2017

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BackgroundBmi-1, the B cell-specific moloney murine leukemia virus insertion site 1, is a member of the Polycomb-group (PcG) family and acts as an oncogene in various tumors; however, its expression related to the prognosis of pediatric patients with acute lymphoblastic leukemia (ALL) has not been well studied.MethodsThe Bmi-1 expression levels in the bone marrow of 104 pediatric ALL patients and 18 normal control subjects were determined by using qRT-PCR. The association between the Bmi-1 expression and the clinicopathological characteristics of pediatric ALL patients was analyzed, and the correlation between Bmi-1 and the prognosis of pediatric ALL was calculated according to the Kaplan–Meier method. Furthermore, the association between Bmi-1 expression and its transcriptional regulator Sall4 was investigated.ResultsCompared to normal control subjects, patients with primary pediatric ALL exhibited upregulated levels of Bmi-1. However, these levels were sharply decreased in patients who achieved complete remission. A significant positive association between elevated Bmi-1 levels and a poor response to prednisone as well as an increased clinical risk was observed. Patients who overexpressed Bmi-1 at the time of diagnosis had a lower relapse-free survival (RFS) rate (75.8%), whereas patients with lower Bmi-1 expression had an RFS of 94.1%. Furthermore, in ALL patients, the mRNA expression of Bmi-1 was positively correlated to the mRNA expression of Sall4a.ConclusionsTaken together, these data suggest that Bmi-1 could serve as a novel prognostic biomarker in pediatric primary ALL and may be partially regulated by Sall4a. Our study also showed that Bmi-1 could serve as a new therapeutic target for the treatment of pediatric ALL.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-017-3049-3) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 92%

Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia

et al. 2017

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“…B lymphoma Mo-MLV insertion region 1 homolog (BMI-1), a member of the polycomb group (PcG), functions as a transcriptional repressor and presents with high expression in many tumors including HCC, indicating a poor prognosis (22,23). BMI-1 has been shown to be an oncogene that regulates cell proliferation and transformation (19).…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of miR-218 in human hepatocellular carcinoma and its role in cell growth

Zheng

et al. 2014

Oncology Reports

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MicroRNA-218 (miR-218) is considered a tumor suppressor in human cancer. In the present study, miR-218 expression was found to be significantly lower in human hepatocellular carcinoma (HCC) than in normal tumor-adjacent tissues. miR-218 was clearly silenced or downregulated in five HCC cells (HepG2, Hep3B, SMMC-7721, Huh7 and Bel-7402) compared with normal hepatocytes (LO2). The low expression of miR-218 conferred a poor 5-year survival in HCC patients. Multivariate Cox regression analysis indicated that miR-218 was an independent prognostic factor in HCC. Ectopic expression of miR-218 inhibited proliferation and promoted apoptosis in HepG2 and SMMC-7721 cells. In tumor bearing mice, miR-218 slowed down tumor growth by inducing apoptosis and growth arrest. Restoring miR-218 expression resulted in downregulation of B lymphoma Mo-MLV insertion region 1 homolog (BMI-1) mRNA and protein level in HepG2 and SMMC-7721 cells. In addition, BMI-1 mRNA expression in HCC was significantly higher than that in non-cancerous tissues. BMI-1 mRNA was inversely correlated with miR-218 expression in HCC tissues. In conclusion, miR-218 may serve as a prognostic biomarker and induce apoptosis and growth arrest by downregulating BMI-1 in HCC.

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“…Bmi1 is overexpressed in various solid cancers (47,48), including CRC (49), where increased Bmi1 expression correlates with poor prognosis (50). Bmi-1 is a regulatory subunit of the polycomb repressor complex 1.…”

Section: Discussionmentioning

confidence: 99%

Partial inhibition of gp130-Jak-Stat3 signaling prevents Wnt–β-catenin–mediated intestinal tumor growth and regeneration

et al. 2014

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Most colon cancers arise from somatic mutations in the tumor suppressor gene APC (adenomatous polyposis coli), and these mutations cause constitutive activation of the Wnt-to-β-catenin pathway in the intestinal epithelium. Because Wnt-β-catenin signaling is required for homeostasis and regeneration of the adult intestinal epithelium, therapeutic targeting of this pathway is challenging. We found that genetic activation of the cytokine-stimulated pathway mediated by the receptor gp130, the associated Jak (Janus kinase) kinases, and the transcription factor Stat3 (signal transducer and activator of transcription 3) was required for intestinal regeneration in response to irradiation-induced damage in wild-type mice and for tumorigenesis in Apc-mutant mice. Systemic pharmacological or partial genetic inhibition of gp130-Jak-Stat3 signaling suppressed intestinal regeneration, the growth of tumors in Apc-mutant mice, and the growth of colon cancer xenografts. The growth of Apc-mutant tumors depended on gp130-Jak-Stat3 signaling for induction of the polycomb repressor Bmi-1, and the associated repression of genes encoding the cell cycle inhibitors p16 and p21. However, suppression of gp130-Jak-Stat3 signaling did not affect Wnt-β-catenin signaling or homeostasis in the intestine. Thus, these data not only suggest a molecular mechanism for how the gp130-Jak-Stat3 pathway can promote cancer but also provide a rationale for therapeutic inhibition of Jak in colon cancer.

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Overexpression of BMI‐1 is associated with poor prognosis in cervical cancer

Cited by 32 publications

References 25 publications

Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia

Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia

Prognostic significance of miR-218 in human hepatocellular carcinoma and its role in cell growth

Partial inhibition of gp130-Jak-Stat3 signaling prevents Wnt–β-catenin–mediated intestinal tumor growth and regeneration

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