<i>MiR‐125b</i> targets BCL3 and suppresses ovarian cancer proliferation

Guan, Yunqian; Yao, Hailan; Zheng, Zhaohui; Qiu, Guang-Rong; Sun, Kun

doi:10.1002/ijc.25575

Cited by 132 publications

(107 citation statements)

References 34 publications

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“…Decreased expression of miR-125b was further detected in 13 ERBB2 (v-erb-b2 erythroblastic leukemia viral oncogene homolog 2) positive compared to 7 ERBB2 negative breast tumors (Mattie et al, 2006). Consistent with a potential tumor suppressor gene function, miR-125b was also shown to target the proto-oncogene BCL3 (B-cell CLL/ lymphoma 3) in ovarian cancer (Guan et al, 2011;Zhang et al, 2011) and E2F3 (E2F transcription factor 3), a major cell cycle regulator, in bladder cancer and ETS1, a member of ETS transcription factor family, in breast cancer (Zhang et al, 2011). Another confirmed target of miR-125 family is MUC I (Mucin I) oncogene in breast cancer (Rajabi et al, 2010).…”

mentioning

confidence: 80%

miR-125b Targets ARID3B in Breast Cancer Cells

Akhavantabasi¹,

Sapmaz²,

Tuna³

et al. 2012

Cell Struct. Funct.

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ABSTRACT. Mounting evidence suggests involvement of deregulated microRNA (miRNA) expression during the complex events of tumorigenesis. Among such deregulated miRNAs in cancer, miR-125b expression is reported to be consistently low in breast cancers. In this study, we screened a panel of breast cancer cell lines (BCCLs) for miR-125b expression and detected decreased expression in 14 of 19 BCCLs. Due to the heterogeneity of breast cancers, MCF7 cells were chosen as a model system for ERBB2 independent breast cancers to restore miR-125b expression (MCF7-125b) to investigate the phenotypical and related functional changes. Earlier, miR-125b was shown to regulate cell motility by targeting ERBB2 in ERBB2 overexpressing breast cancer cells. Here we showed decreased motility and migration in miR-125b expressing MCF7 cells, independent of ERBB2. MCF7-125b cells demonstrated profoundly decreased cytoplasmic protrusions detected by phalloidin staining of filamentous actin along with decreased motility and migration behaviors detected by in vitro wound closure and transwell migration assays compared to empty vector transfected cells (MCF7-EV). Among possible numerous targets of miR-125b, we showed ARID3B (AT-rich interactive domain 3B) to be a novel target with roles in cell motility in breast cancer cells. When ARID3B was transiently silenced, the decreased cell migration was also observed. In light of these findings, miR-125b continues to emerge as an interesting regulator of cancer related phenotypes.

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mentioning

confidence: 80%

miR-125b Targets ARID3B in Breast Cancer Cells

Akhavantabasi¹,

Sapmaz²,

Tuna³

et al. 2012

Cell Struct. Funct.

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“…MiR-125b-5p is upregulated in many cancers but downregulated in others, such as breast cancer, and controls many different cellular processes by targeting numerous transcription factors such as ETS1, E2F3, and BCL3 (23)(24)(25). In addition, we have identified new miRNAs that have not been associated with breast cancer before, such as miR-3613-3p, miR-4668-5p, miR-4516, miR-548as-3p, miR-4488, miR-3656, and miR-5704, expanding the knowledge on miRNA deregulation in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Tumor MicroRNA Expression Profiling Identifies Circulating MicroRNAs for Early Breast Cancer Detection

Vargas²,

et al. 2015

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“…Despite this, the role of Bcl3 in endogenous tumor pathology is poorly defined. Previous studies have focused on the effects of Bcl3 in tumor cell lines and have identified roles in proliferation (8)(9)(10)(11) and cell survival (12) in vitro, whereas one study showed that ectopic expression of Bcl3 in an estrogen receptor (ER)-positive breast cancer cell line (MCF-7) promoted hormone-independent growth in xenografts (44). Here, we addressed the role of Bcl3 in endogenous tumor development in vivo, using a transgenic mouse model of spontaneous breast cancer progression.…”

Section: Discussionmentioning

confidence: 99%

“…One of these Stat3-responsive genes, Bcl3, is a proto-oncogene originally described in B-cell lymphomas that has previously been shown to be constitutively expressed in a small study of breast cancer tissues (6,7). The precise role for Bcl3 in tumor pathology is currently unknown, but studies in cell lines suggest that it upregulates cell proliferation and survival (8)(9)(10)(11)(12). Similarly, there is no known role for Bcl3 in either the normal or neoplastic mammary gland, yet is a cofactor of the inflammatory mediator NF-kB (6), which is associated with mammary epithelial cell survival (13) and malignant progression in HER2-and EGFR1-positive mammary tumors (14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Bcl3 Selectively Promotes Metastasis of ERBB2-Driven Mammary Tumors

et al. 2013

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Bcl3 is a putative proto-oncogene deregulated in hematopoietic and solid tumors. Studies in cell lines suggest that its oncogenic effects are mediated through the induction of proliferation and inhibition of cell death, yet its role in endogenous solid tumors has not been established. Here, we address the oncogenic effect of Bcl3 in vivo and describe how this Stat3-responsive oncogene promotes metastasis of ErbB2-positive mammary tumors without affecting primary tumor growth or normal mammary function. Deletion of the Bcl3 gene in ErbB2-positive (MMTV-Neu) mice resulted in a 75% reduction in metastatic tumor burden in the lungs with a 3.6-fold decrease in cell turnover index in these secondary lesions with no significant effect on primary mammary tumor growth, cyclin D1 levels, or caspase-3 activity. Direct inhibition of Bcl3 by siRNA in a transplantation model of an Erbb2-positive mammary tumor cell line confirmed the effect of Bcl3 in malignancy, suggesting that the effect of Bcl3 was intrinsic to the tumor cells. Bcl3 knockdown resulted in a 61% decrease in tumor cell motility and a concomitant increase in the cell migration inhibitors Nme1, Nme2, and Nme3, the GDP dissociation inhibitor Arhgdib, and the metalloprotease inhibitors Timp1 and Timp2. Independent knockdown of Nme1, Nme2, and Arhgdib partially rescued the Bcl3 motility phenotype. These results indicate for the first time a cell-autonomous disease-modifying role for Bcl3 in vivo, affecting metastatic disease progression rather than primary tumor growth. Cancer Res; 73(2); 745-55. Ó2012 AACR.

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MiR‐125b targets BCL3 and suppresses ovarian cancer proliferation

Cited by 132 publications

References 34 publications

miR-125b Targets ARID3B in Breast Cancer Cells

miR-125b Targets ARID3B in Breast Cancer Cells

Tumor MicroRNA Expression Profiling Identifies Circulating MicroRNAs for Early Breast Cancer Detection

Bcl3 Selectively Promotes Metastasis of ERBB2-Driven Mammary Tumors

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