MicroRNA-191, an estrogen-responsive microRNA, functions as an oncogenic regulator in human breast cancer

Nagpal, Neha; Ahmad, Hafiz; Molparia, Bhuvan; Kulshreshtha, Ritu

doi:10.1093/carcin/bgt107

Cited by 102 publications

(124 citation statements)

References 57 publications

(48 reference statements)

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“…These data are not surprising as it is widely reported that the cellular context, and, thereby, the expression of the miRNA-targettable genes may have a critical role in determining the oncogenic or tumor suppressor effect of a miRNA. Consistently, it has been demonstrated miR-191 expression strongly correlates with cellular ERa (Estrogen Receptor a) status in breast cancer cells: in ERa-positive cells miR-191/425 act as oncogenes promoting cell proliferation, migration and chemoresistance [32,33]. Conversely, in ERa-negative cells, the same miRNAs impair tumor growth and cell invasion leading to a more epithelial phenotype to highly aggressive breast cancer cells [33].…”

Section: Ctx: Cetuximabmentioning

confidence: 67%

MiR-199a-5p and miR-375 affect colon cancer cell sensitivity to cetuximab by targeting PHLPP1

Mussnich¹,

Rosa

Bianco

et al. 2015

Expert Opinion on Therapeutic Targets

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Section: Ctx: Cetuximabmentioning

confidence: 67%

MiR-199a-5p and miR-375 affect colon cancer cell sensitivity to cetuximab by targeting PHLPP1

Mussnich¹,

Rosa

Bianco

et al. 2015

Expert Opinion on Therapeutic Targets

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“…15 Mounting evidence has shown that SOCS2 is overexpressed in multiple cancers and can enhance cell proliferation and neoplastic transformation. 16,17 However, the status and function of SOCS2 have never been documented in GC. Previous studies had demonstrated that H. pylori infection could lead to the activation of SOCS protein expression.…”

Section: Discussionmentioning

confidence: 99%

MiR-101 inhibits cell growth and tumorigenesis of Helicobacter pylori related gastric cancer by repression of SOCS2

Zhou¹,

Xia

Li³

et al. 2015

Cancer Biology & Therapy

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These authors contributed equally to the work.Keywords: cell growth, cell-cycle regulators, gastric cancer, Helicobacter pylori, miR-101; SOCS2, tumorigenesis Abbreviations: CDK, cyclin-dependent kinase; GC, gastric cancer; miRNA, microRNA; MOI, multiplicity of infection; mt, mutant; PVDF, polyvinylidene difluoride; qRT-PCR, quantitative real-time; UTR, untranslated regions; wt, wild-type Several microRNAs (miRNA) have been implicated in H. pylori related gastric cancer (GC). However, the molecular mechanism of miRNAs in gastric cancer has not been fully understood. In this study, we reported that miR-101 is significantly down-regulated in H. pylori positive tissues and cells and in tumor tissues with important functional consequences. Ectopic expression of miR-101 dramatically suppressed cell proliferation and colony formation by inducing G1-phase cell-cycle arrest. We found that miR-101 strongly reduced the expression of SOCS2 oncogene in GC cells. Similar to the restoring miR-26 expression, SOCS2 down-regulation inhibited cell growth and cell-cycle progression, whereas SOCS2 over-expression rescued the suppressive effect of miR-101. Mechanistic investigations revealed that miR-101 suppressed the expression of c-myc, CDK2, CDK4, CDK6, CCND2, CCND3, and CCNE2, while promoted tumor suppressor p14, p16, p21 and p27 expression. In clinical specimens, SOCS2 was over-expressed in tumors and H. pylori positive tissues and its mRNA levels were inversely correlated with miR-101 expression. Taken together, our results indicated that miR-101 functions as a growth-suppressive miRNA in H. pylori related GC, and that its suppressive effects are mediated mainly by repressing SOCS2 expression.

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“…Human breast cancer line used, regarded as a non-aggressive one, has been widely used as a model in the studies of the SATB1 protein due to its easy-to-control expression level [37][38][39][40]. There are studies showing that SATB1 reprograms chromatin organization and transcription profiles of breast tumors to promote growth and metastasis [39].…”

Section: Discussionmentioning

confidence: 99%

The alterations in SATB1 and nuclear F-actin expression affect apoptotic response of the MCF-7 cells to geldanamycin

Grzanka

Izdebska

Klimaszewska‐Wiśniewska

et al. 2015

Folia Histochem Cytobiol.

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Introduction. The function and localization of actin in the nucleus have not yet been fully described. However, actin seems to be a key protein in nuclear processes interacting with chromatin and matrix proteins. The aim of the study was to evaluate the effect of controlled expression of nuclear pool of F-actin and special AT-rich sequence-binding protein 1 (SATB1) on the in vitro induction of active cell death by geldanamycin (GA). Material and methods. The expression of SATB1 was regulated by the transfection of non-aggressive breast cancer MCF-7 cells with siRNA against SATB1 or expression plasmid with cloned cDNA of SATB1. The altered expression of cofilin-1 in these cells was used to regulate the nuclear expression and localization of F-actin. The effect of GA was analyzed in the context of cell death induction and cell cycle alterations. Results. Our studies revealed that the targeted regulation of SATB1 and cofilin-1 expression changed the apoptotic response of the MCF-7 cells to GA. The overexpression of these proteins potentiated GA-induced arrest of the cells in the G1 phase of cell cycle and increased the population of the hypodiploid cells. Conclusion. The alterations in the nuclear expression of SATB1 and F-actin in MCF-7 cells may affect their active cell death in response to GA.

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MicroRNA-191, an estrogen-responsive microRNA, functions as an oncogenic regulator in human breast cancer

Cited by 102 publications

References 57 publications

MiR-199a-5p and miR-375 affect colon cancer cell sensitivity to cetuximab by targeting PHLPP1

MiR-199a-5p and miR-375 affect colon cancer cell sensitivity to cetuximab by targeting PHLPP1

MiR-101 inhibits cell growth and tumorigenesis of Helicobacter pylori related gastric cancer by repression of SOCS2

The alterations in SATB1 and nuclear F-actin expression affect apoptotic response of the MCF-7 cells to geldanamycin

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