MiR-205 in cancer: An angel or a devil?

Qin, Ai Ying; Zhang, Xin Wei; Liu, Liang; Yu, Jin; Li, Hui; Wang, Shi Zhen Emily; Ren, Xiu Bao; Cao, Shui

doi:10.1016/j.ejcb.2012.11.002

Cited by 118 publications

(117 citation statements)

References 68 publications

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“…MiR-205, transcribed from the MIR205HG gene located in the second intron of LOC642587 locus in chromosome 1, is observed to express predominantly in epithelial tissues [25]. As a highly conserved miRNA, it was originally predicted by computational approaches according to the conservation with mouse and Fugu rubripes sequences [26].…”

Section: Discussionmentioning

confidence: 99%

MiR-205 promotes motility of ovarian cancer cells via targeting ZEB1

Ning

Shen

Zhang

et al. 2015

Gene

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Section: Discussionmentioning

confidence: 99%

MiR-205 promotes motility of ovarian cancer cells via targeting ZEB1

Ning

Shen

Zhang

et al. 2015

Gene

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“…As a consequence, tumor cells shed from the primary tumor into the circulation system, and position in the new site. In addition, Qin et al (49) showed that hnRNP K is a target of miR-205. miR-205 has a complex regulatory role in tumor initiation and growth processes.…”

Section: Hnrnp K Interacts With Non-coding Rnas (Ncrnas) To Promote Tmentioning

confidence: 98%

Role and molecular mechanism of heterogeneous nuclear ribonucleoprotein K in tumor development and progression

Gao

2016

Biomedical Reports

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Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is a member of the hnRNP family, which exists in the nucleus and the cytoplasm simultaneously. It is a multifunctional protein that can participate in a variety of regulatory progressions of gene expression and signal transduction, such as chromatin remodeling, transcription, RNA alternative splicing and translation. hnRNP K not only directly binds to the kinases, but also recruits the associated factors regarding transcription, splicing and translation to control gene expression, and therefore, it serves as a docking platform for integrating transduction pathways to nucleic acid-directed processes. Numerous studies also show that abnormal expression of hnRNP K is closely associated with the tumor formation. This protein is overexpressed in numerous types of cancer and its aberrant cytoplasmic localization is also associated with a worse prognosis for patients. These results consistently indicate that hnRNP K has a key role in cancer progression. To understand the hnRNP K pathophysiological process in tumor disease, the previous research results regarding the association between hnRNP K and tumors were reviewed.

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“…Notably, low expression of miR-205 predicts a chemotherapy relapse in cancer patients who have triple-negative breast cancer (TNBC) (9), where a high content of the cancer stem cell population is enriched. It is intriguing that emerging in vitro studies reveal complex roles of miR-205 as either a tumor suppressor or an oncogene, depending on different cell contexts (10). Nonetheless, the role of miR-205 in breast cancer in vivo and the mechanism by which miR-205 is regulated during tumorigenesis still remain unclear.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

Chao¹,

Chang²,

Wu³

et al. 2014

J. Clin. Invest.

100

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Dysregulation of epigenetic controls is associated with tumorigenesis in response to microenvironmental stimuli; however, the regulatory pathways involved in epigenetic dysfunction are largely unclear. We have determined that a critical epigenetic regulator, microRNA-205 (miR-205), is repressed by the ligand jagged1, which is secreted from the tumor stroma to promote a cancer-associated stem cell phenotype. Knockdown of miR-205 in mammary epithelial cells promoted epithelial-mesenchymal transition (EMT), disrupted epithelial cell polarity, and enhanced symmetric division to expand the stem cell population. Furthermore, miR-205-deficient mice spontaneously developed mammary lesions, while activation of miR-205 markedly diminished breast cancer stemness. These data provide evidence that links tumor microenvironment and microRNA-dependent regulation to disruption of epithelial polarity and aberrant mammary stem cell division, which in turn leads to an expansion of stem cell population and tumorigenesis. This study elucidates an important role for miR-205 in the regulation of mammary stem cell fate, suggesting a potential therapeutic target for limiting breast cancer genesis.

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MiR-205 in cancer: An angel or a devil?

Cited by 118 publications

References 68 publications

MiR-205 promotes motility of ovarian cancer cells via targeting ZEB1

MiR-205 promotes motility of ovarian cancer cells via targeting ZEB1

Role and molecular mechanism of heterogeneous nuclear ribonucleoprotein K in tumor development and progression

MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

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