Growth inhibition by microRNAs that target the insulin receptor substrate-1

Rocca, Gaspare La; Shi, Bin; Badin, Margherita; Angelis, Tiziana De; Sepp‐Lorenzino, Laura; Baserga, Renato

doi:10.4161/cc.8.14.9026

Cited by 18 publications

(11 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1 miR-145 inhibits cancer cell growth by targeting the Insulin receptor substrate-1. 41 This miR can downregulate estrogen receptor-α (ER-α) protein expression through direct interaction with two complementary sites within its coding sequence. 42 In the same study it was reported that miR-145 exhibited a pro-apoptotic effect that was Tp53 activation-dependent.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA expression analysis in triple-negative (ER, PR and Her2/neu) breast cancer

Zaravinos²,

et al. 2011

View full text Add to dashboard Cite

miRNAs are small, regulatory molecules approximately 21-24 nucleotides in length. They function at the post-transcriptional level by controlling the expression of more than 50% of human protein-coding genes and play an essential role in cell signaling pathways. The objective of the present study was to explore the expression profile of oncomiRs and tumor-suppressor miRs, and to define their possible correlations in triple-negative (ER, PR and Her2/neu) primary breast cancers. Forty-nine primary triple-negative breast cancer cases, along with 34 matched tumor-associated normal samples were investigated for the expression of 9 miRNAs using qPCR. Relationships between the expression of miR-10b, miR-21, miR-122a, miR-145, miR-205, miR-210, miR-221, miR-222 and miR-296 and the pathologic features of the tumors were examined, as were the influences of miR expression on patient overall and cancer-specific survival. miR-21, miR-210 and miR-221 were significantly overexpressed, whereas miR-10b, miR-145, miR-205, miR-122a were significantly underexpressed in the triple-negative primary breast cancers. Significant correlations among all of the studied miRs were scored both in the breast cancer and control tissue. Expression of miR-222 and miR-296 did not exhibit any significant difference between the breast cancer and normal tissue. There was a non-significant trend for high expression levels of the microRNAs, miR-21, miR-210, miR-221 and miR-222, to be associated with worse patient disease-free and overall survival. miR-21, miR-210 and miR-221 expression plays a significant role in triple- negative primary breast cancers.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA expression analysis in triple-negative (ER, PR and Her2/neu) breast cancer

Zaravinos²,

et al. 2011

View full text Add to dashboard Cite

show abstract

“…ATRA induces down-regulation of IRS-1 (but not IRS-2) in MCF-7 cells and over-expression of IRS-1 causes resistance to ATRA [24]. miR145 down-regulates both the type 1 insulin-like growth factor receptor (IGF-IR) and its docking protein, the insulin receptor substrate-1 (IRS-1), but not the other docking protein, IRS-2, and inhibits growth of human cancer cells [14,15,25]. The differential effect of ATRA on the two IRS proteins suggested a role of miR145 in ATRA action.…”

Section: All-trans Retinoic Acid Increases Mir145 Expressionmentioning

confidence: 99%

Regulation of microRNA-145 by growth arrest and differentiation

Rocca

Shu

Audia

et al. 2011

Experimental Cell Research

Self Cite

View full text Add to dashboard Cite

“…Previous studies have also identified IGF-I/IRS1 as direct targets of miR-145. 29,30 Importantly, although most of miRNAs have multiple targets, miR-145 seems to affect its tumor suppressor activity predominantly by repressing IRS1, the docking protein of the IGF-IR. 30 Our data have suggested that miR-145 also directly target N-RAS and VEGF-A, further enhancing knowledge about the miR-145-dependent network.…”

Section: Discussionmentioning

confidence: 99%

“…27,28 Interestingly, IGF-I/IRS1 was found to be a predominant target of miR-145. 29,30 Therefore, it is reasonable to speculate that miR-145 regulates the downstream genes of IGF-I/IRS1, including N-RAS and VEGF. However, it remains unclear to date whether these two genes are direct targets of miR-145 and whether miR-145 functionally affects angiogenesis.…”

Section: Introductionmentioning

confidence: 99%