NRG-3 in human breast cancers: activation of multiple erbB family proteins.

Hijazi, Mai; Young, Philippa; Dougherty, M. K.; Bressette, D. S.; Cao, Tianzhu; Pierce, Jacalyn H.; Wong, Ling M.; Alimandi, Maurizio; King, C. Richter

doi:10.3892/ijo.13.5.1061

Cited by 17 publications

(18 citation statements)

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“…Our results are consistent with the published observation that a recombinant NRG3 fusion protein fails to compete with radiolabeled NRG1b for binding to a recombinant ErbB3 fusion protein (Jones et al, 1999). However, the observation that NRG3 stimulates ErbB2 and ErbB3 tyrosine phosphorylation in 32D cells devoid of endogenous ErbB family receptors (Hijazi et al, 1998) contrasts our results. Of course, coexpression of ErbB2 and ErbB3 in 32D cells permits EGF stimulation of receptor coupling to IL3 independence and mitogenesis (Pinkas-Kramarski et al, 1998).…”

Section: Discussioncontrasting

confidence: 51%

Neuregulin isoforms exhibit distinct patterns of ErbB family receptor activation

Hobbs

Coffing

et al. 2002

Oncogene

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Section: Discussioncontrasting

confidence: 51%

Neuregulin isoforms exhibit distinct patterns of ErbB family receptor activation

Hobbs

Coffing

et al. 2002

Oncogene

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“…Cell lines MDA-MD-453 and T47D were stimulated to grow by two NRG2 isoforms. 89 NRG3 was expressed in breast cancer cell lines, and the EGF-like domain of NRG3, as a recombinant protein, activated ERBB2/ ERBB3 in breast cancer cells and altered their growth, 90 although it had little affinity in a direct-binding assay. 84 NRG4 appears to be specific for ERBB4.…”

Section: Erbb3 Interacting Proteins: Activation Signaling and Regulamentioning

confidence: 99%

The ERBB3 receptor in cancer and cancer gene therapy

2008

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ERBB3, a member of the epidermal growth factor receptor (EGFR) family, is unique in that its tyrosine kinase domain is functionally defective. It is activated by neuregulins, by other ERBB and nonERBB receptors as well as by other kinases, and by novel mechanisms. Downstream it interacts prominently with the phosphoinositol 3-kinase/AKT survival/mitogenic pathway, but also with GRB, SHC, SRC, ABL, rasGAP, SYK and the transcription regulator EBP1. There are likely important but poorly understood roles for nuclear localization and for secreted isoforms. Studies of ERBB3 expression in primary cancers and of its mechanistic contributions in cultured cells have implicated it, with varying degrees of certainty, with causation or sustenance of cancers of the breast, ovary, prostate, certain brain cells, retina, melanocytes, colon, pancreas, stomach, oral cavity and lung. Recent results link high ERBB3 activity with escape from therapy targeting other ERBBs in lung and breast cancers. Thus a wide and centrally important role for ERBB3 in cancer is becoming increasingly apparent. Several approaches for targeting ERBB3 in cancers have been tested or proposed. Small inhibitory RNA (siRNA) to ERBB3 or AKT is showing promise as a therapeutic approach to treatment of lung adenocarcinoma.

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“…The mammary phenotypes observed in the A/J strain are all consistent with defective specification events occurring prior to the morphological appearance of the mammary bud. Here we provide evidence that the gene affected in ska mice encodes the Erbb4 ligand, Neuregulin3 (Nrg3) (Zhang et al 1997;Hijazi et al 1998;Gizatullin et al 2000). Taken together, these results indicate that Nrg3 is a specification signal for mammary buds.…”

mentioning

confidence: 99%

Identification of the scaramanga gene implicates Neuregulin3 in mammary gland specification

Howard

Panchal²,

McCarthy³

et al. 2005

Genes Dev.

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The mouse scaramanga (ska) mutation impairs mammary gland development such that both abrogation and stimulation of gland formation occurs. We used positional cloning to narrow the interval containing scaramanga (ska) to a 75.6-kb interval containing the distal part of the Neuregulin3 (Nrg3) gene. Within this region the only sequence difference between ska and wild-type mice is in a microsatellite repeat within intron 7. This alteration correlates with variations in Nrg3 expression profiles both at the whole embryo level and locally in the presumptive mammary region in ska mice. Localized expression of Nrg3 and its receptor, Erbb4, in the presumptive mammary region around the future bud site prior to morphological appearance of buds and the expression of bud epithelial markers further support an inductive role. Finally, Neuregulin3 (Nrg3)-soaked beads can induce expression of the early bud marker Lef1 in mouse embryo explant cultures, and epithelial bud formation can be observed histologically, suggesting that initiation of mammary bud development occurs. Taken together, these results indicate that a Neuregulin signaling pathway is involved in specification of mammary gland morphogenesis and support the long-held view that mesenchymal signal(s) are responsible for mammary gland inductive/initiating events.[Keywords: Mammary gland development; Neuregulin3; specification] Supplemental material is available at http://www.genesdev.org.

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NRG-3 in human breast cancers: activation of multiple erbB family proteins.

Cited by 17 publications

References 0 publications

Neuregulin isoforms exhibit distinct patterns of ErbB family receptor activation

Neuregulin isoforms exhibit distinct patterns of ErbB family receptor activation

The ERBB3 receptor in cancer and cancer gene therapy

Identification of the scaramanga gene implicates Neuregulin3 in mammary gland specification

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