Regulation of mammary epithelial cell phenotypes by the helix-loop-helix protein, Id-1.

Lin, Claudia Q.; Parrinello, Simona; Campisi, Judith; Desprez, Pierre Yves

doi:10.1677/erc.0.0060049

Cited by 11 publications

(4 citation statements)

References 6 publications

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“…Id1 was previously reported to be expressed in the mammary gland during the early stages of pregnancy, followed by a downregulation of Id1 concomitant with an upregulation of milk protein genes [6]. Id1 expression has also been shown to prevent terminal differentiation and production of milk proteins by immortalised mammary epithelial cells in culture [6], [7], [8], [17], [18]. While our earlier results suggested that Id1 is not expressed by luminal epithelia, it is possible that our histological analysis failed to identify a role for Id1 in luminal cell biology.…”

Section: Resultsmentioning

confidence: 99%

Redefining the Expression and Function of the Inhibitor of Differentiation 1 in Mammary Gland Development

et al. 2010

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The accumulation of poorly differentiated cells is a hallmark of breast neoplasia and progression. Thus an understanding of the factors controlling mammary differentiation is critical to a proper understanding of breast tumourigenesis. The Inhibitor of Differentiation 1 (Id1) protein has well documented roles in the control of mammary epithelial differentiation and proliferation in vitro and breast cancer progression in vivo. However, it has not been determined whether Id1 expression is sufficient for the inhibition of mammary epithelial differentiation or the promotion of neoplastic transformation in vivo. We now show that Id1 is not commonly expressed by the luminal mammary epithelia, as previously reported. Generation and analysis of a transgenic mouse model of Id1 overexpression in the mammary gland reveals that Id1 is insufficient for neoplastic progression in virgin animals or to prevent terminal differentiation of the luminal epithelia during pregnancy and lactation. Together, these data demonstrate that there is no luminal cell-autonomous role for Id1 in mammary epithelial cell fate determination, ductal morphogenesis and terminal differentiation.

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Section: Resultsmentioning

confidence: 99%

Redefining the Expression and Function of the Inhibitor of Differentiation 1 in Mammary Gland Development

et al. 2010

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“…It appears that Id-1 protein may be an important new target molecule for antiangiogenic drug design in cancer treatment. Several investigations have demonstrated that Id protein affects cell growth via the mechanisms of cell proliferation and/or apoptosis (Kim et al, 1999;Lin et al, 1999;Norton, 2000;Alani et al, 2001). It has been suggested that Id-1 and Id-2 proteins may function in the bHLH-mediated inactivation of the cyclindependent kinase inhibitors, for example, p21 WAF1 , p16 INK4a and p27 KIP1 (Prabhu et al, 1997;Polsky et al, 2001;Ouyang et al, 2002b;Singh et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Id-1 is significantly associated with tumour angiogenesis in human pancreas cancers

Lee

et al. 2004

Br J Cancer

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It has been suggested that Id-1 has a critical role in the tumour progression and aggressiveness of several human cancers. However, the clinicopathological and biological significance of Id-1 overexpression remains unclear in human primary cancer. To investigate the association between Id-1 expression and cell proliferation or tumour angiogenesis, we examined the cell cycle kinetic indices (the proliferation and apoptotic indices, PI and AI) and intratumoral microvessel density (MVD) in 65 human pancreatic cancers. We also investigated the relationship between its expression and various clinicopathological factors to determine the clinical significance of Id-1 overexpression. Out of a total 65 cases, 32 (49.3%) showed overexpression of Id-1 vs normal tissues. Id-1 expression was found to be significantly associated with MVD (P ¼ 0.002). In further analysis of subgroups with higher and lower Id-1 expression, tumours with higher Id-1 expression (scores 4 and 5) showed significantly higher MVD than tumours with lower expression of Id-1 (scores 2 and 3) (111.18757.14 vs 64.13728.19, Po0.001). However, no significant association was found between Id-1 overexpression and patient survival rate. No significant association was also found between Id-1 expression and cell cycle kinetic indices (PI or AI) in pancreatic cancer. Moreover, the overexpression of Id-1 protein was not correlated with any significant clinicopathologic factors. These findings indicate that Id-1 overexpression is closely related with tumour angiogenesis and a higher density of intratumoral vessel, but that it is not associated with a poorer prognosis of survival or a higher cell proliferative potential in human pancreatic cancer.

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“…Id-1 has multiple roles in cell proliferation, invasion, differentiation ,and antiapoptosis and it has shown to be necessary for mammary gland development and remodeling (Lin et al, 1999(Lin et al, , 2000Parrinello et al, 2001). Here, we generated a MMTV-Id-1 transgenic mouse model and investigated the role of Id-1 as a potential controller of mouse mammary gland development.…”

Section: Discussionmentioning

confidence: 99%

Constitutive overexpression of Id‐1 in mammary glands of transgenic mice results in precocious and increased formation of terminal end buds, enhanced alveologenesis, delayed involution

Shin

Jang

Kang

et al. 2011

Journal Cellular Physiology

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Inhibitor of differentiation-1 (Id-1) has been shown to play an essential role in cell proliferation, invasion, migration, and anti-apoptosis. However, the effect of Id-1 in mammary gland development remains unknown. Here, we generated MMTV-Id-1 transgenic mice to study the role of Id-1 in mammary gland development. In virgin mice, Id-1 overexpression led to precocious development and delayed regression of terminal end buds (TEBs) compared with wild-type mice. The number of BrdU-positive cells and the expression of Wnt signaling molecules, β-catenin and cyclin D1, which regulate ductal extension and TEB formation in virgin, were statistically higher in Id-1 transgenic mice than in wild-type mice. Id-1 also had an effect on the formation and proliferation of lobuloalveolar structures during early and mid-pregnancy. Id-1 transgenic mice had more lobulated and prominent alveolar budding than wild-type mice and had significantly greater counts of lobuloalveolar structures in early pregnancy. The expression of BrdU, β-catenin, and cyclin D1 was also predominantly increased in Id-1 transgenic mice. Moreover, Id-1 transgenic mice showed delayed involution. Id-1 regulated the expression levels of anti-apoptotic Bcl-2 and pro-apoptotic Bax, and resulted in delay of apoptotic peak during postlactational involution. We also found that Id-1 was able to modulate expression of the regulators of Wnt/β-catenin signaling such as phospho-Akt, BMP2, FGF3, and RAR-β in tubuloalveolar development of mammary glands. Taken together, our results suggest that Id-1 plays a pivotal role in mammary gland development through Wnt signaling-mediated acceleration of precocity and alveologenesis and Bcl-2 family members-mediated delay of involution.

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Regulation of mammary epithelial cell phenotypes by the helix-loop-helix protein, Id-1.

Cited by 11 publications

References 6 publications

Redefining the Expression and Function of the Inhibitor of Differentiation 1 in Mammary Gland Development

Redefining the Expression and Function of the Inhibitor of Differentiation 1 in Mammary Gland Development

Overexpression of Id-1 is significantly associated with tumour angiogenesis in human pancreas cancers

Constitutive overexpression of Id‐1 in mammary glands of transgenic mice results in precocious and increased formation of terminal end buds, enhanced alveologenesis, delayed involution

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