WISP-2 Gene in Human Breast Cancer: Estrogen and Progesterone Inducible Expression and Regulation of Tumor Cell Proliferation

Banerjee, Snigdha; Saxena, Neela K.; Sengupta, Krishanu; Tawfik, Ossama; Mayo, Matthew S.

doi:10.1016/s1476-5586(03)80018-0

Cited by 62 publications

(118 citation statements)

References 33 publications

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“…Importantly, they were able to extend this observation to the in vivo setting by showing a strong correlation between expression of CCN5 protein and estrogen receptor alpha (ER-α) positivity in human breast cancer samples (Banerjee et al 2003). Progesterone was also shown to induce CCN5 protein in ER-positive human breast cancer cells.…”

Section: Estrogen Signalingmentioning

confidence: 86%

“…Addition of 17β-estradiol to MCF-7 cells in culture increases expression of CCN5 mRNA and protein in a dose-dependent manner (Banerjee et al 2003;Inadera et al 2002). CCN5 protein levels in MCF-7 cells increase over 24 h and can reach maximum levels by 72 h (Banerjee et al 2003;Inadera et al 2002).…”

Section: Estrogen Signalingmentioning

confidence: 99%

“…However, stable transfection of ER-α into these cells restores the ability of estrogen to induce CCN5 expression (Banerjee et al 2003). There is some evidence to suggest that estrogen might also function to stabilize CCN5 mRNA (Banerjee et al 2003).…”

Section: Estrogen Signalingmentioning

confidence: 99%

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CCN5: biology and pathophysiology

Russo

Castellot

2010

Journal of Cell Communication and Signaling

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CCN5 is one of six proteins in the CCN family. This family of proteins has been shown to play important roles in many processes, including proliferation, migration, adhesion, extracellular matrix regulation, angiogenesis, tumorigenesis, fibrosis, and implantation. In this review, we focus on the biological and putative pathophysiological roles of CCN5. This intriguing protein is structurally unique among the CCN family members, and has a unique biological activity profile as well.

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Section: Estrogen Signalingmentioning

confidence: 86%

Section: Estrogen Signalingmentioning

confidence: 99%

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CCN5: biology and pathophysiology

Russo

Castellot

2010

Journal of Cell Communication and Signaling

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“…CCN5 has also been described in human fetal bone (Kumar et al 1999); human pancreas (Dhar et al 2007); and breast ductal and lobular epithelium (Banerjee et al 2003). CCN5 protein and mRNA has also been detected in numerous cultured cells and tissue specimens using Western and Northern blots, respectively (summarized in Gray and Castellot 2004).…”

Section: Discussionmentioning

confidence: 99%

CCN5 Expression in mammals. II. Adult rodent tissues

Gray

Malmquist

Sullivan

et al. 2007

J. Cell Commun. Signal.

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CCN5 is a secreted heparin-and estrogenregulated matricellular protein that inhibits vertebrate smooth muscle cell proliferation and motility. CCN5 is expressed throughout murine embryonic development in most organs and tissues. However, after embryonic development is complete, we hypothesized that CCN5 distribution would be largely restricted to small set of tissues, including smooth muscle cells of the arteries, uterus, airway, and digestive tract. Because CCN5 inhibits proliferation of smooth muscle cells in vitro, it might function to prevent excessive growth in vivo. In contrast, another member of the CCN family, CCN2, promotes smooth muscle cell proliferation in vitro, and thus it was expected that its expression levels would be low in uninjured normal adult tissues. Frozen sections from adult tissues and organs were analyzed immunohistochemically using anti-CCN5 and anti-CCN2 antibodies. Both proteins were detected in arteries, the uterus, bronchioles, and the digestive tract as expected, and also in many other tissues including the pancreas, spleen, liver, skeletal muscle, ovary, testis, thymus, brain, olfactory epithelium, and kidney. CCN5 and CCN2 protein was found in smooth muscle, endothelial cells, epithelial cells, skeletal muscle, cells of the nervous system, and numerous other cell types. In many cells, both CCN5 and CCN2 was present in the nucleus. Rather than having opposite patterns of localization, CCN5 and CCN2 often had similar sites of expression. The wide distribution of both CCN5 and CCN2 suggests that both proteins have additional biological functions beyond those previously identified in specific cellular and pathological models.

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“…Recent studies from our laboratory and others have suggested that WISP-2/CCN5 has a particular relevance to human breast disease (1,7,8). This is because WISP-2/CCN5 mRNA and protein levels were elevated in different human breast tumor-derived cell lines as well as in breast tumor samples while being barely detectable, or undetectable, in normal breast epithelial cells (7)(8)(9). Additionally, abnormal expression of the WISP-2/CCN5 gene was significantly higher in noninvasive carcinoma cells compared with invasive carcinoma cells.…”

Section: Introductionmentioning

confidence: 99%

Epidermal Growth Factor Induces WISP-2/CCN5 Expression in Estrogen Receptor-α-Positive Breast Tumor Cells through Multiple Molecular Cross-talks

Banerjee

Sengupta²,

Saxena³

et al. 2005

Molecular Cancer Research

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Epidermal growth factor (EGF) is a mitogen for estrogen receptor (ER) -positive breast tumor cells, and it has been proven that EGF occasionally mimicked estrogen action and cross-talks with ER-A to exert its activity. Therefore, the present study was undertaken to explore whether EGF is able to modulate the expression of Wnt-1-induced signaling protein-2/connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed 5 (WISP-2/CCN5), an estrogenresponsive gene, in normal and transformed cell lines of the human breast and, if so, whether this induction is critical for EGF mitogenesis and what downstream signaling pathways are associated with this event. Here, we show that EGF-induced WISP-2 expression in ER-and EGF receptor -positive noninvasive MCF-7 breast tumor cells was dose and time dependent and that expression was modulated at transcription level. A synergism was seen in combination with estrogen. Moreover, small interfering RNA -mediated inhibition of WISP-2/CCN5 activity in MCF-7 cells resulted in abrogation of proliferation by EGF. The multiple molecular cross-talks, including the interactions between phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase signaling pathways and two diverse receptors (i.e., ER-A and EGFR), were essential in the event of EGF-induced WISP-2/CCN5 up-regulation in MCF-7 cells. Moreover, EGF action on WISP-2/CCN5 is restricted to ER-and EGFR-positive noninvasive breast tumor cells, and this

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WISP-2 Gene in Human Breast Cancer: Estrogen and Progesterone Inducible Expression and Regulation of Tumor Cell Proliferation

Cited by 62 publications

References 33 publications

CCN5: biology and pathophysiology

CCN5: biology and pathophysiology

CCN5 Expression in mammals. II. Adult rodent tissues

Epidermal Growth Factor Induces WISP-2/CCN5 Expression in Estrogen Receptor-α-Positive Breast Tumor Cells through Multiple Molecular Cross-talks

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