Down-regulation of SPARC/Osteonectin/BM-40 expression in methylcholanthrene-induced fibrosarcomas and in kirsten-MSV transformed fibroblasts

Colombo, Mario P.; Ferrari, G.; Biondi, G.; Galasso, Daniela; Howe, Chin C.; Parmiani, Giorgio

doi:10.1016/0277-5379(91)90062-i

Cited by 12 publications

(6 citation statements)

References 24 publications

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“…In rat and chick embryo fibroblasts, c-Jun expression downregulates SPARC (Kraemer et al, 1999;Mettouchi et al, 1994;. This downregulation is required for fibrosarcoma development (Colombo et al, 1991;. In contrast, in our MCF7 model, c-Jun highly upregulates SPARC ( (Rinehart-Kim et al, 2000), and Figures 1 and 4) and this upregulation plays an important role in tumor cell invasion in vitro (Figure 3).…”

Section: Discussionmentioning

confidence: 96%

“…For example, SPARC upregulation is associated with invasive behavior of breast, prostate and colorectal carcinomas as well as invasive meningioma and melanoma (Bellahcene and Castronovo, 1995;Graham et al, 1997;Jacob et al, 1999;Kato et al, 2000;Ledda et al, 1997a;Porte et al, 1995;Porter et al, 1995;Sturm et al, 2002;Thomas et al, 2000). In contrast, ovarian carcinoma and fibrosarcoma development exhibit an inverse correlation with SPARC expression Colombo et al, 1991;Mok et al, 1996;Yiu et al, 2001) perhaps related to increased apoptotic activity (Yiu et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

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Transcriptional upregulation of SPARC, in response to c-Jun overexpression, contributes to increased motility and invasion of MCF7 breast cancer cells

et al. 2002

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Transcriptional upregulation of SPARC, in response to c-Jun overexpression, contributes to increased motility and invasion of MCF7 breast cancer cells

et al. 2002

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“…In mammalian cells, independent reports also show repression of SPARC mRNA and protein in primary rat embryo ®broblasts which transiently express cJun (Mettouchi et al, 1994) as well as in immortalized rodent ®broblasts stably transformed by cJun, Ha-ras (Mettouchi et al, 1994), vAbl, vSrc (Mason et al, 1986a,b), and Ki-Ras (Colombo et al, 1991). In contrast, the simian virus 40 and bovine papilloma virus 1 oncogenes exert little or no repressive eect on SPARC (Colombo et al, 1991;Kraemer et al, 1999). Together these data strongly suggest a functional link between the transformed state as established in cultured cells by certain oncoproteins and the down-regulation of SPARC.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of the extracellular matrix protein SPARC in vSrc- and vJun-transformed chick embryo fibroblasts contributes to tumor formation in vivo

Vial

Castellazzi

2000

Oncogene

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In vitro transformation of primary cultures of chick embryo ®broblasts by the membrane-bound vSrc or the nuclear vJun oncoproteins is correlated with a downregulation of the secreted glycoprotein SPARC (also called BM-40 or osteonectin). This protein is a nonstructural component of the extracellular matrix that is thought to regulate cell ± matrix interaction during development, wound repair, and carcinogenesis. Its precise function remains unclear. To estimate the contribution of SPARC down-regulation to the major aspects of the transformed phenotype, we have reexpressed this protein from a self-replicating retrovirus Rcas, designated R-SPARC, in the transformed cultures. These R-SPARC-infected cultures display the following main properties: (i) they accumulate the SPARC protein to a level identical to or only slightly higher than the level in normal chick embryo ®broblasts; (ii) they retain the main phenotypic properties characteristic of in vitro transformed cells, that is, altered morphology, capacity to grow in a reduced amount of serum, and capacity to develop colonies from single cells in agar; (iii) they display a clearly reduced capacity to develop local ®brosarcomas in vivo. Taken together, these data strongly suggest that down-regulation of SPARC contributes to the transformed phenotype triggered by vSrc and vJun in primary avian ®broblasts, by facilitating in vivo tumorigenesis.

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“…A variety of in vitro papers have suggested a role for SPARC in the regulation of cell adhesion and proliferation, and in the modulation of cytokine activity (17)(18)(19)(20). Although SPARC expression appears to be deregulated in transformed cells (21)(22)(23), its inhibition by antisense RNA diminished both the adhesive and invasive capacities of human melanoma cells in vitro and in xenotransplanted nu/nu mice (24). The role of SPARC in neoplastic cell transformation, conditioning inflammation, and leukocyte trafficking has not been well defined in vivo, where the major phenotypes reported so far in SPARC KO mice are cataract formation (25)(26)(27) and osteopenia (28,29).…”

Section: Introductionmentioning

confidence: 99%

Leukocyte, Rather than Tumor-produced SPARC, Determines Stroma and Collagen Type IV Deposition in Mammary Carcinoma

Sangaletti

Stoppacciaro

Guiducci

et al. 2003

The Journal of Experimental Medicine

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121

110

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Secreted protein, acidic and rich in cysteine (SPARC), also known as osteonectin or BM-40, is a Ca2+-binding matricellular glycoprotein involved in development, wound healing, and neoplasia. However, the role of SPARC in tumors is ill defined mostly because it is expressed by both tumor and stromal cells, especially inflammatory cells. We analyzed the respective roles of host- and tumor-derived SPARC in wild-type and congenic SPARC knockout (SPARC−/−) mice on a BALB/c genetic background injected into the mammary fat pad with SPARC-producing mammary carcinoma cells derived from c-erB2 transgenic BALB/c mice. Reduced tumor growth but massive parenchyma infiltration, with large areas of necrosis and impaired vascularization were observed in SPARC−/− mice. Immunohistochemical analysis showed a defect in collagen type IV deposition in the stroma of lobular tumors from SPARC−/− mice. Chimeric mice expressing SPARC only in bone marrow–derived cells were able to organize peritumoral and perilobular stroma, whereas reciprocal chimeras transplanted with bone marrow from SPARC−/− mice developed tumors with less defined lobular structures, lacking assembled collagen type IV and with a parenchyma heavily infiltrated by leukocytes. Together, the data indicate that SPARC produced by host leukocytes, rather than the tumor, determines the assembly and function of tumor-associated stroma through the organization of collagen type IV.

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Down-regulation of SPARC/Osteonectin/BM-40 expression in methylcholanthrene-induced fibrosarcomas and in kirsten-MSV transformed fibroblasts

Cited by 12 publications

References 24 publications

Transcriptional upregulation of SPARC, in response to c-Jun overexpression, contributes to increased motility and invasion of MCF7 breast cancer cells

Transcriptional upregulation of SPARC, in response to c-Jun overexpression, contributes to increased motility and invasion of MCF7 breast cancer cells

Down-regulation of the extracellular matrix protein SPARC in vSrc- and vJun-transformed chick embryo fibroblasts contributes to tumor formation in vivo

Leukocyte, Rather than Tumor-produced SPARC, Determines Stroma and Collagen Type IV Deposition in Mammary Carcinoma

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