Ultrastructural evidence of collagenolytic activity in ductal infiltrating carcinoma of the human breast

Pucci‐Minafra, Ida; Luparello, Claudio; Schillaci, Rosario; Sciarrino, Serafina

doi:10.1002/ijc.2910390510

Cited by 18 publications

(9 citation statements)

References 26 publications

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“…These pathways, subjected to a dynamic and zonal turn‐over of synthetic and degradative events (e.g. [37]), conceivably participate in feeding or restraining the autocrine/paracrine circuits which are likely to exist between PTHrP and sensitive breast cancer (and other) cells; the resulting differential effects on cell behavior might contribute in concert with other microenvironmental signals to control tumor growth and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Extracellular matrix regulation of PTHrP and PTH/PTHrP receptor in a human breast cancer cell line

et al. 1999

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It was previously reported that 8701-BC breast cancer cells express the gene for parathyroid hormone-related peptide (PTHrP) and its cognate receptor (PTHrP-R), and release immunoreactive PTHrP in the extracellular medium; it was also found that PTHrP, in turn, exerts a role on the proliferative and invasive behavior in vitro of the same cell line. On the other hand, evidence has been produced that adhesion of 8701-BC cells onto different collagen substrates influences in various ways a number of phenotypic expressions, such as cell growth, motility, invasion of reconstituted basement membrane and production of lytic enzymes of the extracellular matrix (ECM). In light of these previous data, we have examined whether substrates of either reconstituted basement membrane or representative collagen components of the breast tumor stroma (type I, V and OF/LB) might (i) regulate the PTHrP promoter usage and mRNA splicing patterns, (ii) modulate quantitatively the extracellular release of immunoreactive PTHrP (iPTHrP), and (iii) affect the expression of PTHrP-R. The results obtained give evidence that (i) 8701-BC cells are able to utilize different start sites and mRNA splicing patterns for PTHrP transcription; (ii)`structural' components of the stroma, such as collagens, are by themselves capable of controlling both the expression pattern of the PTHrP gene and the extent of extracellular release of iPTHrP, and (iii) PTHrP-R expression can be up-or downregulated in response to the ECM substrate present. These data demonstrate that PTHrP and PTHrP-R expression by 8701-BC neoplastic cells can be modulated by ECM molecules, indirectly supporting the active participation of stromal collagen composition in the regulation of PTHrP-controlled circuits which may play a role in carcinogenesis.z 1999 Federation of European Biochemical Societies.

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Section: Discussionmentioning

confidence: 99%

Extracellular matrix regulation of PTHrP and PTH/PTHrP receptor in a human breast cancer cell line

et al. 1999

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“…[1][2][3][4][5][6][7][8] The degradation of the collagen fibrils in breast tissue is known to occur with infiltrating disease. [9][10][11][12] Tumor cell secreted proteases cause degradation of basement membranes around epithelial cells as well as the extracellular matrix ͑ECM͒, which are abundant in connective proteins, such as collagen. 13,14 The interactions of tumor cells with these connective tissues are important events in the metastasis of cancer, and the implication that cancer cells become invasive by adhesion to, and degradation of, the basement membranes and ECM is central to the activity of tumor cells entering and exiting blood vessels and lymphatics in order to proliferate at distant sites.…”

Section: Introductionmentioning

confidence: 99%

“…13,15 Degradation of fibrillar collagen in cancerous tissues, which has been seen with electron micrograph images, may indicate that the new collagen is unable to aggregate properly to reconstitute the typical bundles found in healthy tissues. 11,12 It has also been suggested that the accumulation of altered collagen molecules during cancer progression impairs the correct supramolecular organization of the collagenous stroma and may provide a permissive pathway for the invasive growth of neoplastic cells. 5,16 Since SAXS is sensitive to the supramolecular structures of tissues, it can be used to evaluate if systematic variations in structure are correlated with disease progression, and hence to improved understanding of the spread of invasive disease.…”

Section: Introductionmentioning

confidence: 99%

Mapping structural changes in breast tissue disease using x‐ray scattering

et al. 2009

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Spread of invasive carcinoma throughout breast tissue is believed to occur at supramolecular levels, beyond the range of standard histopathology identification. Small angle x-ray scattering (SAXS) is capable of characterizing the structural properties of collagen and tissue found in the breast at the scale of tens to hundreds of nanometers. Fifty-six patients who were treated with wide-local excision or mastectomy had tissue biopsy samples analyzed at 2 cm intervals along two perpendicular axes over their excised mass, up to 6 cm away from the primary site of the tumor. Two SAXS parameters, the integrated amorphous scatter and the third order collagen axial d spacing, showed significant differences between the center (0 cm) and distant tissues (2, 4, or 6 cm from the primary lesion). There was no evidence of directional trends (superior, inferior, or lateral sides of the nipple) of these two parameters over the breast. Mapping of these two variables over a two-dimensional grid showed good matching with independent histopathology diagnosis. These results suggest that SAXS may be capable of identifying areas of invasion or directional spread of disease as well as providing more information at the supramolecular level for aiding tissue diagnosis.

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“…The invasive properties of primary tumours are partially dependent on degradation of the extracellular matrix (ECM), which under normal circumstances is crucial for cell-cell and cell-substratum interaction (7). Increased collagen degradation and reduced collagen synthesis are key features in the series of pathological events that aid tumour cell invasion and metastasis (8,9).…”

Section: Introductionmentioning

confidence: 99%

Infrequent Somatic Deletion of the 5' Region of the COL1A2 Gene in Oesophageal Squamous Cell Cancer Patients

Dietzsch¹,

Parker²

2002

Clinical Chemistry and Laboratory Medicine

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Oesophageal squamous cell cancer is the leading cause of cancer death amongst African males in South Africa. DNA was isolated from normal and tumour biopsies of the oesophagi of 33 African patients with squamous cell carcinoma of the oesophagus and was analysed with two dinucleotide repeat polymorphisms, a GT repeat sequence in the first intron, and a CA repeat in the promoter of the human alpha2(I) procollagen gene (COL1A2), using the polymerase chain reaction (PCR). Normal and tumour DNAs from each individual were compared to identify changes present in the tumour DNA, but absent in normal DNA. Twenty two cases were informative (heterozygous) for the promoter polymorphism and 24 cases were informative for the intronic polymorphism. Loss of heterozygosity (LOH) was seen in 2/22 (9.1%) for the promoter and 3/24 (12.5%) for the intronic polymorphism. These changes involved a total of three patients: two patients displayed the lost allele incorporating both the CA repeat and GT repeat loci; the third patient revealed LOH at the intronic polymorphism, but was non-informative (homozygous) for the promoter polymorphism. Deletions within the procollagen genes may represent an as yet unrecognised but rare event in the multistep process of carcinogenesis.

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Ultrastructural evidence of collagenolytic activity in ductal infiltrating carcinoma of the human breast

Cited by 18 publications

References 26 publications

Extracellular matrix regulation of PTHrP and PTH/PTHrP receptor in a human breast cancer cell line

Extracellular matrix regulation of PTHrP and PTH/PTHrP receptor in a human breast cancer cell line

Mapping structural changes in breast tissue disease using x‐ray scattering

Infrequent Somatic Deletion of the 5' Region of the COL1A2 Gene in Oesophageal Squamous Cell Cancer Patients

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