Differential nuclear matrix-intermediate filament expression in human prostate cancer in respect to benign prostatic hyperplasia

Alberti, Ingles; Parodi, Silvio; Barboro, Paola; Sanna, Paola; Nicoló, Guido; Allera, Caterina; Patrone, Eligio; Galli, Stefano; Balbi, Cecilia

doi:10.1016/s0304-3835(96)04444-8

Cited by 10 publications

(6 citation statements)

References 16 publications

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“…Finally, the data reported in Table III show that the increase in lamin B is strongly correlated with Gleason score. This finding indicates that the expression of this protein is differentiation related, as already noted for the minor components of the NM showing differences between tumor and normal tissue (4)(5)(6).…”

Section: Resultssupporting

confidence: 80%

“…We have recently shown that the development of human prostate cancer (PCa) is characterized by an increase in the complexity of the protein pattern of the NM. Poorly differentiated tumors express proteins that are not detected in more differentiated tumors (4,5); moreover, a few newly expressed proteins are significantly correlated with the risk of biochemical progression (6).…”

Section: Introductionmentioning

confidence: 99%

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Differential expression of nuclear lamins in normal and cancerous prostate tissues

et al. 2006

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The process of carcinogenesis is characterized by definite changes in the protein composition of the nuclear matrix. We have recently found that lamins form, in addition to the nuclear lamina, an intranuclear web of thin fibrils. This finding prompted us to address the question of whether changes in the expression of lamins occur in the course of tumor development. In prostate cancer, lamin B undergoes a significant increase; interestingly, its nuclear content strongly correlates with tumor differentiation. Moreover, all the lamins show reproducible alterations in the distribution of the isoelectric variants, suggesting that dephosphorylation events could trigger changes in the pattern of gene expression by inducing structural rearrangements of the nuclear scaffold.

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Section: Resultssupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Differential expression of nuclear lamins in normal and cancerous prostate tissues

et al. 2006

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“…2a). Therefore, as already observed, 21,22 the complexity of protein patterns increased from normal to tumor tissues, whereas no significant differences were observed among PCa with different Gleason scores in terms of number of expressed proteins (Fig. 1b).…”

Section: Resultssupporting

confidence: 75%

Expression of nuclear matrix proteins binding matrix attachment regions in prostate cancer. PARP‐1: New player in tumor progression

Barboro

Ferrari

Capaia

et al. 2015

Intl Journal of Cancer

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Prostate cancer (PCa) displays infrequent point mutations, whereas genomic rearrangements are highly prevalent. In eukaryotes, the genome is compartmentalized into chromatin loop domains by the attachment to the nuclear matrix (NM), and it has been demonstrated that several recombination hot spots are situated at the base of loops. Here, we have characterized the binding between NM proteins and matrix attachment regions (MARs) in PCa. Nontumor and 44 PCa tissues were analyzed. More aggressive tumors were characterized by an increase in the complexity of the NM protein patterns that was synchronous with a decrease in the number of proteins binding the MAR sequences. PARP-1 was the protein that showed the most evident changes. The expression of the PARP-1 associated with NM increased and it was dependent on tumor aggressiveness. Immunohistochemical analysis showed that the protein was significantly overexpressed in tumor cells. To explore the role of PARP-1 in PCa progression, PCa cells were treated with the PARP inhibitor, ABT-888. In androgen-independent PC3 cells, PARP inhibition significantly decreased cell viability, migration, invasion, chromatin loop dimensions and histone acetylation. Collectively, our study provides evidence that MAR-binding proteins are involved in the development and progression of PCa. PARP could play a key role in the compartmentalization of chromatin and in the development of the more aggressive phenotype. Thus, PARP can no longer be viewed only as an enzyme involved in DNA repair, but that its role in chromatin modulation could provide the basis for a new therapeutic approach to the treatment of PCa.Although significant advancements have been made in the understanding of the molecular events responsible for the development and progression of prostate cancer (PCa), this tumor remains the most frequently diagnosed among males in economically developed countries.1 The pathogenesis of this cancer is complex; it has an extremely heterogeneous clinical behavior and, different from many other cancers, the events associated with its initiation and progression remain poorly understood.2 Therefore, an improved comprehension of the molecular aspects of PCa progression could help to detect new diagnostic and prognostic markers and define new therapeutic strategies.PCa displays infrequent point mutations, whereas genomic rearrangements are highly prevalent.3 Recently, Baca et al. 4sequenced the whole genomes of 57 PCa cases and identified abundant DNA translocations and deletions. These large-scale chromosomal rearrangements arise through a single and highly interdependent process, rather than through independent multiple steps. The authors coined the term "chromoplexy" to describe this phenomenon of complex genome restructuring. It is known that in eukaryotes, the genome is compartmentalized into chromatin loop domains by the attachment to nuclear matrix (NM). 5 The interactions of chromatin with the NM are a dynamic event that is functionally dependent, 6 and occur via noncoding AT-rich DNA se...

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“…The protein composition and organization of the nuclear matrix reflects and appears to mediate changes in cellular growth, differentiation, and transformation (39,76–78) . Tumor‐specific, nuclear matrix proteins have been characterized in prostate, breast, and bladder tissues (79–81) . The diagnostic and prognostic value of these proteins is under investigation and may be the molecular correlate to the pathologist's observation that cancer is often heralded by changes in nuclear morphology (82) …”

Section: The Substructure Of the Nucleus Is The Nuclear Matrix A Unimentioning

confidence: 99%

Nuclear Matrix Proteins and Osteoblast Gene Expression

Bidwell

Alvarez

Feister

et al. 1998

Journal of Bone and Mineral Research

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The molecular mechanisms that couple osteoblast structure and gene expression are emerging from recent studies on the bone extracellular matrix, integrins, the cytoskeleton, and the nucleoskeleton (nuclear matrix). These proteins form a dynamic structural network, the tissue matrix, that physically links the genes with the substructure of the cell and its substrate. The molecular analog of cell structure is the geometry of the promoter. The degree of supercoiling and bending of promoter DNA can regulate transcriptional activity. Nuclear matrix proteins may render a change in cytoskeletal organization into a bend or twist in the promoter of target genes. We review the role of nuclear matrix proteins in the regulation of gene expression with special emphasis on osseous tissue. Nuclear matrix proteins bind to the osteocalcin and type I collagen promoters in osteoblasts. One such protein is Cbfa1, a recently described transcriptional activator of osteoblast differentiation. Although their mechanisms of action are unknown, some nuclear matrix proteins may act as "architectural" transcription factors, regulating gene expression by bending the promoter and altering the interactions between other trans-acting proteins. The osteoblast nuclear matrix is comprised of cell-and phenotype-specific proteins including proteins common to all cells. Nuclear matrix proteins specific to the osteoblast developmental stage and proteins that distinguish osteosarcoma from the osteoblast have been identified. Recent studies indicating that nuclear matrix proteins mediate bone cell response to parathyroid hormone and vitamin D are discussed. (J Bone Miner Res 1998;13:155-167) THE CONNECTION BETWEEN THE SHAPE OF A BONE CELL AND ITS GENETIC PROGRAMT HE COUPLING OF CELL SHAPE and gene expression through the linkage of dynamic skeletal networks provides a molecular framework for sensing and responding to mechanical stimuli, fluid flow, and diffusion-based chemical signaling pathways that induce changes in cell morphology.(1-10) This is particularly relevant to osteoblast gene expression. That the shape of a cell is somehow related to what that cell does has been a venerable article of faith in pathology. However, data to support the concept that molecular mechanisms link cell structure to gene expression are only recently emerging from studies in cell and molecular biology.(1-15) In the tensegrity paradigm, a subcellular scaffolding consisting of proteins from the extracellular matrix (ECM), the integrin receptors, and the cyto-and nucleoskeletons, is physically linked or "hard-wired" to the genes. (16 -18) An outstanding question of this paradigm is how a mechanical tug on the DNA contributes to the regulation of

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Differential nuclear matrix-intermediate filament expression in human prostate cancer in respect to benign prostatic hyperplasia

Cited by 10 publications

References 16 publications

Differential expression of nuclear lamins in normal and cancerous prostate tissues

Differential expression of nuclear lamins in normal and cancerous prostate tissues

Expression of nuclear matrix proteins binding matrix attachment regions in prostate cancer. PARP‐1: New player in tumor progression

Nuclear Matrix Proteins and Osteoblast Gene Expression

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