Identification of a Gene That Reverses the Immortal Phenotype of a Subset of Cells and Is a Member of a Novel Family of Transcription Factor-Like Genes

Bertram, Michael J.; Bérubé, Nathalie G.; Hang-Swanson, X.; Ran, Qitao; Leung, James K.; Bryce, Steven D.; Spurgers, Kevin B.; Bick, Roger J.; Baldini, Antonio; Ning, Yi; Clark, Louise; Parkinson, E.K.; Barrett, J. Carl; Smith, James R.; Pereira‐Smith, Olivia M.

doi:10.1128/mcb.19.2.1479

Cited by 131 publications

(119 citation statements)

References 40 publications

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“…Analysis of these mechanical stress-induced genes (MSGens) showed marked induction of MSGen-15 mRNA expression in the cells subjected to mechanical loading (Myokai et al, 2003). Interestingly, MSGen-15 showed homology with MRG-15 (mortality factor on a chromosome-4-related gene), which belongs to a novel family of transcription factor-like genes whose RNA level changes during cell growth and at times of senescence (Bertram et al, 1999). In human PDL cells, mRNA for transcription factors such as c-fos is also shown to be induced after mechanical stretching without any significant change in the matrix proteins (Yamaguchi et al, 2002).…”

Section: Regulation Of Gene Expression In Fibroblasts By Mechanical Lmentioning

confidence: 99%

Mechanoregulation of gene expression in fibroblasts

Wang

Thampatty

Lin

et al. 2007

Gene

225

187

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Mechanical loads placed on connective tissues alter gene expression in fibroblasts through mechanotransduction mechanisms by which cells convert mechanical signals into cellular biological events, such as gene expression of extracellular matrix components (e.g., collagen). This mechanical regulation of ECM gene expression affords maintenance of connective tissue homeostasis. However, mechanical loads can also interfere with homeostatic cellular gene expression and consequently cause the pathogenesis of connective tissue diseases such as tendinopathy and osteoarthritis. Therefore, the regulation of gene expression by mechanical loads is closely related to connective tissue physiology and pathology. This article reviews the effects of various mechanical loading conditions on gene regulation in fibroblasts and discusses several mechanotransduction mechanisms. Future research directions in mechanoregulation of gene expression are also suggested.

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Section: Regulation Of Gene Expression In Fibroblasts By Mechanical Lmentioning

confidence: 99%

Mechanoregulation of gene expression in fibroblasts

Wang

Thampatty

Lin

et al. 2007

Gene

225

187

View full text Add to dashboard Cite

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“…The dominant nature of cellular senescence has provided an opportunity to identify senescence loci by microcell transfer of individual human chromosomes into immortal cell lines (Ohmura et al, 1995;Bertram et al, 1999;Tominaga et al, 2002). Applying this approach, we have previously identified cell senescence loci on human chromosomes 6 and 16 (Sandhu et al, 1994(Sandhu et al, , 1996Reddy et al, 1999Reddy et al, , 2000.…”

Section: Introductionmentioning

confidence: 99%

Functional identification of a BAC clone from 16q24 carrying a senescence gene SEN16 for breast cancer cells

et al. 2004

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We have identified an 85 kb BAC clone, 346J21, that carries a cell senescence gene (SEN16), previously mapped to 16q24.3. Transfer and retention of 346J21 in breast cancer cell lines leads to growth arrest after 8-10 cell doublings, accompanied by the appearance of characteristic senescent cell morphology and senescence-associated acid b-galactosidase activity. Loss of transferred BAC results in reversion to the immortal growth phenotype of the parental cancer cell lines. BAC 346J21 restores senescence in the human breast cancer cell lines, MCF.7 and MDA-MB468, and the rat mammary tumor cell line LA7, but not in the human glioblastoma cell line T98G. We postulate that inactivation of both copies of SEN16 is required for the immortalization of breast epithelial cells at an early stage of tumorigenesis. Positional mapping of 346J21 shows that SEN16 is distinct from other candidate tumor suppressor genes reported at 16q24.

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“…So far only one gene, MORF4, which restores senescence in immortal Hela cells has been cloned (Bertram et al, 1999). However, the role of this gene in cellular senescence has not been established as yet.…”

mentioning

confidence: 99%

Identification of a YAC from 16q24 carrying a senescence gene for breast cancer cells

Popescu

et al. 2000

Oncogene

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We have identi®ed a 360 kb YAC that carries a cell senescence gene, SEN16. In our earlier studies, we localized SEN16 within a genetic interval of 3 ± 7 cM at 16q24.3. Six overlapping YACs spanning the chromosomal region of senescence activity, were assembled in a contig. Candidate YACs, identi®ed by the markers located in the vicinity of SEN16, were retro®tted to introduce a neo selectable marker. Retro®tted YACs were ®rst transferred into mouse A9 cells to generate A9/YAC hybrids. YAC DNA present in A9/YAC hybrids was further transferred by microcell fusion into immortal cell lines derived from human and rat mammary tumors. YAC d792t2 restored senescence in both human and rat mammary tumor cell lines, while an unrelated YAC from chromosome 6q had no senescence activity. Oncogene (2000) 19, 217 ± 222.

show abstract

Identification of a Gene That Reverses the Immortal Phenotype of a Subset of Cells and Is a Member of a Novel Family of Transcription Factor-Like Genes

Cited by 131 publications

References 40 publications

Mechanoregulation of gene expression in fibroblasts

Mechanoregulation of gene expression in fibroblasts

Functional identification of a BAC clone from 16q24 carrying a senescence gene SEN16 for breast cancer cells

Identification of a YAC from 16q24 carrying a senescence gene for breast cancer cells

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