Role of cell shape in growth control

Folkman, Judah; Moscona, Anne

doi:10.1038/273345a0

Cited by 2,291 publications

(1,222 citation statements)

References 16 publications

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“…Thereafter, we examined the involvement of XEDAR in detachment-induced apoptosis. Fortyeight hours after transfection with plasmid expressing XEDAR, HEK293 cells were detached and cultured in suspension for 24 h using a poly-2-hydroxyethyl methacrylate-coated plate (Folkman and Moscona, 1978). Subsequent analyses indicated that XEDAR introduction reduced the number of viable cells through caspase-3 activation (Figure 3d).…”

Section: Role Of Xedar In Anoikismentioning

confidence: 99%

XEDAR as a putative colorectal tumor suppressor that mediates p53-regulated anoikis pathway

et al. 2009

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Colorectal cancers with mutations in the p53 gene have an invasive property, but its underlying mechanism is not fully understood. Through the screening of two data sets of the genome-wide expression profile, one for p53-introduced cells and the other for the numbers of cancer tissues, we report here X-linked ectodermal dysplasia receptor (XEDAR), a member of the TNFR superfamily, as a novel p53 target that has a crucial role in colorectal carcinogenesis. p53 upregulated XEDAR expression through two p53-binding sites within intron 1 of the XEDAR gene. We also found a significant correlation between decreased XEDAR expressions and p53 gene mutations in breast and lung cancer cell lines (P ¼ 0.0043 and P ¼ 0.0122, respectively). Furthermore, promoter hypermethylation of the XEDAR gene was detected in 20 of 20 colorectal cancer cell lines (100%) and in 6 of 12 colorectal cancer tissues (50%), respectively. Thus, the XEDAR expression was suppressed to o25% of surrounding normal tissues in 12 of 18 colorectal cancer tissues (66.7%) due to either its epigenetic alterations and/or p53 mutations. We also found that XEDAR interacted with and subsequently caused the accumulation of FAS protein, another member of p53-inducible TNFR. Moreover, XEDAR negatively regulated FAK, a central component of focal adhesion. As a result, inactivation of XEDAR resulted in the enhancement of cell adhesion and spreading, as well as resistance to p53-induced apoptosis. Taken together, our findings showed that XEDAR is a putative tumor suppressor that could prevent malignant transformation and tumor progression by regulating apoptosis and anoikis.

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Section: Role Of Xedar In Anoikismentioning

confidence: 99%

XEDAR as a putative colorectal tumor suppressor that mediates p53-regulated anoikis pathway

et al. 2009

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“…29 Addition of growth factors.Growth factors were added at a concentration of 10 ng/ml to AG 1518 fibroblasts cultured on poly[HEMA]-coated microtiter plates as described above. The growth factors were added after an initial incubation period of 2.5 hr and present during the entire [ 14 C]Glycine pulse period.…”

Section: Cell Culture Protocolsmentioning

confidence: 99%

Collagen type I expression in experimental anaplastic thyroid carcinoma: Regulation and relevance for tumorigenicity

Dahlman

Lammerts

Bergström

et al. 2001

Intl Journal of Cancer

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Fibrosis in solid malignancies plays a significant role in tumor pathophysiology. Potential mechanisms for collagen type I deposition in anaplastic thyroid carcinoma (ATC) were investigated using 6 characterized ATC cell lines. Three of these cell lines, which produced collagen type I, had, as a group, a poor tumorigenicity when inoculated in athymic mice. This group of cells generated tumors in 4 of 24 injected animals (17%). Pro-␣1(I) collagen mRNA-expressing carcinoma and stromal cells were interdispersed in the tumors generated by these ATC cells. By contrast, the 3 noncollagen-producing ATC cell lines were all tumorigenic with a tumor take of 60% in the whole group. In the latter tumors, pro-␣1(I) collagen mRNA-expressing cells were confined to the stromal compartment, well delineated from carcinoma cell islets. To study the influence of ATC cells on collagen type I synthesis by fibroblasts, we used AG 1518 diploid human fibroblasts cultured on poly-(2-hydroxyethyl methacrylate) (poly[HEMA])-coated plates. This culture condition allows the study of the effect of collagen mRNA translation in the regulation of collagen type I synthesis. Conditioned media from the 6 ATC cell lines did not influence collagen synthesis. The ATC cell line KAT-4 stimulated fibroblast synthesis of collagen type I when the two cell types were cocultured on poly[HEMA]-coated substrates. Specific inhibitors of PDGF and TGF-␤ reduced the KAT 4 carcinoma cell-induced stimulation of collagen type I synthesis. Our data suggest that collagen type I production by carcinoma cells correlates negatively with tumorigenicity and that the formation of a well-defined stroma is of importance for tumor growth. Furthermore, our data suggest that tumor cells are able to stimulate collagen mRNA translation in stromal fibroblasts in direct cell-cell contact by, at least in part, transferring PDGF or TGF-␤.

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“…These considerations suggest that CAM vascular growth may be initiated by a global trigger, but is placed under local control for down-regulation of endothelial cell proliferation in response to the hemodynamic and geometric constraints. It appears reasonable that intussusceptive mesh formation is the optimum way to realize this task of growth control via cell shape (compare Folkman and Moscona, 1978). This study is aimed at extending the concept of Patan et al (19931, by relating capillary endothelial cell proliferation to precapillary vessel formation.…”

Section: Introductionmentioning

confidence: 95%

Proliferation pattern of capillary endothelial cells in chorioallantoic membrane development indicates local growth control, which is counteracted by vascular endothelial growth factor application

Kurz

Ambrosy

Wilting

et al. 1995

Developmental Dynamics

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Role of cell shape in growth control

Cited by 2,291 publications

References 16 publications

XEDAR as a putative colorectal tumor suppressor that mediates p53-regulated anoikis pathway

XEDAR as a putative colorectal tumor suppressor that mediates p53-regulated anoikis pathway

Collagen type I expression in experimental anaplastic thyroid carcinoma: Regulation and relevance for tumorigenicity

Proliferation pattern of capillary endothelial cells in chorioallantoic membrane development indicates local growth control, which is counteracted by vascular endothelial growth factor application

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