Suppression of tumorigenic and metastatic potentials of human melanoma cell lines by mutated (143 Val-Ala) p53

Rauth, Sikha; Green, A; Kichina, Julia V.; Shilkaitis, Anne

doi:10.1038/bjc.1998.369

Cited by 6 publications

(7 citation statements)

References 34 publications

(27 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The first aim of the study was to evaluate the relative toxicity of the three MLs towards six different human melanoma cell lines, two established from a primary melanoma (Rauth et al, 1998) and four established from melanoma lymph node metastases (Fodstad et al, 1988a(Fodstad et al, , 1988bEdward, 2001;Carey et al, 1976). All three MLs inhibited cell proliferation of the six cell lines in a dose dependent manner, however, distinct differences between the cytotoxicity of the three lectins were noted.…”

Section: Discussionmentioning

confidence: 99%

“…The human melanoma cell lines UISO-Mel6 (established from a primary malignant melanoma, Rauth et al, 1998), MV3 (established from a metastatic melanoma lymph node, Edward, 2001), and MeWo (established from a metastatic melanoma lymph node of a white, 78-year-old male, Carey et al, 1976) were kindly provided from the Klinik für Dermatologie, Universitätsklinikum Hamburg-Eppendorf, Germany. The human melanoma cell lines Lox and FemX-1, both established from a metastatic lymph node, (Fodstad et al, 1988a(Fodstad et al, , 1988b were kindly provided by Dr. O. Fodstad (Department of Tumour Biology University of Oslo, Norway).…”

Section: Cell Linesmentioning

confidence: 99%

See 1 more Smart Citation

Influence of mistletoe lectins and cytokines induced by them on cell proliferation of human melanoma cells in vitro

et al. 2005

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Section: Cell Linesmentioning

confidence: 99%

Influence of mistletoe lectins and cytokines induced by them on cell proliferation of human melanoma cells in vitro

et al. 2005

View full text Add to dashboard Cite

“…The effects of mutation or loss of p53 have been elucidated in numerous studies. Rauth and co‐workers suggested that mutated ( 143 Val‐Ala ) p53 , which retains DNA binding and some of the transactivation functions of the wild‐type (wt) p53 protein, suppresses tumorigenic and metastatic potentials of human melanoma cell lines in vivo [19]. Furthermore, despite the presence of SV‐40 T‐antigen, p53 levels influence the characteristics of the late stages of mammary tumor growth and accelerate metastasis.…”

Section: Introductionmentioning

confidence: 99%

p53 is a regulator of the metastasis suppressor gene Nm23‐H1

Chen

Shieh

et al. 2003

Molecular Carcinogenesis

View full text Add to dashboard Cite

p53, a tumor suppressor gene involved in the G1 cell cycle checkpoint, is also the most frequently mutated gene in human cancer. In addition, p53 modifies the ability of tumor cells to metastasize. The metastasis-associated gene Nm23-H1, which encodes an 18-kDa nucleoside diphosphate kinase, was previously identified in cells with low metastatic potential. Although p53 and Nm23-H1 proteins play an important part in regulating the progression of cancer, any functional relationship between these two proteins is currently unknown. Here we report an association between p53 levels and expression of the Nm23-H1 gene. Our data indicate that wild-type (wt) p53 upregulated the expression of Nm23-H1 at protein and mRNA levels in MCF-7 and J7B cells. This capacity of wt p53 to regulate expression of Nm23-H1 was not only dependent on the endogenous but also the exogenous origin of p53, and could not be reproduced with mutant p53. Subsequently, the invasive ability of MCF-7 and J7B cells was suppressed upon induction of the Nm23-H1 protein by p53. In contrast, increased levels of p53 downregulated the expression of Nm23-H1 at the protein and mRNA levels in RKO and H1299 cells and, as a consequence, increased the invasive ability of both cell types. Thus, our results implicated the differential regulation of Nm23-H1 by p53 in different cell types as an important component in the molecular mechanisms of tumor metastasis.

show abstract

“…The human melanoma cell lines UISO-Mel6 (established from a primary malignant melanoma; see Rauth et al (1998)), MV3 (established from a metastatic melanoma lymph node; see Edward (2001)) and MeWo (established from a metastatic melanoma lymph node of a white, 78-year-old male; see Carey et al (1976)) were kindly provided by the Klinik für Dermatologie, Universitätsklinikum Hamburg-Eppendorf, Germany. The human melanoma cell lines LOX and FEMX-1 were both established from a metastatic lymph node (Fodstad et al, 1988a, b).…”

Section: Cell Linesmentioning

confidence: 99%

Clinically proven markers of metastasis predict metastatic spread of human melanoma cells engrafted in scid mice

et al. 2007

View full text Add to dashboard Cite

Metastasis formation is a complex process and as such can only be modelled in vivo. As markers indicating metastatic spread in syngenic mouse models differ significantly from those in man, this study aimed to develop a human melanoma xenograft mouse model that reflects the clinical situation. Six human melanoma cell lines (LOX, MV3, FEMX-1, G361, MeWo and UISO-Mel6) were xenografted into severe combined immunodeficient mice and tumour growth, metastatic behaviour and number of lung metastases were assessed. Tumours and metastases were analysed for HPA binding and expression of CEACAM-1 and L1, all markers indicative of metastasis in clinical studies. Development of primary tumour nodules ranged from 3 weeks (MV3) to 3 months (MeWo). Whereas G361 and FEMX-1 rarely formed lung metastases, MeWo, MV3 and LOX were moderately and UISO-Mel6 was highly metastatic. Similar to clinical studies, HPA, CEACAM1 and L1 indicated metastatic spread in the xenograft melanoma model, but were not all simultaneously expressed in all cell lines. Considering the strongest expression of one marker combined with an absent or low expression of the other two markers, we conclude that LOX is the cell line of choice for analyses of the functional role of HPA-binding glycoconjugates, UISO-Mel6 is ideally suited to study CEACAM1 function in melanoma spread and L1 function can best be modelled using MeWo. Malignant melanoma, being the most aggressive form of skin cancer, represents a considerable clinical problem worldwide, where about 1 : 35 Caucasians will suffer from malignant melanoma during their lifetime with an incidence furthermore accelerating (Lens and Dawes, 2004). If the primary melanoma can be excised completely before it has spread to distant sites, the patient is cured. However, if metastases occur the patient's fate is sealed, as in spite of intensive research no curative treatment is yet available (Garbe and Blum, 2001;Eigentler et al, 2003). In order to make progress in the field of metastasis treatment, the process of malignant melanoma spread has to be better understood. Metastasis formation is a complex process, which involves many different steps, each of which has to be passed sequentially in order to lead to a clinically detectable metastasis (Hart and Saini, 1992). As this whole metastatic cascade is such a complex process, simple in vitro experiments can only partially mimick the course of metastatic spread and only animal experiments of metastasis can represent the full picture of this multistep phenomenon (Eccles, 2001).In melanoma metastasis research, the mouse B16 melanoma model has found widespread application (Tao et al, 1982). However, as this model represents a syngenic mouse model, it suffers the inherent problems of all murine models of metastasis, namely whether it is directly transferable to humans. Concerning carbohydrate expression, which has profound influence on the metastatic behaviour of tumour cells , murine B16 melanoma cells significantly differ from human melanoma cells. Expression of WGA and PHA...

show abstract

Suppression of tumorigenic and metastatic potentials of human melanoma cell lines by mutated (143 Val-Ala) p53

Cited by 6 publications

References 34 publications

Influence of mistletoe lectins and cytokines induced by them on cell proliferation of human melanoma cells in vitro

Influence of mistletoe lectins and cytokines induced by them on cell proliferation of human melanoma cells in vitro

p53 is a regulator of the metastasis suppressor gene Nm23‐H1

Clinically proven markers of metastasis predict metastatic spread of human melanoma cells engrafted in scid mice

Contact Info

Product

Resources

About