Identification of Tumor-Suppressor Genes Using Human Melanoma Cell Lines UACC903, UACC903(+6), and SRS3 by Comparison of Expression Profiles

Su, Yan; Bittner, Michael; Chen, Yidong; Tao, Lian; Jiang, Yuan; Zhang, Yinghua; Stephan, Dietrich A.; Trent, Jeffrey M.

doi:10.1002/1098-2744(200006)28:2<119::aid-mc8>3.0.co;2-n

Cited by 60 publications

(48 citation statements)

References 31 publications

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“…In this sense, the mitogenic effect of ET-1, its ability to inhibit gap junctional communication, to downregulate Cx43, the protein forming gap junction channels, and to increase the rate of glucose uptake is well known (Blomstrand and Giaume, 2006;Supattapone et al, 1989;Tabernero et al, 2001;Teixeira et al, 2000). To address the possible participation of Cx43, a tumor suppressor protein (Huang et al, 1998;Metha et al, 1991;Naus, 2002;Su et al, 2000;Yamasaki et al, 1999;Zhu et al, 1991), in the proliferation and glucose uptake brought about by ET-1, astrocytes were transfected with Cx43-siRNA, which decreased the level of Cx43 by about 80% (see Fig. 1), resulting in a strong reduction in gap junctional permeability (see Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the role of Cx43 in the expression of some genes linked to growth regulation is well documented (for review, see Kardami et al, 2007), and the association between Cx43 and several proteins responsible for regulating the cell cycle is also well known (Koffler et al, 2000;Sin et al, 2007;Zhang et al, 2001Zhang et al, , 2003. Although most studies indicate that Cx43 behaves as a tumor suppressor protein (Huang et al, 1998;Metha et al, 1991;Naus, 2002;Su et al, 2000;Yamasaki et al, 1999;Zhu et al, 1991), there is also an important body of evidence suggesting that Cx43 would be required for cell proliferation. Thus, astrocytes from Cx43 KO mice exhibit a reduced rate of growth (Dermietzel et al, 2000;Naus et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

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Connexin43 is involved in the effect of endothelin‐1 on astrocyte proliferation and glucose uptake

Herrero-González

Valle-Casuso

Sánchez‐Alvarez

et al. 2008

Glia

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In previous studies, we showed that endothelin-1 increased astrocyte proliferation and glucose uptake. These effects were similar to those observed with other gap junction inhibitors, such as carbenoxolone (CBX). Because 24-h treatment with endothelin-1 or CBX downregulates the expression of connexin43, the main protein forming astrocytic gap junctions, which can also be involved in proliferation, in this study, we addressed the possible role of connexin43 in the effects of endothelin-1. To do so, connexin43 was silenced in astrocytes by siRNA. The knock down of connexin43 increased the rate of glucose uptake, characterized by the upregulation of GLUT-1 and type I hexokinase. Neither endothelin-1 nor CBX were able to further increase the rate of glucose uptake in connexin43-silenced astrocytes. In agreement, no effects of endothelin-1 and CBX on GLUT-1 and type I hexokinase were observed in connexin-43 silenced astrocytes or in astrocytes from connexin43 knock-out (KO) mice. Our previous studies suggested a close relationship between glucose uptake and astrocyte proliferation. Consistent with this, connexin43-silenced astrocytes exhibited an increase in Ki-67, a marker of proliferation. The effects of ET-1 on retinoblastoma phosphorylation on Ser780 and on the upregulation of cyclins D1 and D3 were affected by the levels of connexin43. In conclusion, our results indicate that connexin43 participates in the effects of endothelin-1 on glucose uptake and proliferation in astrocytes. Interestingly, although the rate of growth in connexin43 KO astrocytes has been reported to be reduced, we observed that an acute reduction in connexin43 by siRNA increased proliferation and glucose uptake. V V C

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Connexin43 is involved in the effect of endothelin‐1 on astrocyte proliferation and glucose uptake

Herrero-González

Valle-Casuso

Sánchez‐Alvarez

et al. 2008

Glia

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“…RGP, radial growth phase melanoma; VGP, vertical growth phase melanoma. overall gene expression in successive genetic alterations that have lead to different cellular phenotypes (Su et al, 2000). Using this strategy, it was possible to identify 12 candidate genes that display a higher level of expression in the tumorigenic, anchorage-independent growth melanoma cell line.…”

Section: Cdna Arrays In Melanomamentioning

confidence: 99%

cDNA array technology in melanoma: An overview

Baldi¹,

Santini²,

Luca³

et al. 2003

Journal Cellular Physiology

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Genetic aberrations, mostly resulting in changes in gene expression, are critical events in cancer onset and progression. The advent of the cDNA array technology allows the screening and the efficient measurement of expression of thousands genes simultaneously in a wide spectrum of experimental and clinical models. This genomic scale approach is being currently used to obtain global views of human cancer gene expression and to identify genetic markers that might be important for diagnosis, prognosis, and therapy. This review discusses some recent findings obtained by means of cDNA arrays investigating the human melanoma.

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“…Taken together, these results suggested the presence of several TS genes on chromosome 6q that play a role in the formation and development of a variety of tumours. Several putative TS genes were subsequently identified, these being PRDM1 on chromosome q21-q22.1 in B-cell NHL (Mock et al, 1996), GJA1 on chromosome 6q21-23 for human melanoma (Su et al, 2000), PLAGL1 on chromosome 6q25 in many solid tumours (Abdollahi et al, 1997), LATS1 on chromosome 6q24-25AE2 in human breast cancer (Morinaga et al, 2000), and IGF2R on 6q25.3 in breast and liver cancers (DaCosta et al, 2000). It is not known why so many different TS genes, and probably others not yet identified, are clustered within the chromosome 6q region.…”

Section: Discussionmentioning

confidence: 99%

A 2·6 Mb interval on chromosome 6q25.2–q25.3 is commonly deleted in human nasal natural killer/T‐cell lymphoma

Sun

Lin

et al. 2003

Br J Haematol

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Summary. Natural killer (NK)/T-cell lymphoma is a special subtype of rare malignant lymphoma that is more prevalent in Asia than in America and Europe. This newly characterized haemato-lymphoid malignancy is highly aggressive and frequently present in nasal and upper aerodigestive sites. Several studies have reported the commonly deleted region of chromosome 6q21-25 in this particular type of lymphoma. To refine the smallest region of overlapping (SRO) deletion for localization of potential tumour suppressor (TS) genes, we performed loss of heterozygosity (LOH) and homozygosity mapping of deletion (HOMOD) analyses on 37 nasal and nasal-type NK/T-cell lymphoma patients using a panel of 25 microsatellite markers, covering the 6q21-q25 region. In all patients studied, LOH was detected in eight (89%) paired-sample patients, while hemizygous deletion was detected in three (11%) singlesample patients. Combination of the LOH and HOMOD results defined a distinct 3 Mb SRO on chromosome 6q25. Quantitative multiplex polymerase chain reaction analysis of 10 sequence-tagged sites further refined the putative TS-gene-containing region to a 2AE6 Mb interval between TIAM2 and SNX9. Eighteen known genes/Unigene clusters and 25 hypothetical genes are located within this 2AE6 Mb region, but none are previously identified TS genes. These results provide a framework for future positional cloning of novel TS gene(s) at 6q25.2-q25.3.

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Identification of Tumor-Suppressor Genes Using Human Melanoma Cell Lines UACC903, UACC903(+6), and SRS3 by Comparison of Expression Profiles

Cited by 60 publications

References 31 publications

Connexin43 is involved in the effect of endothelin‐1 on astrocyte proliferation and glucose uptake

Connexin43 is involved in the effect of endothelin‐1 on astrocyte proliferation and glucose uptake

cDNA array technology in melanoma: An overview

A 2·6 Mb interval on chromosome 6q25.2–q25.3 is commonly deleted in human nasal natural killer/T‐cell lymphoma

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