Experimental metastasis correlates with cyclic AMP accumulation in B16 melanoma clones

Sheppard, J. R.; Koestler, Thomas P.; Corwin, Steven P.; Buscarino, Charles; Doll, John; Lester, Bruce R.; Greig, Russell; Poste, George

doi:10.1038/308544a0

Cited by 50 publications

(46 citation statements)

References 22 publications

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“…In an earlier investigation we examined the responsiveness of a series of B16 melanoma clones with different metastatic capacities to stimulation by MSH and forskolin (Sheppard et al, 1984). Based on the accumulation of cAMP following exposure to these agents, it was found that the B16 melanoma cell clones segregated into high and low responders.…”

Section: Discuss I 0 Nmentioning

confidence: 98%

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Biochemical regulation of adenylate cyclase in murine melanoma clones with different metastatic properties

Sheppard¹,

Lester²,

Doll³

et al. 1986

Intl Journal of Cancer

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The regulation of adenylate cyclase in murine melanoma tumor cell clones with different metastatic capacities has been studied in intact cells and isolated membrane preparations. Analysis of the responses of intact cells from a number of B16 melanoma clones revealed that treatment with melanocyte-stimulating hormone (MSH) or the diterpene, forskolin, produced significantly greater accumulation of intracellular cyclic adenosine 3',5' monophosphate (cAMP) in strongly metastatic clones than in weakly metastatic tumor cell clones. In contrast, in isolated membranes from the same panel of clones, the extent of activation by forskolin but not by MSH correlated with metastatic capacity. Sodium fluoride and 5'-guanyl-beta-gamma-imidodiphosphate [Gpp(NH)p] also stimulated adenylate cyclase in isolated membranes but the extent of activation did not correlate with the metastatic behavior of the donor cells. A combination of forskolin and Gpp(NH)p proved to be a sensitive prospective indicator for identifying differences in the metastatic capabilities of individual B16 melanoma clones. Adenylate cyclase in membrane preparations from strongly metastatic B16 clones displayed synergistic activation but stimulation of the enzyme from weakly metastatic clones was less than additive. To test the generality of these findings, similar investigations were performed on B16-BL6 melanoma cells, a highly invasive subline of the B16 melanoma, and the K1735, an ultraviolet-light-induced murine melanoma arising in a different mouse strain (C3H). Consistent with their high metastatic potential, clones derived from the B16-BL6 melanoma displayed elevated levels of hormonally-stimulated adenylate cyclase, thereby confirming, for this tumor system, a close association between hormonal responsiveness and metastatic capacity. In contrast, K1735 melanoma cell clones exhibited significant interclonal variation in adenylate cyclase activity and metastatic performance, but no consistent relationship between the two traits was detected. Differences in the regulation and/or the intrinsic catalytic capacity of adenylate cyclase may account, at least in part, for the variation in hormonal responsiveness observed among B16 clones with distinct metastatic properties and suggest that cAMP-dependent molecular processes may be required for the expression of B16 melanoma experimental metastatic potential.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Discuss I 0 Nmentioning

confidence: 98%

“…Clones were isolated as described . From a panel of over 30 B16 melanoma clones that had been characterized in terms of their hormonal responsiveness and metastatic capacity (Sheppard et al, 1984), 5 were chosen for detailed analysis of adenylate cyclase func-…”

Section: Cell Culturesmentioning

confidence: 99%

Biochemical regulation of adenylate cyclase in murine melanoma clones with different metastatic properties

Sheppard¹,

Lester²,

Doll³

et al. 1986

Intl Journal of Cancer

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“…Compared with normal cells, lower cAMP concentrations were found in certain tumor cells, which revealed that cAM Phas a negative role in cell proliferation (30). Additionally, intracellular cAMP levels were reported to be associated with the metastatic ability of tumor cells (31,32). Epidermal growth factor signaling has been well studied with regards to controlling cell proliferation, differentiation and migration (33).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of calcyphosine is associated with poor prognosis in esophageal squamous cell carcinoma

Zhu

Yang

et al. 2017

Oncol Lett

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Abstract. Calcyphosine (CAPS), a calcium-binding protein, has been identified as a potential diagnostic and prognostic biomarker in several human carcinomas. However, little is known about CAPS in esophageal squamous cell carcinoma (ESCC). The present study aimed to investigate the expression levels of CAPS in ESCC tissues and evaluate its clinicopathological significance. Reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining were conducted to detect the expression of CAPS in ESCC tissues and adjacent non-cancerous tissues. ESCC samples exhibited higher levels of CAPS mRNA than paired non-cancerous samples (P=0.0015), and the mRNA level of CAPS was positively associated with histological grade (P=0.0013) and tumor invasion depth (P=0.0206). In addition, Kaplan-Meier survival analysis revealed that patients with high CAPS expression experienced significantly shorter 5-year overall survival times than those with low CAPS expression (P=0.0112). Multivariate analysis demonstrated that CAPS protein expression was an independent prognostic biomarker for patients with ESCC. In conclusion, the findings of the present study demonstrated that CAPS may represent a novel diagnostic indicator and an independent prognostic biomarker in ESCC.

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“…However, a-MSH is reported to both stimulate and inhibit melanoma invasion in vitro and in vivo. Murine melanoma cells respond to a-MSH stimulation in vitro with a higher number of metastases in vivo, and a positive correlation exists between murine melanoma cell response to a-MSH (assessed by cAMP elevation) in vitro and metastatic success in vivo (Sheppard et al, 1984;Hill et al, 1990). However, a-MSH can inhibit B16-BL6 melanoma invasion through reconstituted (Matrigel) basement membrane (Murata et al, 1997), and reduce colony formation by 50%, in agreement with similar work in B16-F10 cells (Kameyama et al, 1990).…”

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confidence: 99%

Anti-inflammatory and anti-invasive effects of α-melanocyte-stimulating hormone in human melanoma cells

et al. 2003

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a-Melanocyte stimulating hormone (a-MSH) is known to have pleiotrophic functions including pigmentary, anti-inflammatory, antipyretic and immunoregulatory roles in the mammalian body. It is also reported to influence melanoma invasion with levels of a-, b-and g-MSH correlated clinically with malignant melanoma development, but other studies suggest a-MSH acts to retard invasion. In the present study, we investigated the action of a-MSH on three human melanoma cell lines (HBL, A375-SM and C8161) differing in metastatic potential. a-melanocyte-simulating hormone reduced invasion through fibronectin and also through a human reconstructed skin composite model for the HBL line, and inhibited proinflammatory cytokine-stimulated activation of the NF-kB transcription factor. However, A375-SM and C8161 cells did not respond to a-MSH. Immunofluorescent microscopy and Western blotting identified melanocortin-1 receptor (MC-1R) expression for all three lines and MC-2R on HBL and A375-SM lines. Receptor binding identified a similar affinity for a-MSH for all three lines with the highest number of binding sites on HBL cells. Only the HBL melanoma line demonstrated a detectable cyclic adenosine monophosphate (cAMP) response to a-MSH, although all three lines responded to acute a-MSH addition ( þ (À)-N 6 -(2-phenylisopropyl)-adenosine (PIA)) with an elevation in intracellular calcium. The nonresponsive lines displayed MC-1R polymorphisms (C8161, Arg (wt) 151/Cys 151; A375-SM, homozygous Cys 151), whereas the HBL line was wild type. Stable transfection of the C8161 line with wild-type MC-1R produced cells whose invasion was significantly inhibited by a-MSH. From this data, we conclude that a-MSH can reduce melanoma cell invasion and protect cells against proinflammatory cytokine attack in cells with the wild-type receptor (HBL).

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Experimental metastasis correlates with cyclic AMP accumulation in B16 melanoma clones

Cited by 50 publications

References 22 publications

Biochemical regulation of adenylate cyclase in murine melanoma clones with different metastatic properties

Biochemical regulation of adenylate cyclase in murine melanoma clones with different metastatic properties

Overexpression of calcyphosine is associated with poor prognosis in esophageal squamous cell carcinoma

Anti-inflammatory and anti-invasive effects of α-melanocyte-stimulating hormone in human melanoma cells

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