Biological and enzymatic features of human melanoma clones with different invasive potential

Supino, Rosanna; Mapelli, Elena; Sanfilippo, Ornella; Silvestro, L

doi:10.1097/00008390-199212000-00012

Cited by 26 publications

(18 citation statements)

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“…Human metastatic melanoma cells Me665/2/21 (henceforth called Me21) (kindly provided by Dr. Zunino and Dr. Supino, Istituto Nazionale Tumori, Milan) [17] and human metastatic melanoma cells HT-144 (from ATCC) were cultured in RPMI-1640 medium (Sigma, R5886) containing 10% heat-inactivated foetal bovine serum (Invitrogen, 10270), 50 mg/L gentamycin (Sigma, G1264), 2 mM L-glutamine (Sigma, G6392), at 37°C, in a humidified atmosphere with 5% CO 2 . Human melanoma cells A375 (from ATCC) were cultured in Dulbecco's modified Eagle's medium (DMEM) with 4.5 g/L glucose (Sigma, D5671), containing 5% heat-inactivated foetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

Cisplatin-Induced Apoptosis Inhibits Autophagy, Which Acts as a Pro-Survival Mechanism in Human Melanoma Cells

et al. 2013

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The interplay between a non-lethal autophagic response and apoptotic cell death is still a matter of debate in cancer cell biology. In the present study performed on human melanoma cells, we investigate the role of basal or stimulated autophagy in cisplatin-induced cytotoxicity, as well as the contribution of cisplatin-induced activation of caspases 3/7 and conventional calpains. The results show that, while down-regulating Beclin-1, Atg14 and LC3-II, cisplatin treatment inhibits the basal autophagic response, impairing a physiological pro-survival response. Consistently, exogenously stimulated autophagy, obtained with trehalose or calpains inhibitors (MDL-28170 and calpeptin), protects from cisplatin-induced apoptosis, and such a protection is reverted by inhibiting autophagy with 3-methyladenine or ATG5 silencing. In addition, during trehalose-stimulated autophagy, the cisplatin-induced activation of calpains is abrogated, suggesting the existence of a feedback loop between the autophagic process and calpains. On the whole, our results demonstrate that in human melanoma cells autophagy may function as a beneficial stress response, hindered by cisplatin-induced death mechanisms. In a therapeutic perspective, these findings suggest that the efficacy of cisplatin-based polychemotherapies for melanoma could be potentiated by inhibitors of autophagy.

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Section: Methodsmentioning

confidence: 99%

Cisplatin-Induced Apoptosis Inhibits Autophagy, Which Acts as a Pro-Survival Mechanism in Human Melanoma Cells

et al. 2013

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“…In fact, GGT-positive foci were found in animals exposed to prooxidant carcinogens, suggesting the hypothesis of GGT as an early marker of neoplastic transformation [40, 41]. Moreover, increased levels of GGT have been observed in cancers of the ovaries [42], colon [43], liver [44], melanoma [45], and leukemias [46]. In studies on melanoma cells in vitro and in vivo , elevated GGT activity has been found to accompany an increased invasive growth [45, 47, 48], and a positive correlation has been described between GGT expression and unfavourable prognostic signs in human breast cancer [49].…”

Section: Role Of Gsh In Regulating Cancer Development and Growthmentioning

confidence: 99%

Role of Glutathione in Cancer Progression and Chemoresistance

Traverso

Ricciarelli

Nitti

et al. 2013

Oxidative Medicine and Cellular Longevity

952

779

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Glutathione (GSH) plays an important role in a multitude of cellular processes, including cell differentiation, proliferation, and apoptosis, and disturbances in GSH homeostasis are involved in the etiology and progression of many human diseases including cancer. While GSH deficiency, or a decrease in the GSH/glutathione disulphide (GSSG) ratio, leads to an increased susceptibility to oxidative stress implicated in the progression of cancer, elevated GSH levels increase the antioxidant capacity and the resistance to oxidative stress as observed in many cancer cells. The present review highlights the role of GSH and related cytoprotective effects in the susceptibility to carcinogenesis and in the sensitivity of tumors to the cytotoxic effects of anticancer agents.

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“…Cell lines and chemicals: Three human melanoma cell lines, JR8, SK-MEL-5, MEL501, and two melanoma cell clones, 2/21 and 2/60 (selected from the human melanoma cell line 665/2 by micromanipulation in soft agar), were used in the study [43][44][45]. Cell lines were maintained in logarithmic growth phase at 37°C in a 5% CO 2 humidified atmosphere in air.…”

Section: Biological Studymentioning

confidence: 99%

Synthesis, spectroscopy (IR, multinuclear NMR, ESI-MS), diffraction, density functional study and in vitro antiproliferative activity of pyrazole-beta-diketone dihalotin(IV) compounds on 5 melanoma cell lines

Pettinari¹,

Caruso²,

Zaffaroni³

et al. 2006

Journal of Inorganic Biochemistry

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Biological and enzymatic features of human melanoma clones with different invasive potential

Cited by 26 publications

References 0 publications

Cisplatin-Induced Apoptosis Inhibits Autophagy, Which Acts as a Pro-Survival Mechanism in Human Melanoma Cells

Cisplatin-Induced Apoptosis Inhibits Autophagy, Which Acts as a Pro-Survival Mechanism in Human Melanoma Cells

Role of Glutathione in Cancer Progression and Chemoresistance

Synthesis, spectroscopy (IR, multinuclear NMR, ESI-MS), diffraction, density functional study and in vitro antiproliferative activity of pyrazole-beta-diketone dihalotin(IV) compounds on 5 melanoma cell lines

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