Effect of proteasome inhibitors on proliferation and apoptosis of human cutaneous melanoma-derived cell lines

Sorolla, Anabel; Yeramian, Andrée; Dolcet, Xavier; Santos, Ana M.; Llobet, David; Schoenenberger, Joan Antoni; Casanova, Josep Manel; Gili, Xavier Soria; Egido, R.; Llombart, Antonio; Vilella, Ramón; Matías‐Guiu, Xavier; Martí, Rosa M.

doi:10.1111/j.1365-2133.2007.08390.x

Cited by 38 publications

(33 citation statements)

References 44 publications

(45 reference statements)

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“…20,21 The cell lines were cultured in Dulbecco's Modified Eagle Medium (DMEM) (Gibco ® Cell Culture, Barcelona, Spain) with 10% fetal calf serum (FCS; Gibco ® ) and 20 mM penicillin/ streptomycin/glutamine (Sigma-Aldrich, Madrid, Spain) at 37°C and in 5% CO 2 . The cells were trypsinized and plated in 96-well plates and incubated with octreotide or SOM230 (Novartis, Basel, Switzerland) for 1, 3 and 6 days.…”

Section: Malignant Melanoma Cell Lines and Cell Culturementioning

confidence: 99%

Expression of Somatostatin Receptors in Human Melanoma Cell Lines: Effect of Two Different Somatostatin Analogues, Octreotide and SOM230, on Cell Proliferation

Martínez-Alonso¹,

Llecha²,

Mayorga

et al. 2009

J Int Med Res

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Section: Malignant Melanoma Cell Lines and Cell Culturementioning

confidence: 99%

Expression of Somatostatin Receptors in Human Melanoma Cell Lines: Effect of Two Different Somatostatin Analogues, Octreotide and SOM230, on Cell Proliferation

Martínez-Alonso¹,

Llecha²,

Mayorga

et al. 2009

J Int Med Res

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“…Therefore, inhibition of proteasome activity has emerged as a new chemotherapy strategy for malignant tumors. Although studies have shown that inhibition of proteasome activity could inhibit cellular proliferation in several tumor cell lines including melanoma, prostate cancer and glioma cells [3][4][5][6] , its underlying mechanism is not fully understood. The proteasome inhibitor bortezomib has been authorized by the US Food and Drug Administration to enter clinical trials, but it is used mainly in the leukemia field.…”

Section: Introductionmentioning

confidence: 99%

Proteasome inhibitor MG-132 induces C6 glioma cell apoptosis via oxidative stress

et al. 2011

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Aim: Proteasome inhibitors have been found to suppress glioma cell proliferation and induce apoptosis, but the mechanisms are not fully elucidated. In this study we investigated the mechanisms underlying the apoptosis induced by the proteasome inhibitor MG-132 in glioma cells. Methods: C6 glioma cells were used. MTT assay was used to analyze cell proliferation. Proteasome activity was assayed using Succinyl-LLVY-AMC, and intracellular ROS level was evaluated with the redox-sensitive dye DCFH-DA. Apoptosis was detected using fluorescence and transmission electron microscopy as well as flow cytometry. The expression of apoptosis-related proteins was investigated using Western blot analysis. Results: MG-132 inhibited C6 glioma cell proliferation in a time-and dose-dependent manner (the IC 50 value at 24 h was 18.5 μmol/L). MG-132 (18.5 μmol/L) suppressed the proteasome activity by about 70% at 3 h. It induced apoptosis via down-regulation of antiapoptotic proteins Bcl-2 and XIAP, up-regulation of pro-apoptotic protein Bax and caspase-3, and production of cleaved C-terminal 85 kDa PARP). It also caused a more than 5-fold increase of reactive oxygen species. Tiron (1 mmol/L) effectively blocked oxidative stress induced by MG-132 (18.5 μmol/L), attenuated proliferation inhibition and apoptosis in C6 glioma cells, and reversed the expression pattern of apoptosis-related proteins. Conclusion: MG-132 induced apoptosis of C6 glioma cells via the oxidative stress.

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“…41 Preclinical studies revealed bortezomib to be effective at inhibiting the in vitro growth of several human melanoma cell lines. 42 A phase II study of bortezomib alone in the treatment of metastatic melanoma proved to be ineffective. 43 Bortezomib may achieve better results if used in combination with chemotherapeutic drugs.…”

Section: Fibrohistiocytic Tumorsmentioning

confidence: 99%

Angiogenesis in cutaneous disease: Part II

Laquer

Hoang

Nguyen

et al. 2009

Journal of the American Academy of Dermatology

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This review will discuss the role of angiogenesis in specific cutaneous diseases. Scientific evidence now points to the role of angiogenesis in tumor development and many other cutaneous disorders. Angiogenesis is a complex process that involves angiogenic growth factors and inhibitors, many of which could be a potential target for pharmacologic intervention. Antiangiogenic agents have recently been applied to dermatologic diseases with promising efficacy. ( J Am Acad Dermatol 2009;61:945-58.)Learning objectives: After completing this learning activity, participants should be able to recognize cutaneous diseases where angiogenesis is likely to be an important factor, recognize scenarios where angiogenic therapy may be useful in conjunction with traditional therapies, and be able to use angiogenicmediating agents in the treatment of dermatologic disease.

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Effect of proteasome inhibitors on proliferation and apoptosis of human cutaneous melanoma-derived cell lines

Cited by 38 publications

References 44 publications

Expression of Somatostatin Receptors in Human Melanoma Cell Lines: Effect of Two Different Somatostatin Analogues, Octreotide and SOM230, on Cell Proliferation

Expression of Somatostatin Receptors in Human Melanoma Cell Lines: Effect of Two Different Somatostatin Analogues, Octreotide and SOM230, on Cell Proliferation

Proteasome inhibitor MG-132 induces C6 glioma cell apoptosis via oxidative stress

Angiogenesis in cutaneous disease: Part II

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