Mitogen-Activated Protein Kinase Signaling Pathway in Cutaneous Melanoma: An Updated Review

Acosta, Andrés; Kadkol, Shrihari S.

doi:10.5858/arpa.2015-0475-rs

Cited by 15 publications

(22 citation statements)

References 33 publications

(71 reference statements)

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“…The most complicated intracellular signal transduction structures are present in the MAPK signaling pathway and, in common, are activated using an extensive cluster of intracellular or extracellular stimuli [52]. Three common components of the MAPK signaling pathway are ERK, JNK, and p38 MAPK pathways, frequently participating in genetic processes despite crosstalk between these signaling pathways at the upper levels of cascades [53]. In this study, we observed ROS uptake in U87 MG cancer cells treated with NBP-J.…”

Section: Discussionmentioning

confidence: 69%

Non-Thermal Atmospheric Pressure Bio-Compatible Plasma Stimulates Apoptosis via p38/MAPK Mechanism in U87 Malignant Glioblastoma

Akter

Jangra

Choi

et al. 2020

Cancers

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Nonthermal plasma is a promising novel therapy for the alteration of biological and clinical functions of cells and tissues, including apoptosis and inhibition of tumor progression. This therapy generates reactive oxygen and nitrogen species (RONS), which play a major role in anticancer effects. Previous research has verified that plasma jets can selectively induce apoptosis in various cancer cells, suggesting that it could be a potentially effective novel therapy in combination with or as an alternative to conventional therapeutic methods. In this study, we determined the effects of nonthermal air soft plasma jets on a U87 MG brain cancer cell line, including the dose- and time-dependent effects and the physicochemical and biological correlation between the RONS cascade and p38/mitogen-activated protein kinase (MAPK) signaling pathway, which contribute to apoptosis. The results indicated that soft plasma jets efficiently inhibit cell proliferation and induce apoptosis in U87 MG cells but have minimal effects on astrocytes. These findings revealed that soft plasma jets produce a potent cytotoxic effect via the initiation of cell cycle arrest and apoptosis. The production of reactive oxygen species (ROS) in cells was tested, and an intracellular ROS scavenger, N-acetyl cysteine (NAC), was examined. Our results suggested that soft plasma jets could potentially be used as an effective approach for anticancer therapy.

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Section: Discussionmentioning

confidence: 69%

Non-Thermal Atmospheric Pressure Bio-Compatible Plasma Stimulates Apoptosis via p38/MAPK Mechanism in U87 Malignant Glioblastoma

Akter

Jangra

Choi

et al. 2020

Cancers

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“…It has been reported that MAPK signal transduction pathway plays an important regulatory role in tumourigenesis and development. Different MAPK signaling pathways can regulate each other and mediate a variety of cellular biological reactions, regulating the proliferation, differentiation and apoptosis of cancer cells [21]. MAPK7, one of its family members, is also known as extracellular signal-regulated kinase 5 (ERK5) and is expressed in a variety of tissues.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of osteosarcoma cells by targeting MAPK7

Hou

Feng

Jiao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objective: To investigate the effects of miR-143-3p and MAPK7 on the proliferation, migration, and invasion of U2OS human osteosarcoma (OS) cells. Methods: The expression of miR-143-3p and MAPK7 in U2OS cells were detected by qRT-PCR, and the protein level of MAPK7 was measured by western blot assay. The targeting relationship between miR-143-3p and MAPK7 was predicted by TargetScan and verified by dual luciferase reporter assay. MTT and Transwell assays were used to detect cell viability, migrated cells and invaded cells of U2OS cells. Results: Compared with hFOB1.19 cells, the expression of miR-143-3p was down-regulated and MAPK7 was up-regulated in U2OS cells. Cell viability, migration and invasion ability significantly decreased induced by miR-143-3p overexpression or MAPK7 knockdown in U2OS cells. The results of dual luciferase reporter assay indicated that miR-143-3p interacted with MAPK7. Furthermore, overexpression of MAPK7 could reverse the inhibitory effects on cell proliferation, migration and invasion in U2OS cells induced by miR-143-3p mimics. Conclusion: miR-143-3p could inhibit proliferation, migration and invasion of U2OS cells by targeting MAPK7.

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“…imlygic (talimogene laherparepvec/T-Vec, a herpesvirus-based vector optimised for oncolytic and immunomodulatory activities) represent a new class of anti-melanoma agents that have recently been approved for treatment [42]. Currently, the highest survival rates are obtained for melanoma patients with the BRAF V600E mutation with vemurafenib, dabrafenib or trametinib that are low molecular weight inhibitors of the B-Raf serinethreonine kinase [43,44]. In melanoma cells harboring the BRAF V600E mutations, the mitogen-activated protein kinase (MAPK) pathway is permanently activated, which ultimately leads to uncontrolled cell proliferation and which can be reversed by inhibition of B-Raf.…”

Section: Introductionmentioning

confidence: 99%

Synthetic Peptide Drugs for Targeting Skin Cancer: Malignant Melanoma and Melanotic Lesions

Eberlé

Rout

et al. 2017

CMC

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Peptides play decisive roles in the skin, ranging from host defense responses to various forms of neuroendocrine regulation of cell and organelle function. Synthetic peptides conjugated to radionuclides or photosensitizers may serve to identify and treat skin tumors and their metastatic forms in other organs of the body. In the introductory part of this review, the role and interplay of the different peptides in the skin are briefly summarized, including their potential application for the management of frequently occurring skin cancers. Special emphasis is given to different targeting options for the treatment of melanoma and melanotic lesions. Radionuclide Targeting: α-Melanocyte-stimulating hormone (α-MSH) is the most prominent peptide for targeting of melanoma tumors via the G protein-coupled melanocortin-1 receptor that is (over-)expressed by melanoma cells and melanocytes. More than 100 different linear and cyclic analogs of α-MSH containing chelators for 111In, 67/68Ga, 64Cu, 90Y, 212Pb, 99mTc, 188Re were synthesized and examined with experimental animals and in a few clinical studies. Linear Ac-Nle-Asp-His-D-Phe-Arg-Trp-Gly-Lys-NH2 (NAP-amide) and Re-cyclized Cys- Cys-Glu-His-D-Phe-Arg-Trp-Cys-Arg-Pro-Val-NH2 (Re[Arg11]CCMSH) containing different chelators at the N- or C-terminus served as lead compounds for peptide drugs with further optimized characteristics. Alternatively, melanoma may be targeted with radiopeptides that bind to melanin granules occurring extracellularly in these tumors. Photosensitizer targeting: A more recent approach is the application of photosensitizers attached to the MSH molecule for targeted photodynamic therapy using LED or coherent laser light that specifically activates the photosensitizer. Experimental studies have demonstrated the feasibility of this approach as a more gentle and convenient alternative compared to radionuclides.

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Mitogen-Activated Protein Kinase Signaling Pathway in Cutaneous Melanoma: An Updated Review

Cited by 15 publications

References 33 publications

Non-Thermal Atmospheric Pressure Bio-Compatible Plasma Stimulates Apoptosis via p38/MAPK Mechanism in U87 Malignant Glioblastoma

Non-Thermal Atmospheric Pressure Bio-Compatible Plasma Stimulates Apoptosis via p38/MAPK Mechanism in U87 Malignant Glioblastoma

Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of osteosarcoma cells by targeting MAPK7

Synthetic Peptide Drugs for Targeting Skin Cancer: Malignant Melanoma and Melanotic Lesions

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