Related Experiment Video
Updated: Aug 12, 2026

Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
Published on: September 7, 2013
Death receptors and melanoma resistance to apoptosis
Vladimir N Ivanov1, Anindita Bhoumik, Ze'ev Ronai
1Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, NY 10029, USA.
Abstract:
Impaired ability to undergo programmed cell death in response to a wide range of external stimuli acquires melanomas a selective advantage for progression and metastasis as well as their notorious resistance to therapy. Better understanding of mechanisms that govern apoptosis has enabled identification of diverse routes by which melanomas manage to escape stimuli of apoptosis. Changes at genomic, transcriptional and post-translational levels of G-proteins and protein kinases (Ras, B-Raf) and their transcription factor effectors (c-Jun, ATF2, Stat3 and NF-kappaB) affects TNF, Fas and TRAIL receptors, which play important roles in acquiring melanoma's resistance to apoptosis. Here, we summarize our current understanding of changes that alters the regulation of death receptors during melanoma development.
Insights
Melanomas evade apoptosis, programmed cell death, enabling progression and therapy resistance. Understanding altered death receptor regulation in melanoma is key to overcoming this resistance.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Research
Background:
- Melanomas exhibit impaired apoptosis, contributing to progression, metastasis, and therapeutic resistance.
- Understanding the mechanisms of apoptosis evasion is crucial for developing effective melanoma treatments.
Purpose of the Study:
- To summarize current knowledge on how altered death receptor regulation contributes to melanoma's resistance to apoptosis.
- To highlight key molecular players involved in melanoma's evasion of programmed cell death.
Main Methods:
- Review and synthesis of existing research on melanoma apoptosis evasion.
- Analysis of genomic, transcriptional, and post-translational alterations affecting signaling pathways.
Main Results:
- Melanomas escape apoptosis through diverse mechanisms.
- Alterations in G-proteins and protein kinases (Ras, B-Raf) and their transcription factors (c-Jun, ATF2, Stat3, NF-kappaB) impact TNF, Fas, and TRAIL receptor signaling.
- These changes are critical for melanoma's resistance to apoptosis.
Conclusions:
- Altered regulation of death receptors is a significant factor in melanoma development and resistance.
- Targeting these altered pathways may offer new therapeutic strategies for melanoma.
More Related Videos
09:53Using X-ray Crystallography, Biophysics, and Functional Assays to Determine the Mechanisms Governing T-cell Receptor Recognition of Cancer Antigens
Published on: February 6, 2017
06:09Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
Published on: June 7, 2019
Related Concept Videos
Treatment Resistant Cancers
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
Apoptosis
The Extrinsic Apoptotic Pathway
The Intrinsic Apoptotic Pathway
Cellular Injury V: Apoptosis and Autophagy