Botanical root transforming into cellular structure attacked by light particles

Melanoma Breakthrough: A Natural Compound Offers New Hope

Nico Varela in Health & Wellness June 2025 • 3 min read.

"New research highlights how a compound derived from a traditional medicinal plant could revolutionize melanoma treatment by triggering cell death and inhibiting cancer growth."

Skin cancer diagnoses are increasing, with melanoma being the deadliest form, responsible for a significant percentage of skin cancer fatalities. Melanoma's aggressive nature and rapid progression underscore the urgent need for more effective treatments.

Natural compounds have long been a source of innovative medicines. Researchers are exploring the potential of β-β-Dimethylacrylshikonin (DMAS), a compound isolated from the roots of the Onosma paniculata plant, traditionally used in medicine. This study investigates DMAS's impact on melanoma cells, offering hope for novel therapies.

Past research indicates that DMAS demonstrates potent anti-cancer properties, particularly against melanoma. This study delves deeper, examining how DMAS affects gene expression in melanoma cells to understand its mechanisms and potential therapeutic uses.

How Does DMAS Fight Melanoma?

Botanical root transforming into cellular structure attacked by light particles

The study examined how DMAS impacts gene expression in WM164 melanoma cells. After treating cells with DMAS, researchers identified significant changes in gene expression, pointing to DMAS's ability to alter cellular functions.

The most significant change observed was the increase in sequestosome 1 (p62) levels. P62 is crucial in regulating cell growth, survival, and autophagy—a process where cells break down and recycle their components. This suggests DMAS promotes autophagy, potentially leading to the death of melanoma cells.

Autophagy Induction: DMAS triggers autophagy, a process where cells degrade and recycle their own components.
ROS Generation: DMAS leads to the generation of reactive oxygen species (ROS), which can damage cells.
Mitochondrial Damage: DMAS causes a loss of mitochondrial membrane potential, disrupting cellular energy production.

Further experiments showed that DMAS not only induces autophagy but also leads to the generation of reactive oxygen species (ROS) and disrupts mitochondrial function in melanoma cells. These combined effects contribute to cell death and inhibit cancer growth.

The Future of Melanoma Treatment

DMAS holds promise as a potential melanoma therapy by inducing autophagy, ROS generation, and mitochondrial damage. While further research is needed to refine its application and minimize side effects, DMAS represents a significant step forward in developing more effective and less toxic treatments for melanoma.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.3390/molecules23112823, Alternate LINK

Title: Comparative Gene Expression Analysis In Wm164 Melanoma Cells Revealed That Β-Β-Dimethylacrylshikonin Leads To Ros Generation, Loss Of Mitochondrial Membrane Potential, And Autophagy Induction

Subject: Chemistry (miscellaneous)

Journal: Molecules

Publisher: MDPI AG

Authors: Nadine Kretschmer, Alexander Deutsch, Christin Durchschein, Beate Rinner, Alexander Stallinger, Juan Higareda-Almaraz, Marcel Scheideler, Birgit Lohberger, Rudolf Bauer

Published: 2018-10-30

Everything You Need To Know

How does β-β-Dimethylacrylshikonin (DMAS) specifically target and destroy melanoma cells, and what makes this approach promising?

β-β-Dimethylacrylshikonin, or DMAS, works against melanoma cells by inducing autophagy, generating reactive oxygen species (ROS), and damaging mitochondria. Autophagy involves cells breaking down and recycling their components, while ROS can damage cells. Mitochondrial damage disrupts cellular energy production, all contributing to melanoma cell death and inhibited cancer growth. The combined effect of DMAS disrupting cellular functions offers a multi-pronged approach to combating melanoma. More studies will reveal how these pathways may lead to therapeutics.

What is the significance of increased sequestosome 1 (p62) levels in melanoma cells treated with DMAS, and how does it relate to cell survival?

Sequestosome 1, or p62, plays a vital role in regulating cell growth, survival, and autophagy. Autophagy is a cellular process where cells degrade and recycle their own components. The observed increase in p62 levels upon DMAS treatment suggests that DMAS promotes autophagy in melanoma cells, potentially leading to their death. Further research into how DMAS modulates p62 could reveal more targeted cancer treatment strategies.

Where does β-β-Dimethylacrylshikonin (DMAS) come from, and what is the history of its use in traditional medicine?

DMAS, or β-β-Dimethylacrylshikonin, is a compound isolated from the roots of the Onosma paniculata plant. This plant has been traditionally used in medicine, and DMAS has demonstrated anti-cancer properties, particularly against melanoma. The study of DMAS's effects on melanoma cells offers hope for novel therapies that leverage natural compounds to combat cancer. Further research might explore if other compounds from Onosma paniculata have similar anti-cancer properties.

How do reactive oxygen species (ROS) contribute to the anti-cancer effects of DMAS on melanoma cells?

Reactive oxygen species, or ROS, are generated as a result of DMAS treatment, and can cause damage to melanoma cells. This oxidative stress contributes to cell death and inhibited cancer growth. Understanding the specific mechanisms by which DMAS induces ROS generation could lead to the development of more targeted and effective melanoma therapies.

What role does mitochondrial membrane potential play in the effectiveness of DMAS against melanoma, and how does its disruption lead to cancer cell death?

Mitochondrial membrane potential is crucial for cellular energy production. DMAS causes a loss of this potential, disrupting the energy supply to melanoma cells. This disruption, combined with DMAS-induced autophagy and ROS generation, contributes to the death of cancer cells and inhibits tumor growth. Further research might explore the long term impact of DMAS on mitochondrial health.