Cold Atmospheric Plasma and Silymarin Nanoemulsion Activate Autophagy in Human Melanoma Cells.

Publication date: Mar 12, 2020

Autophagy is reported as a survival or death-promoting pathway that is highly debatable in different kinds of cancer. Here, we examined the co-effect of cold atmospheric plasma (CAP) and silymarin nanoemulsion (SN) treatment on G-361 human melanoma cells via autophagy induction.

The temperature and pH of the media, along with the cell number, were evaluated. The intracellular glucose level and PI3K/mTOR and EGFR downstream pathways were assessed. Autophagy-related genes, related transcriptional factors, and autophagy induction were estimated using confocal microscopy, flow cytometry, and ELISA.

CAP treatment increased the temperature and pH of the media, while its combination with SN resulted in a decrease in intracellular ATP with the downregulation of PI3K/AKT/mTOR survival and RAS/MEK transcriptional pathways. Co-treatment blocked downstream paths of survival pathways and reduced PI3K (2 times), mTOR (10 times), EGFR (5 times), HRAS (5 times), and MEK (10 times). CAP and SN co-treated treatment modulates transcriptional factor expressions (ZKSCAN3, TFEB, FOXO1, CRTC2, and CREBBP) and specific genes (BECN-1, AMBRA-1, MAP1LC3A, and SQSTM) related to autophagy induction.

CAP and SN together activate autophagy in G-361 cells by activating PI3K/mTOR and EGFR pathways, expressing autophagy-related transcription factors and genes.

Open Access PDF

Adhikari, M., Adhikari, B., Ghimire, B., Baboota, S., and Choi, E.H. Cold Atmospheric Plasma and Silymarin Nanoemulsion Activate Autophagy in Human Melanoma Cells. 26141. 2020 Int J Mol Sci (21):6.

Concepts Keywords
ATP Programmed cell death
Autophagy Autophagy
BECN Protein kinases
Cancer Oncology
Confocal Microscopy Signal transduction
CREBBP Branches of biology
Downregulation Enzymes
EGFR Melanoma
ELISA Temperature media combination
Flow Cytometry Phosphoinositide 3-kinase
Glucose Protein kinase B
Intracellular Ras GTPase
Transcription Factors
Transcriptional Factors


Type Source Name
pathway KEGG Autophagy
disease MESH Melanoma
pathway KEGG Melanoma
disease MESH death
disease MESH cancer
drug DRUGBANK Dextrose unspecified form
drug DRUGBANK Rasagiline
drug DRUGBANK Coenzyme M
drug DRUGBANK Oxygen
drug DRUGBANK Nitrogen
disease MESH oxidative stress
pathway KEGG Apoptosis
drug DRUGBANK Gold
drug DRUGBANK Methionine
drug DRUGBANK Water
disease MESH growth
drug DRUGBANK Medical air
drug DRUGBANK Dimercaprol
drug DRUGBANK Nitric Oxide
drug DRUGBANK Albendazole
disease MESH dissociation
disease MESH metabolic stress
drug DRUGBANK Sirolimus
drug DRUGBANK Chloroquine
drug DRUGBANK Isoxaflutole
pathway KEGG Lysosome
disease MESH repression
drug DRUGBANK Phosphate ion
drug DRUGBANK Streptomycin
drug DRUGBANK Trypsin
drug DRUGBANK Edetic Acid
drug DRUGBANK Silver
drug DRUGBANK Dacarbazine
drug DRUGBANK Ethanol
drug DRUGBANK Inositol
drug DRUGBANK Adenosine
drug DRUGBANK Zinc
disease MESH Skin Cancer
drug DRUGBANK Guanosine
disease MESH Community
disease MESH Tumorigenesis
drug DRUGBANK Polyethylene glycol
disease MESH Glioblastoma
disease MESH Metastasis
disease MESH Aging
disease MESH Hepatocellular Carcinoma
pathway KEGG Hepatocellular carcinoma
disease MESH Infectious Diseases
pathway KEGG Oxidative phosphorylation
drug DRUGBANK Trihexyphenidyl
drug DRUGBANK Profenamine
drug DRUGBANK Dabrafenib
disease MESH Endoplasmic Reticulum Stress


Original Article

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