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

2020 ◽  
Vol 21 (6) ◽  
pp. 1939 ◽  
Author(s):  
Manish Adhikari ◽  
Bhawana Adhikari ◽  
Bhagirath Ghimire ◽  
Sanjula Baboota ◽  
Eun Ha Choi
Keyword(s):  
Melanoma Cells ◽  
Cell Number ◽  
Human Melanoma ◽  
Atmospheric Plasma ◽  
Cold Atmospheric Plasma ◽  
Human Melanoma Cells ◽  
Survival Pathways ◽  
Autophagy Induction ◽  
The Media ◽  
Intracellular Glucose

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

Adipocytes Contribute to Resistance of Human Melanoma Cells to Chemotherapy and Targeted Therapy

2014 ◽  
Vol 21 (10) ◽  
pp. 1255-1267 ◽  
Author(s):  
M. Chi ◽  
J. Chen ◽  
Y. Ye ◽  
Hsin-Yi Tseng ◽  
F. Lai ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Human Melanoma Cells

scholarly journals Phosphorylation of ectopically expressed L-plastin enhances invasiveness of human melanoma cells

2007 ◽  
Vol 120 (12) ◽  
pp. 2590-2599 ◽  
Author(s):  
Martin Klemke ◽  
Maria T. Rafael ◽  
Guido H. Wabnitz ◽  
Tatjana Weschenfelder ◽  
Mathias H. Konstandin ◽  
...  
Keyword(s):  
Melanoma Cells ◽  
Human Melanoma ◽  
Human Melanoma Cells

scholarly journals Mitochondrial function is controlled by melatonin and its metabolites in vitro in human melanoma cells

2021 ◽  
Vol 70 (3) ◽  
Author(s):  
Bernadetta Bilska ◽  
Fiona Schedel ◽  
Anna Piotrowska ◽  
Joanna Stefan ◽  
Michal Zmijewski ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Human Melanoma Cells

scholarly journals Ca2+ overload- and ROS-associated mitochondrial dysfunction contributes to δ-tocotrienol-mediated paraptosis in melanoma cells

APOPTOSIS ◽  
2021 ◽  
Author(s):  
Michela Raimondi ◽  
Fabrizio Fontana ◽  
Monica Marzagalli ◽  
Matteo Audano ◽  
Giangiacomo Beretta ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Atp Synthesis ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Ros Generation ◽  
Therapy Outcomes ◽  
Human Melanoma Cells ◽  
Oxphos Complex

Abstract Melanoma is an aggressive tumor with still poor therapy outcomes. δ-tocotrienol (δ-TT) is a vitamin E derivative displaying potent anti-cancer properties. Previously, we demonstrated that δ-TT triggers apoptosis in human melanoma cells. Here, we investigated whether it might also activate paraptosis, a non-canonical programmed cell death. In accordance with the main paraptotic features, δ-TT was shown to promote cytoplasmic vacuolization, associated with endoplasmic reticulum/mitochondrial dilation and protein synthesis, as well as MAPK activation in A375 and BLM cell lines. Moreover, treated cells exhibited a significant reduced expression of OXPHOS complex I and a marked decrease in oxygen consumption and mitochondrial membrane potential, culminating in decreased ATP synthesis and AMPK phosphorylation. This mitochondrial dysfunction resulted in ROS overproduction, found to be responsible for paraptosis induction. Additionally, δ-TT caused Ca2+ homeostasis disruption, with endoplasmic reticulum-derived ions accumulating in mitochondria and activating the paraptotic signaling. Interestingly, by using both IP3R and VDAC inhibitors, a close cause-effect relationship between mitochondrial Ca2+ overload and ROS generation was evidenced. Collectively, these results provide novel insights into δ-TT anti-melanoma activity, highlighting its ability to induce mitochondrial dysfunction-mediated paraptosis. Graphic Abstract δ-tocotrienol induces paraptotic cell death in human melanoma cells, causing endoplasmic reticulum dilation and mitochondrial swelling. These alterations induce an impairment of mitochondrial function, ROS production and calcium overload.

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