Cellular Characteristics of Protein Autophagy and Mitophagy in the Tumor Microenvironment

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (1 April 2023) | Viewed by 3056

Special Issue Editor


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Guest Editor
Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
Interests: mitophagy; autophagy; tumor microenvironment; mitophagy/autophgay targeting molecular; reactive oxygen species; mitochondrial dysfunction

Special Issue Information

Dear Colleagues,

Autophagy and mitophagy are important cellular processes responsible for breaking down cellular contents and preserving energy against the accumulation of damaged biomolecules. The stimuli for autophagy and mitophagy, such as chemotherapy agents, nonbiological stresses, extracellular physiological stress signals (cytokines), growth factors/hormones and DNA damage, determine the degree to which they are induced. Therefore, exploring the mechanism between autophagy signaling and mitophagy in tumor cells is critical to therapeutic development. In this Special Issue, we encourage submissions on the functional role and molecular mechanisms underlying autophagy and mitophagy in the tumor microenvironment. We also welcome studies researching the cell model and in vivo targeting of autophagy/mitophagy in animal for the treatment of various tumor cells. Original research and review articles are highly encouraged.

Dr. Yi-Hsien Hsieh
Guest Editor

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Keywords

  • mitophagy
  • autophagy
  • tumor microenvironment
  • cellular signaling cascades
  • mitophagy/autophagy targeting molecular
  • reactive oxygen species
  • chemotherapy agents
  • anticancer agents

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Published Papers (1 paper)

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Research

12 pages, 10433 KiB  
Article
Mitophagy Effects of Protodioscin on Human Osteosarcoma Cells by Inhibition of p38MAPK Targeting NIX/LC3 Axis
by Chien-Feng Huang, Yi-Hsien Hsieh, Shun-Fa Yang, Chao-Hung Kuo, Pei-Han Wang, Chung-Jung Liu and Renn-Chia Lin
Cells 2023, 12(3), 395; https://doi.org/10.3390/cells12030395 - 21 Jan 2023
Cited by 5 | Viewed by 2752
Abstract
Protodioscin (PD) is a steroidal saponin with various pharmacological activities, including neuro-protective, anti-inflammatory, and anti-tumor activities. However, the effect of PD on human osteosarcoma (OS) cells is unclear. In this study, we found that PD significantly inhibits the growth of human HOS and [...] Read more.
Protodioscin (PD) is a steroidal saponin with various pharmacological activities, including neuro-protective, anti-inflammatory, and anti-tumor activities. However, the effect of PD on human osteosarcoma (OS) cells is unclear. In this study, we found that PD significantly inhibits the growth of human HOS and 143B OS cells through the upregulation of apoptotic-related proteins (cleaved caspase-3, cleaved caspase-9, and cleaved PARP) and mitophagy-related proteins (LC3B and NIX), which contribute to the induction of apoptosis, and MMP (mitochondrial membrane potential) dysfunction and mitophagy. The inhibition of LC3 or NIX was shown to decrease apoptosis and mitophagy in PD-treated OS cells. The knockdown of p38MAPK by siRNA decreased mitochondrial dysfunction, autophagy, mitophagy, and the NIX/LC3B expression in the PD-treated OS cells. A binding affinity analysis revealed that the smaller the KD value (−7.6 Kcal/mol and −8.9 Kcal/mol, respectively), the greater the binding affinity in the PD-NIX and PD-LC3 complexes. These findings show the inhibitory effects of PD-induced mitophagy in human OS cells and may represent a novel therapeutic strategy for human OS, by targeting the NIX/LC3 pathways. Full article
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