scholarly journals Mitophagy in carcinogenesis and cancer treatment

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tatiana V. Denisenko ◽  
Vladimir Gogvadze ◽  
Boris Zhivotovsky
Keyword(s):  
Quality Control ◽  
Cancer Treatment ◽  
Cancer Progression ◽  
Control Mechanism ◽  
Current Knowledge ◽  
Mitochondrial Proteins ◽  
Mitochondrial Network ◽  
Cellular Homeostasis ◽  
Anticancer Treatment ◽  
Quality Control Mechanism

AbstractIn order to maintain a functional mitochondrial network, cells have developed a quality control mechanism, namely mitophagy. This process can be induced through different pathways. The most studied is the so-called PINK1/Parkin pathway, which is associated with ubiquitylation of several mitochondrial proteins that were initially found to be related to Parkinson’s disease. Another type of mitophagy is known as receptor-mediated mitophagy, which includes proteins, such as BNIP3 and BNIP3L, also known as Nix. Through these two mechanisms, mitophagy fulfills its functions and maintains cellular homeostasis. Here, we summarize the current knowledge about the mechanisms of mitophagy regulation and their interplay with cancer progression as well as anticancer treatment.

scholarly journals Quality-Control Mechanism for Telomerase RNA Folding in the Cell

Cell Reports ◽  
2020 ◽  
Vol 33 (13) ◽  
pp. 108568
Author(s):  
Xichan Hu ◽  
Jin-Kwang Kim ◽  
Clinton Yu ◽  
Hyun-Ik Jun ◽  
Jinqiang Liu ◽  
...  
Keyword(s):  
Quality Control ◽  
Rna Folding ◽  
Control Mechanism ◽  
Telomerase Rna ◽  
Quality Control Mechanism

scholarly journals Intra- and Intercellular Quality Control Mechanisms of Mitochondria

2017 ◽  
Author(s):  
Yoshimitsu Kiriyama ◽  
Hiromi Nochi
Keyword(s):  
Quality Control ◽  
Cell Death ◽  
Extracellular Vesicles ◽  
Mitochondrial Function ◽  
Current Knowledge ◽  
Control Mechanisms ◽  
Tunneling Nanotubes ◽  
Cellular Homeostasis

Mitochondria function to generate ATP and also play important roles in cellular homeostasis, signaling, apoptosis, autophagy, and metabolism. The loss of mitochondrial function results in cell death and various types of diseases. Therefore, quality control of mitochondria via intra- and intercellular pathways is crucial. Intracellular quality control consists of biogenesis, fusion and fission, and degradation of mitochondria in the cell, whereas intercellular quality control involves tunneling nanotubes and extracellular vesicles. In this review, we outline the current knowledge on the intra- and intercellular quality control mechanisms of mitochondria.

Rho GTPase Activating Protein 9 (ARHGAP9) in Human Cancers

2021 ◽  
Vol 16 ◽  
Author(s):  
Wenping Song ◽  
Jinhua Chen ◽  
Shuolei Li ◽  
Ding Li ◽  
Yongna Zhang ◽  
...  
Keyword(s):  
Cancer Treatment ◽  
Cancer Progression ◽  
Rho Gtpases ◽  
Rho Gtpase ◽  
Current Knowledge ◽  
Clinical Success ◽  
Predictive Biomarker ◽  
Migration And Invasion ◽  
Targeted Drugs ◽  
Gtpase Activating Protein

Background: In recent years, targeted therapy combined with traditional chemoradiotherapy and surgery has brought new opportunities for cancer treatment. However, the complex characteristics of cancer, such as heterogeneity and diversity, limit the clinical success of targeted drugs. The discovery of new cancer targets and deepening the understanding of their functional mechanisms will bring additional promising application prospects for the research and development of personalized cancer-targeted drugs. Objective: This study aimed to summarize the role of the Rho GTPase activating protein 9 (ARHGAP9) gene in tumorigenesis and development to discover therapeutic targets for cancer in the future. Methods: For this review, we collected patents from the databases of Espacenet and WIPO and articles from PubMed that were related to the ARHGAP9 gene. Results: Genetic/epigenetic variations and abnormal expression of the ARHGAP9 gene are closely associated with a variety of diseases, including cancer. ARHGAP9 can inactivate Rho GTPases by hydrolyzing GTP into GDP and regulate cancer cellular events, including proliferation, differentiation, apoptosis, migration and invasion, by inhibiting JNK/ERK/p38 and PI3K/AKT signaling pathways. In addition to reviewing these mechanisms, we assessed various patents on ARHGAP9 to determine whether ARHGAP9 might be used as a predictive biomarker for diagnosis/prognosis evaluation and a druggable target for cancer treatment. Conclusion: In this review, the current knowledge of ARHGAP9 in cancer is summarized with an emphasis on its molecular function, regulatory mechanism and disease implications. Its characterization is crucial to understanding its important roles during different stages of cancer progression and therapy as a predictive biomarker and/or target.

Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila

Genome ◽  
2017 ◽  
Vol 60 (3) ◽  
pp. 241-247
Author(s):  
P. Githure M’Angale ◽  
Brian E. Staveley
Keyword(s):  
Gene Expression ◽  
Quality Control ◽  
Early Onset ◽  
Autosomal Recessive ◽  
Control Mechanism ◽  
Nigrostriatal Neurons ◽  
Climbing Ability ◽  
Quality Control Mechanism ◽  
Locomotor Ability ◽  
Early Onset Parkinson’S Disease

Mutations in parkin (PARK2) and Pink1 (PARK6) are responsible for autosomal recessive forms of early onset Parkinson’s disease (PD). Attributed to the failure of neurons to clear dysfunctional mitochondria, loss of gene expression leads to loss of nigrostriatal neurons. The Pink1/parkin pathway plays a role in the quality control mechanism aimed at eliminating defective mitochondria, and the failure of this mechanism results in a reduced lifespan and impaired locomotor ability, among other phenotypes. Inhibition of parkin or Pink1 through the induction of stable RNAi transgene in the Ddc-Gal4-expressing neurons results in such phenotypes to model PD. To further evaluate the effects of the overexpression of the Bcl-2 homologue Buffy, we analysed lifespan and climbing ability in both parkin-RNAi- and Pink1-RNAi-expressing flies. In addition, the effect of Buffy overexpression upon parkin-induced developmental eye defects was examined through GMR-Gal4-dependent expression. Curiously, Buffy overexpression produced very different effects: the parkin-induced phenotypes were enhanced, whereas the Pink1-enhanced phenotypes were suppressed. Interestingly, the overexpression of Buffy along with the inhibition of parkin in the neuron-rich eye results in the suppression of the developmental eye defects.

Where Parkin Parks

2013 ◽  
Vol 6 (273) ◽  
pp. ec96-ec96
Author(s):  
L. Bryan Ray
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Quality Control ◽  
Protein Kinase ◽  
Full Text ◽  
Control Mechanism ◽  
Membrane Depolarization ◽  
Mitofusin 2 ◽  
Link Type ◽  
Quality Control Mechanism

Damaged mitochondria are removed from cells in a process known as mitophagy. Failure of this quality-control mechanism contributes to Parkinson’s disease. When damaged mitochondria lose membrane depolarization, the protein kinase, PINK1, accumulates on the mitochondrial surface, recruits Parkin, and promotes mitophagy. Chen and Dorn describe another component of this process, mitofusin 2, which appears to function as the receptor for Parkin on the surface of damaged mitochondria.Y. Chen, G. W. Dorn II, PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria. Science340, 471–475 (2013). [Abstract] [Full Text]

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