PUMA dependent mitophagy by Abrus agglutinin contributes to apoptosis through ceramide generation

Panda, Prashanta Kumar; Naik, Prajna Paramita; Meher, Biswa Ranjan; Das, Durgesh Nandini; Mukhopadhyay, Subhadip; Praharaj, Prakash Priyadarshi; Maiti, Tapas K.; Bhutia, Sujit K.

doi:10.1016/j.bbamcr.2017.12.002

Cited by 42 publications

(26 citation statements)

References 43 publications

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“…This bioactive sphingolipid is involved in senescence, inhibition of cell proliferation, inflammation, and in the induction of several pathways of cell death, including apoptosis, autophagy, and parthanatos (15,49,54,55). Cer-mediated cell death is frequently associated with mitochondrial dysfunction (56)(57)(58)(59).…”

Section: Ceramide: the Death Orchestratormentioning

confidence: 99%

Sphingolipids as critical players in retinal physiology and pathology

Simón

Basu

Qaladize

et al. 2021

Journal of Lipid Research

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Sphingolipids have emerged as bioactive lipids involved in the regulation of many physiological and pathological processes. In the retina, they have been established to participate in numerous processes, such as neuronal survival and death, proliferation and migration of neuronal and vascular cells, inflammation, and neovascularization. Dysregulation of sphingolipids is, therefore, crucial in the onset and progression of retinal diseases. This review examines the involvement of sphingolipids in retinal physiology and diseases. Ceramide (Cer) emerges as a common mediator of inflammation and death of neuronal and retinal pigment epithelium cells in animal models of retinopathies such as glaucoma, age-related macular degeneration (AMD), and retinitis pigmentosa. Sphingosine-1-phosphate (S1P) has opposite roles, preventing photoreceptor and ganglion cell degeneration but also promoting inflammation, fibrosis, and neovascularization in AMD, glaucoma, and pro-fibrotic disorders. Alterations in Cer, S1P, and ceramide-1-phosphate may also contribute to uveitis. Notably, use of inhibitors that either prevent Cer increase or modulate S1P signaling, such as Myriocin, desipramine, and Fingolimod (FTY720), preserves neuronal viability and retinal function. These findings underscore the relevance of alterations in the sphingolipid metabolic network in the etiology of multiple retinopathies and highlight the potential of modulating their metabolism for the design of novel therapeutic approaches.

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Section: Ceramide: the Death Orchestratormentioning

confidence: 99%

Sphingolipids as critical players in retinal physiology and pathology

Simón

Basu

Qaladize

et al. 2021

Journal of Lipid Research

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“…A pro-apoptotic mechanism of mitophagy was also reported. Induction of mitophagy in cancer cells, by treatment with valinomycin, Abrus agglutinin (AGG), abiraterone or MDV3100 (anti-cancer drugs), led to an increase in apoptosis, facilitating cancer recovery (Panda et al, 2018;Ding et al, 2019;Han et al, 2019). The Bcl-2 family member BCL-B and the levels of phosphorylated Parkin appeared to be central in this response (Ding et al, 2019).…”

Section: Pro-apoptotic Effects Of Mitophagymentioning

confidence: 99%

“…Thus, elimination of dysfunctional mitochondria by mitophagy is critical for cellular survival (Pickles et al, 2018;Allen and Baehrecke, 2020;Markaki and Tavernarakis, 2020). Despite being mostly pro-survival, mitophagy can also synergize with apoptosis to instead promote cell death (Yee et al, 2010;Panda et al, 2018;Ding et al, 2019;Han et al, 2019). Here, we discuss how the mitochondrial fusion factors, mitofusins, impact on mitophagy and apoptosis, present pro-survival and pro-apoptotic roles of mitophagy and detail the roles of mitophagy and mitofusin 2 in non-alcoholic fatty liver disease (NAFLD).…”

Section: Introductionmentioning

confidence: 99%

Role of Mitofusins and Mitophagy in Life or Death Decisions

Joaquim

Escobar-Henriques

2020

Front. Cell Dev. Biol.

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Mitochondria entail an incredible dynamism in their morphology, impacting death signaling and selective elimination of the damaged organelles. In turn, by recycling the superfluous or malfunctioning mitochondria, mostly prevalent during aging, mitophagy contributes to maintain a healthy mitochondrial network. Mitofusins locate at the outer mitochondrial membrane and control the plastic behavior of mitochondria, by mediating fusion events. Besides deciding on mitochondrial interconnectivity, mitofusin 2 regulates physical contacts between mitochondria and the endoplasmic reticulum, but also serves as a decisive docking platform for mitophagy and apoptosis effectors. Thus, mitofusins integrate multiple bidirectional inputs from and into mitochondria and ensure proper energetic and metabolic cellular performance. Here, we review the role of mitofusins and mitophagy at the crossroad between life and apoptotic death decisions. Furthermore, we highlight the impact of this interplay on disease, focusing on how mitofusin 2 and mitophagy affect non-alcoholic fatty liver disease.

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“…More importantly, FoxO3a can be regulated by SIRT1 and thus is implicated in pathogenesis of autoimmune thyroid diseases [17]. In addition, P53-up-regulated modulator of apoptosis (PUMA), a member of Bcl2 family, is identified as an inducer of cell apoptosis [18,19]. Interestingly, FOXO3a can activate PUMA to facilitate the apoptosis of prostate cancer cells, highlighting the importance of their interaction in tumorigenesis [20].…”

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confidence: 99%

WITHDRAWN: Contribution of microRNA-30d to the prevention of the thyroid cancer progression: mechanism and implications

Shao¹,

Zhang²,

Wang³

et al. 2020

Preprint

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Background Thyroid cancer is a major endocrine tumor and represents an emerging health problem worldwide. MicroRNAs (miRNAs) have been addressed to be associated with the pathogenesis and progression of thyroid cancer. However, it remains largely unknown what functions miR-30d may exert on thyroid cancer. This study herein aimed to identify the functional significance and mechanism of miR-30d in the progression of thyroid cancer. Methods The expression of miR-30d and ubiquitin-specific protease 22 (USP22) in cancerous tissues of patients with thyroid cancer was measured using RT-qPCR and Western blot analysis. In response to the gain- or loss-of-function of miR-30d and USP22, cell apoptosis was evaluated by flow cytometry and TUNEL staining in combination with the measurement of apoptosis-related proteins. The interactions among miR-30d, USP22, SIRT1, FOXO3a and PUMA were explored using a series of assays, including dual-luciferase reporter gene assay, Co-IP and ChIP assay. The effects of miR-30d and USP22 on thyroid tumorigenesis were finally validated in vivo. Results MiR-30b presented aberrant low expression in thyroid cancer tissues and this low expression correlated with poor prognosis of thyroid cancer patients. miR-30d promoted apoptosis of thyroid cancer cells through targeting USP22, an up-regulated gene in thyroid cancer. USP22 could enhance the stability of SIRT1 by inducing deubiquitination which consequently contributed to FOXO3a deacetylation-induced PUMA repression. It was verified that this regulatory mechanism was responsible for the pro-apoptotic effect of miR-30d by the in vivo tumorigenicity assay. Conclusion To conclude, the progression of thyroid cancer can be suppressed by miR-30d-mediated inhibition of USP22, provides a promising therapeutic target for thyroid cancer treatment.

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PUMA dependent mitophagy by Abrus agglutinin contributes to apoptosis through ceramide generation

Cited by 42 publications

References 43 publications

Sphingolipids as critical players in retinal physiology and pathology

Sphingolipids as critical players in retinal physiology and pathology

Role of Mitofusins and Mitophagy in Life or Death Decisions

WITHDRAWN: Contribution of microRNA-30d to the prevention of the thyroid cancer progression: mechanism and implications

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