Autophagy in Viral Development and Progression of Cancer

Suares, Alejandra; Medina, María Victoria; Coso, Omar A.

doi:10.3389/fonc.2021.603224

Cited by 16 publications

(8 citation statements)

References 434 publications

(493 reference statements)

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“…The role of autophagy in pathogenic processes and antitumour therapy has been an issue of concern in recent years [20][21][22]. The autophagic process of tumour cells was found to be an important survivaland growth-associated mechanism in many cancers in a previous study [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

The Fgl2 interaction with Tyrobp promotes the proliferation of cutaneous squamous cell carcinoma by regulating ERK-dependent autophagy

Zeng¹,

Li²,

Chen³

et al. 2022

Int. J. Med. Sci.

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Human fibroleukin 2 (Fgl2), a member of the fibrinogen superfamily, can cleave prothrombin to generate thrombin or is secreted in a soluble form as a new type of effector of Tregs with immunomodulatory functions. However, there is little research on the role of Fgl2 in cutaneous squamous cell carcinoma (CSCC) growth. We examined the expression of Fgl2 in samples from CSCC patients and CSCC cell lines. Then, the effect of Fgl2 on CSCC was evaluated in vitro and in animals. Regulation of autophagy by Fgl2 was explored in CSCC. Coimmunoprecipitation (Co-IP) and immunofluorescence colocalization experiments were conducted to identify the regulatory effect of Fgl2 on the downstream protein Tyrobp. Then, gain-or loss-of-function analyses and evaluation of Tyrobp expression were performed to validate its role in autophagy and proliferation promoted by Fgl2. Here, our study demonstrated that Fgl2 promoted the proliferation of CSCC cells in vitro and in vivo. Knocking down Fgl2 reduced CSCC cell proliferation and inhibited autophagy in CSCC. Mechanistically, Fgl2 interacted with Tyrobp and promoted ERK-dependent autophagy, resulting in the proliferation of CSCC cells. Our study suggested that Fgl2 could be a promising prognostic biomarker and useful therapeutic target for CSCC.

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Section: Discussionmentioning

confidence: 99%

The Fgl2 interaction with Tyrobp promotes the proliferation of cutaneous squamous cell carcinoma by regulating ERK-dependent autophagy

Zeng¹,

Li²,

Chen³

et al. 2022

Int. J. Med. Sci.

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“…Viruses, including coronaviruses, suppress autophagy to promote their own replication, and consequently activation of autophagy can effectively limit viral replication. [69][70][71][72] SARS-CoV-2 blocks autophagy, leading to the suggestion that autophagy-inducing agents may overcome infection by reactivating intracellular viral destruction. [73][74][75][76][77][78][79] Supporting this concept, SARS-CoV-2 was shown to promote Beclin-1 degradation, 80 and several autophagy-modifying compounds suppress SAR-CoV-2 replication in vitro (reviewed in 75 ).…”

Section: Induction Of Autophagymentioning

confidence: 99%

Recent Progress in the Development of Opaganib for the Treatment of Covid-19

Smith¹,

Maines²,

Keller³

et al. 2022

DDDT

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The Covid-19 pandemic driven by the SARS-CoV-2 virus continues to exert extensive humanitarian and economic stress across the world. Although antivirals active against mild disease have been identified recently, new drugs to treat moderate and severe Covid-19 patients are needed. Sphingolipids regulate key pathologic processes, including viral proliferation and pathologic host inflammation. Opaganib (aka ABC294640) is a first-in-class clinical drug targeting sphingolipid metabolism for the treatment of cancer and inflammatory diseases. Recent work demonstrates that opaganib also has antiviral activity against several viruses including SARS-CoV-2. A recently completed multinational Phase 2/3 clinical trial of opaganib in patients hospitalized with Covid-19 demonstrated that opaganib can be safely administered to these patients, and more importantly, resulted in a 62% decrease in mortality in a large subpopulation of patients with moderately severe Covid-19. Furthermore, acceleration of the clearance of the virus was observed in opaganib-treated patients. Understanding the biochemical mechanism for the anti-SARS-CoV-2 activity of opaganib is essential for optimizing Covid-19 treatment protocols. Opaganib inhibits three key enzymes in sphingolipid metabolism: sphingosine kinase-2 (SK2); dihydroceramide desaturase (DES1); and glucosylceramide synthase (GCS). Herein, we describe a tripartite model by which opaganib suppresses infection and replication of SARS-CoV-2 by inhibiting SK2, DES1 and GCS. The potential impact of modulation of sphingolipid signaling on multi-organ dysfunction in Covid-19 patients is also discussed.

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“…Also, it is crucial to maintain homeostasis and avoiding from nutritional, metabolic, and infection-mediated stresses [ 91 ]. Moreover, its role in diseases progression especially cancers in different stages of them has been discussed previously [ 92 , 93 ]. Also, autophagy plays important role in viral replication and coordinates adaptive immunity by delivering virus-derived antigens for presentation to T lymphocytes [ 94 ].…”

Section: Similarities Of Treatment For Cancer and Covid-19mentioning

confidence: 99%

An overview on tumor treating fields (TTFields) technology as a new potential subsidiary biophysical treatment for COVID-19

Farmani

Mahdavinezhad

Scagnolari

et al. 2021

Drug Deliv. and Transl. Res.

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Graphical abstract COVID-19 pandemic situation has affected millions of people with tens of thousands of deaths worldwide. Despite all efforts for finding drugs or vaccines, the key role for the survival of patients is still related to the immune system. Therefore, improving the efficacy and the functionality of the immune system of COVID-19 patients is very crucial. The potential new, non-invasive, FDA-approved biophysical technology that could be considered in this regard is tumor treating fields (TTFields) based on an alternating electric field has great biological effects. TTFields have significant effects in improving the functionality of dendritic cell, and cytotoxic T-cells, and these cells have a major role in defense against viral infection. Hence, applying TTFields could help COVID-19 patients against infection. Additionally, TTFields can reduce viral genomic replication, by reducing the expressions of some of the vital members of DNA replication complex genes from the minichromosome maintenance family (MCMs). These genes not only are involved in DNA replication but it has also been proven that they have a crucial role in viral replication. Also, TTFields suppress the formation of the network of tunneling nanotubes (TNTs) which is knows as filamentous (F)-actin-rich tubular structures. TNTs have a critical role in promoting the spread of viruses through improving viral entry and acting as a protective agent for viral components from immune cells and even pharmaceuticals. Moreover, TTFields enhance autophagy which leads to apoptosis of virally infected cells. Thus, it can be speculated that using TTFields may prove to be a promising approach as a subsidiary treatment of COVID-19.

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Autophagy in Viral Development and Progression of Cancer

Cited by 16 publications

References 434 publications

The Fgl2 interaction with Tyrobp promotes the proliferation of cutaneous squamous cell carcinoma by regulating ERK-dependent autophagy

The Fgl2 interaction with Tyrobp promotes the proliferation of cutaneous squamous cell carcinoma by regulating ERK-dependent autophagy

Recent Progress in the Development of Opaganib for the Treatment of Covid-19

An overview on tumor treating fields (TTFields) technology as a new potential subsidiary biophysical treatment for COVID-19

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