Exploiting Extracellular Vesicles Strategies to Modulate Cell Death and Inflammation in COVID-19

Bortot, Barbara; Romani, Arianna; Ricci, Giuseppe; Biffi, Stefania

doi:10.3389/fphar.2022.877422

Cited by 6 publications

(4 citation statements)

References 52 publications

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“…S1C, D ). A549 cells were also transfected with si-p53 or treated with Nutlin-3, which is a common p53 agonist [ 25 ], to assess the effect of different doses of Nutlin-3, and p53 silencing on the proliferation and apoptosis of A549 cells (Supplementary Fig. S2 B and S2C–H ).…”

Section: Resultsmentioning

confidence: 99%

MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer

et al. 2023

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The 5-year survival rate of non-small cell lung cancer (NSCLC) patients is very low. MicroRNAs (miRNAs) are involved in the occurrence of NSCLC. miR-122-5p interacts with wild-type p53 (wtp53), and wtp53 affects tumor growth by inhibiting the mevalonate (MVA) pathway. Therefore, this study aimed to evaluate the role of these factors in NSCLC. The role of miR-122-5p and p53 was established in samples from NSCLC patients, and human NSCLC cells A549 using the miR-122-5p inhibitor, miR-122-5p mimic, and si-p53. Our results showed that inhibiting miR-122-5p expression led to the activation of p53. This inhibited the progression of the MVA pathway in the NSCLC cells A549, hindered cell proliferation and migration, and promoted apoptosis. miR-122-5p was negatively correlated with p53 expression in p53 wild-type NSCLC patients. The expression of key genes in the MVA pathway in tumors of p53 wild-type NSCLC patients was not always higher than the corresponding normal tissues. The malignancy of NSCLC was positively correlated with the high expression of the key genes in the MVA pathway. Therefore, miR-122-5p regulated NSCLC by targeting p53, providing potential molecular targets for developing targeted drugs.

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Section: Resultsmentioning

confidence: 99%

MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer

et al. 2023

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“…Several studies have previously highlighted the role of p53 in SARS-CoV-2 infection [ 34 , 35 ], pointing out p53 as a potential target for the development of antivirals [ 36 , 37 ]. In contrast, our data show that the increase in SARS-CoV-2 replication observed when the cells are stopped in G1 is p53-independent, making the use of p53 targeting antivirals ineffective in this case.…”

Section: Discussionmentioning

confidence: 99%

P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication

Husser,

Kwon,

Andersson

et al. 2024

Microorganisms

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While having already killed more than 7 million of people worldwide in 4 years, SARS-CoV-2, the etiological agent of COVID-19, is still circulating and evolving. Understanding the pathogenesis of the virus is of capital importance. It was shown that in vitro and in vivo infection with SARS-CoV-2 can lead to cell cycle arrest but the effect of the cell cycle arrest on the virus infection and the associated mechanisms are still unclear. By stopping cells in the G1 phase as well as targeting several pathways involved using inhibitors and small interfering RNAs, we were able to determine that the cell cycle arrest in the late G1 is beneficial for SARS-CoV-2 replication. This cell cycle arrest is independent of p53 but is dependent on the CDC25A-CDK2/cyclin E pathway. These data give a new understanding in SARS-CoV-2 pathogenesis and highlight some possible targets for the development of novel therapeutic approaches.

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“…In other words, coronaviruses can evade the host’s natural immune defenses by degrading p53 through their own proteins. At the same time, the application of small molecule inhibitors of MDM2, such as nutlin-3 and idasanutlin, can promote the stable presence of p53 in cells, help regulate the IFN signaling pathway, and inhibit the replication of coronaviruses [ 56 ] ( Figure 3 ).…”

Section: The Interaction Between P53 and Interferonmentioning

confidence: 99%

Roles of p53-Mediated Host–Virus Interaction in Coronavirus Infection

Wang

Liu

et al. 2023

IJMS

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The emergence of the SARS-CoV-2 coronavirus has garnered global attention due to its highly pathogenic nature and the resulting health crisis and economic burden. Although drugs such as Remdesivir have been considered a potential cure by targeting the virus on its RNA polymerase, the high mutation rate and unique 3’ to 5’ exonuclease with proofreading function make it challenging to develop effective anti-coronavirus drugs. As a result, there is an increasing focus on host–virus interactions because coronaviruses trigger stress responses, cell cycle changes, apoptosis, autophagy, and the dysregulation of immune function and inflammation in host cells. The p53 tumor suppressor molecule is a critical regulator of cell signaling pathways, cellular stress responses, DNA repair, and apoptosis. However, viruses can activate or inhibit p53 during viral infections to enhance viral replication and spread. Given its pivotal role in cell physiology, p53 represents a potential target for anti-coronavirus drugs. This review aims to summarize the relationship between p53 and coronaviruses from various perspectives, to shed light on potential targets for antiviral drug development and vaccine design.

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Exploiting Extracellular Vesicles Strategies to Modulate Cell Death and Inflammation in COVID-19

Cited by 6 publications

References 52 publications

MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer

MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer

P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication

Roles of p53-Mediated Host–Virus Interaction in Coronavirus Infection

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