CD147 and cyclophilin A: a promising potential targeted therapy for COVID-19 and associated cancer progression and chemo-resistance

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Coronavirus disease-2019 (COVID-19), as a worldwide serious issue has been shown to lead to progression and poor outcomes in cancer patients. The underlying mechanisms for SARS-CoV-2 infection’s adverse effects on cancer patients have not been fully understood. We hypothesized that CD147 and Cyclophilin A (CyPA) not only can play a significant role in infection severity but also can contribute to cancer progression and chemotherapy resistance in cancer patients with COVID-19. In addition, we hypothesized that the expression of both CD147 and CyPA could be increased by Hypoxia-inducible Factor-1 alpha (HIF-1α) activation during hypoxic conditions that occurred during COVID-19. Therefore, this evidence can open a new window in the management of cancer patients during the pandemic and therapeutic approaches targeting CD147 and CyPA could be a potentially promising therapeutic approach for such patients.

Related collections

Most cited references 21

Record: found
Abstract: found
Article: found

Is Open Access

CD147-spike protein is a novel route for SARS-CoV-2 infection to host cells

Ke Wang, Wei Chen, Zheng Zhang … (2020)

In face of the everlasting battle toward COVID-19 and the rapid evolution of SARS-CoV-2, no specific and effective drugs for treating this disease have been reported until today. Angiotensin-converting enzyme 2 (ACE2), a receptor of SARS-CoV-2, mediates the virus infection by binding to spike protein. Although ACE2 is expressed in the lung, kidney, and intestine, its expressing levels are rather low, especially in the lung. Considering the great infectivity of COVID-19, we speculate that SARS-CoV-2 may depend on other routes to facilitate its infection. Here, we first discover an interaction between host cell receptor CD147 and SARS-CoV-2 spike protein. The loss of CD147 or blocking CD147 in Vero E6 and BEAS-2B cell lines by anti-CD147 antibody, Meplazumab, inhibits SARS-CoV-2 amplification. Expression of human CD147 allows virus entry into non-susceptible BHK-21 cells, which can be neutralized by CD147 extracellular fragment. Viral loads are detectable in the lungs of human CD147 (hCD147) mice infected with SARS-CoV-2, but not in those of virus-infected wild type mice. Interestingly, virions are observed in lymphocytes of lung tissue from a COVID-19 patient. Human T cells with a property of ACE2 natural deficiency can be infected with SARS-CoV-2 pseudovirus in a dose-dependent manner, which is specifically inhibited by Meplazumab. Furthermore, CD147 mediates virus entering host cells by endocytosis. Together, our study reveals a novel virus entry route, CD147-spike protein, which provides an important target for developing specific and effective drug against COVID-19.

0 comments Cited 499 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Is Open Access

Severe Acute Respiratory Syndrome Coronavirus Viroporin 3a Activates the NLRP3 Inflammasome

I-Yin Chen, Miyu Moriyama, Ming-Fu Chang … (2019)

Nod-like receptor family, pyrin domain-containing 3 (NLRP3) regulates the secretion of proinflammatory cytokines interleukin 1 beta (IL-1β) and IL-18. We previously showed that influenza virus M2 or encephalomyocarditis virus (EMCV) 2B proteins stimulate IL-1β secretion following activation of the NLRP3 inflammasome. However, the mechanism by which severe acute respiratory syndrome coronavirus (SARS-CoV) activates the NLRP3 inflammasome remains unknown. Here, we provide direct evidence that SARS-CoV 3a protein activates the NLRP3 inflammasome in lipopolysaccharide-primed macrophages. SARS-CoV 3a was sufficient to cause the NLRP3 inflammasome activation. The ion channel activity of the 3a protein was essential for 3a-mediated IL-1β secretion. While cells uninfected or infected with a lentivirus expressing a 3a protein defective in ion channel activity expressed NLRP3 uniformly throughout the cytoplasm, NLRP3 was redistributed to the perinuclear space in cells infected with a lentivirus expressing the 3a protein. K+ efflux and mitochondrial reactive oxygen species were important for SARS-CoV 3a-induced NLRP3 inflammasome activation. These results highlight the importance of viroporins, transmembrane pore-forming viral proteins, in virus-induced NLRP3 inflammasome activation.

0 comments Cited 245 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages.

Miriam Merad, Jérôme Martin (2020)

The COVID-19 pandemic caused by infection with SARS-CoV-2 has led to more than 200,000 deaths worldwide. Several studies have now established that the hyperinflammatory response induced by SARS-CoV-2 is a major cause of disease severity and death in infected patients. Macrophages are a population of innate immune cells that sense and respond to microbial threats by producing inflammatory molecules that eliminate pathogens and promote tissue repair. However, a dysregulated macrophage response can be damaging to the host, as is seen in the macrophage activation syndrome induced by severe infections, including in infections with the related virus SARS-CoV. Here we describe the potentially pathological roles of macrophages during SARS-CoV-2 infection and discuss ongoing and prospective therapeutic strategies to modulate macrophage activation in patients with COVID-19.

0 comments Cited 239 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Hamidreza Zalpoor:

ORCID: http://orcid.org/0000-0002-8057-2804

hamidreza.zlpr1998@gmail.com

Journal

Journal ID (nlm-ta): Infect Agent Cancer

Journal ID (iso-abbrev): Infect Agent Cancer

Title: Infectious Agents and Cancer

Publisher: BioMed Central (London )

ISSN (Electronic): 1750-9378

Publication date (Electronic): 4 April 2023

Publication date PMC-release: 4 April 2023

Publication date Collection: 2023

Volume: 18

Electronic Location Identifier: 20

Affiliations

[1 ]GRID grid.412606.7, ISNI 0000 0004 0405 433X, Department of Medical Laboratory Sciences, Faculty of Allied Medicine, , Qazvin University of Medical Sciences, ; Qazvin, Iran

[2 ]GRID grid.510410.1, ISNI 0000 0004 8010 4431, Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), , Universal Scientific Education & Research Network (USERN), ; Tehran, Iran

[3 ]GRID grid.508728.0, ISNI 0000 0004 0612 1516, Student Research Committee, , Lorestan University of Medical Sciences, ; Khorramabad, Iran

[4 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, , Shiraz University of Medical Sciences, ; Shiraz, Iran

[5 ]GRID grid.46072.37, ISNI 0000 0004 0612 7950, Department of Virology, Faculty of Veterinary Medicine, , University of Tehran, ; Tehran, Iran

[6 ]GRID grid.411705.6, ISNI 0000 0001 0166 0922, School of Medicine, Tehran University of Medical Sciences, ; Tehran, Iran

[7 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Shiraz Neuroscience Research Center, , Shiraz University of Medical Sciences, ; Shiraz, Iran

Author information

Hamidreza Zalpoor http://orcid.org/0000-0002-8057-2804

Article

Publisher ID: 501

DOI: 10.1186/s13027-023-00501-2

PMC ID: 10072013

PubMed ID: 37016434

SO-VID: 7899bfc6-9c27-4d02-873c-5f10d0b0de32

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 13 May 2022

Date accepted : 29 March 2023

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: covid-19,sars-cov-2,cd147,cyclophilin a,cancer progression,chemo-resistance

Data availability:

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: covid-19, sars-cov-2, cd147, cyclophilin a, cancer progression, chemo-resistance

CD147 and cyclophilin A: a promising potential targeted therapy for COVID-19 and associated cancer progression and chemo-resistance

Read this article at

Abstract

Related collections

Novel Coronavirus Disease COVID-19

Most cited references 21

CD147-spike protein is a novel route for SARS-CoV-2 infection to host cells

Severe Acute Respiratory Syndrome Coronavirus Viroporin 3a Activates the NLRP3 Inflammasome

Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages.

Author and article information

Contributors

Journal

Affiliations

Author information

Article

History

Categories

Custom metadata

Comments

Comment on this article

Similar content 463

Cited by 2

Most referenced authors 950