Evidence map›Paper›PMID 36075565›Full record

ArticleVirologica Sinica2022

Cyclophilin A binds to AKT1 and facilitates the tumorigenicity of Epstein-Barr virus by mediating the activation of AKT/mTOR/NF-κB positive feedback loop.

Shuyu Xin, Lingzhi Liu, Yanling Li, Jing Yang, Lielian Zuo, Pengfei Cao, Qijia Yan, Shen Li, Li Yang, Taimei Cui and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 36% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Article
  7. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 3 countries.

Shuyu XinHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China; China-Africa Research Center of Infectious Diseases, Central South University, Changsha, 410013, China; Department of Hematology, National Clinical Research Center for Geriatric Disorders, Department of Pathology, Xiangya Hospital, Central South University, Changsha, 410080, China.
Lingzhi LiuHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China; China-Africa Research Center of Infectious Diseases, Central South University, Changsha, 410013, China; Department of Hematology, National Clinical Research Center for Geriatric Disorders, Department of Pathology, Xiangya Hospital, Central South University, Changsha, 410080, China.
Yanling LiHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China.
Jing YangHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China.
Lielian ZuoHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China.
Pengfei CaoThe Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China; Department of Hematology, National Clinical Research Center for Geriatric Disorders, Department of Pathology, Xiangya Hospital, Central South University, Changsha, 410080, China.
Qijia YanDepartment of Hematology, National Clinical Research Center for Geriatric Disorders, Department of Pathology, Xiangya Hospital, Central South University, Changsha, 410080, China.
Shen LiHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China.
Li YangHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China.
Taimei CuiDepartment of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China.
Jianhong LuHunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, China; Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, 410078, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, 410078, China; China-Africa Research Center of Infectious Diseases, Central South University, Changsha, 410013, China; Department of Hematology, National Clinical Research Center for Geriatric Disorders, Department of Pathology, Xiangya Hospital, Central South University, Changsha, 410080, China. Electronic address: jianhlu@csu.edu.cn.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The AKT/mTOR and NF-κB signalings are crucial pathways activated in cancers including nasopharyngeal carcinoma (NPC), which is prevalent in southern China and closely related to Epstein-Barr virus (EBV) infection. How these master pathways are persistently activated in EBV-associated NPC remains to be investigated. Here we demonstrated that EBV-encoded latent membrane protein 1 (LMP1) promoted cyclophilin A (CYPA) expression through the activation of NF-κB. The depletion of CYPA suppressed cell proliferation and facilitated apoptosis. CYPA was able to bind to AKT1, thus activating AKT/mTOR/NF-κB signaling cascade. Moreover, the use of mTOR inhibitor, rapamycin, subverted the activation of the positive feedback loop, NF-κB/CYPA/AKT/mTOR. It is reasonable that LMP1 expression derived from initial viral infection is enough to assure the constant potentiation of AKT/mTOR and NF-κB signalings. This may partly explain the fact that EBV serves as a tumor-promoting factor with minimal expression of the viral oncoprotein LMP1 in malignancies. Our findings provide new insight into the understanding of causative role of EBV in tumorigenicity during latent infection.

Indexed as

Cyclophilin AEpstein-Barr Virus InfectionsNasopharyngeal NeoplasmsHerpesvirus 4, HumanHumansNasopharyngeal CarcinomaNF-kappa BProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAKT1 protein, humanCyclophilin AMTOR protein, humanNF-kappa BProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCyclophilin A (CYPA)Epstein-barr virus (EBV)Latent membrane protein 1 (LMP1)NF-κB/AKT/mTOR signalingTumorigenicity

Identifiers

PMID36075565
PMCPMC9797372
OpenAlexW4294692441

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.