Evidence map›Paper›PMID 31320749›Full record

ArticleCell death and differentiation2020

The lncRNA PVT1 regulates nasopharyngeal carcinoma cell proliferation via activating the KAT2A acetyltransferase and stabilizing HIF-1α.

Ying Wang, Wanyuan Chen, Jiayan Lian, Haibo Zhang, Bo Yu, Minjun Zhang, Fangqiang Wei, Jianhui Wu, Jiaxiang Jiang, Yongshi Jia and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 217 citations in OpenAlex.

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65 more citing papers are in PubMed but not listed here.

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

15 authors at 7 institutions in 2 countries.

Ying Wang *Department of Radiation Oncology, Zhejiang Provincial People' s Hospital, People' s Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China.
Wanyuan Chen *Department of Pathology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China.
Jiayan Lian *Department of Pathology, the 7th affiliated hospital of Sun Yat-Sen University, Shenzhen, 510275, Guandong, PR China.
Haibo Zhang *Department of Radiation Oncology, Zhejiang Provincial People' s Hospital, People' s Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China.
Bo Yu *State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 200127, Shanghai, PR China.ORCID http://orcid.org/0000-0001-6039-4249
Minjun ZhangGraduate Department, Bengbu Medical College, Bengbu, 233000, Anhui, PR China.
Fangqiang WeiDepartment of Hepatobiliary and Pancreatic Surgery, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China.
Jianhui WuDepartment of The Otolaryngology, Zhongshan City People's Hospital, Zhongshan Affiliated Hospital of Sun Yan-sen University, Zhongshan, 528403, Guangdong, PR China.
Jiaxiang JiangDepartment of Cardiology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China.
Yongshi JiaDepartment of Radiation Oncology, Zhejiang Provincial People' s Hospital, People' s Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China.
Fan MoVancouver Prostate Centre, University of British Columbia, 2660 Oak St., Vancouver, BC, V6H 3Z6, Canada.
Shirong ZhangTranslational medicine centre, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang, PR China.
Xiaodong LiangDepartment of Radiation Oncology, Zhejiang Provincial People' s Hospital, People' s Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China. lxdctopone@sina.com.
Xiaozhou MouKey Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China. mouxz@zju.edu.cn.ORCID http://orcid.org/0000-0002-3234-1737
Jianming TangDepartment of Radiation Oncology, Zhejiang Provincial People' s Hospital, People' s Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China. 15900792812@163.com.
Zhejiang Provincial People's Hospital · CNBengbu Medical College · CNHangzhou First People's Hospital · CNShanghai Jiao Tong University · CNSun Yat-sen University · CNUniversity of British Columbia · CAZhongshan People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) play important roles in regulating the development and progression of many cancers. However, the clinical significance of specific lncRNAs in the context of nasopharyngeal carcinoma (NPC) and the molecular mechanisms by which they regulate this form of cancer remain largely unclear. In this study we found that the lncRNA PVT1 was upregulated in NPC, and that in patients this upregulation was associated with reduced survival. RNA sequencing revealed that PVT1 was responsible for regulating NPC cell proliferation and for controlling a hypoxia-related phenotype in these cells. PVT1 knockdown reduced NPC cell proliferation, colony formation, and tumorigenesis in a subcutaneous mouse xenograft model systems. We further found that PVT1 serves as a scaffold for the chromatin modification factor KAT2A, which mediates histone 3 lysine 9 acetylation (H3K9), recruiting the nuclear receptor binding protein TIF1β to activate NF90 transcription, thereby increasing HIF-1α stability and promoting a malignant phenotype in NPC cells. Overexpression of NF90 or HIF-1α restored the proliferation in cells that had ceased proliferating due to PVT1 or KAT2A depletion. Conversely, overexpression of active KAT2A or TIF1β, but not of KAT2A acetyltransferase activity-deficient mutants or TIF1β isoforms lacking H3K9ac binding sites, promoted a PVT1-mediated increase in NF90 transcription, as well as increased HIF-1α stability and cell proliferation. PVT1 knockdown enhanced the radiosensitization effect in NPC cells via inhibiting binding between H3K9ac and TIF1β in a manner. Taken together, our results demonstrate that PVT1 serves an oncogenic role and plays an important role in radiosensitivity in malignant NPC via activating the KAT2A acetyltransferase and stabilizing HIF-1α.

Indexed as

Cell ProliferationHistone AcetyltransferasesHumansHypoxia-Inducible Factor 1, alpha SubunitNasopharyngeal CarcinomaNasopharyngeal Neoplasmsp300-CBP-Associated FactorRNA, Long NoncodingSignal TransductionTumor Cells, CulturedHIF1A protein, humanHistone AcetyltransferasesHypoxia-Inducible Factor 1, alpha SubunitKAT2A protein, humanp300-CBP-Associated FactorPVT1 long-non-coding RNA, humanRNA, Long Noncoding

Identifiers

PMID31320749
PMCPMC7206084
OpenAlexW2959018175

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Registered trials

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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 OpenQuestion graph.