Evidence map›Paper›PMID 33431797›Full record

ArticleOncogenesis2021

PBK phosphorylates MSL1 to elicit epigenetic modulation of CD276 in nasopharyngeal carcinoma.

Meng-Yao Wang, Bin Qi, Fang Wang, Zhi-Rui Lin, Ming-Yi Li, Wen-Jing Yin, Yan-Yi Zhu, Lu He, Yi Yu, Fang Yang and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Meng-Yao Wang *Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Bin Qi *Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Fang Wang *Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Zhi-Rui LinState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, 510245, Guangzhou, China.
Ming-Yi LiDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Wen-Jing YinDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Yan-Yi ZhuDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Lu HeDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Yi YuDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Fang YangDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China.
Jin-Quan LiuDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China. liujinquan2018@163.com.
Dong-Ping ChenDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 510245, Guangzhou, China. dongpingchen_20@163.com.ORCID http://orcid.org/0000-0002-5982-355X
Guangzhou Medical University · CNGuangzhou Medical University Cancer Hospital · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81702690
6 · The paper itself

Abstract

CD276 (also known as B7-H3, an immune checkpoint molecule) is aberrantly overexpressed in many cancers. However, the upregulation mechanism and in particular, whether oncogenic signaling has a role, is unclear. Here we demonstrate that a pro-oncogenic kinase PBK, the expression of which is associated with immune infiltration in nasopharyngeal carcinoma (NPC), stimulates the expression of CD276 epigenetically. Mechanistically, PBK phosphorylates MSL1 and enhances the interaction between MSL1 and MSL2, MSL3, and KAT8, the components of the MSL complex. As a consequence, PBK promotes the enrichment of MSL complex on CD276 promoter, leading to the increased histone H4 K16 acetylation and the activation of CD276 transcription. In addition, we show that CD276 is highly upregulated and associated with immune infiltrating levels in NPC. Collectively, our findings describe a novel PBK/MSL1/CD276 signaling axis, which may play an important role in immune evasion of NPC and may be targeted for cancer immunotherapy.

Identifiers

PMID33431797
PMCPMC7801519
OpenAlexW3120726001

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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.