Evidence map›Paper›PMID 34290239›Full record

ArticleCell death & disease2021

PPM1G promotes the progression of hepatocellular carcinoma via phosphorylation regulation of alternative splicing protein SRSF3.

Dawei Chen, Zhenguo Zhao, Lu Chen, Qinghua Li, Jixue Zou, Shuanghai Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
  7. Article
  8. Tumor-promoting effect and tumor immunity of SRSFs.Frontiers in cell and developmental biology · 2025
    Review
  9. BioinformaticsHeliyon · 2024
    Article
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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

6 authors at 2 institutions in 1 country.

Dawei ChenDepartment of Hepatopancreatobiliary Surgery, Jiangyin People's Hospital, School of Medicine, Southeast University, No. 163, Shoushan Road, Jiangyin, 214400, Jiangsu Province, China.
Zhenguo ZhaoDepartment of Hepatopancreatobiliary Surgery, Jiangyin People's Hospital, School of Medicine, Southeast University, No. 163, Shoushan Road, Jiangyin, 214400, Jiangsu Province, China.
Lu ChenDepartment of Hepatopancreatobiliary Surgery, Jiangyin People's Hospital, School of Medicine, Southeast University, No. 163, Shoushan Road, Jiangyin, 214400, Jiangsu Province, China.
Qinghua LiDepartment of Hepatopancreatobiliary Surgery, Jiangyin People's Hospital, School of Medicine, Southeast University, No. 163, Shoushan Road, Jiangyin, 214400, Jiangsu Province, China.
Jixue ZouLiver Cancer Institute, Zhongshan Hospital, Fudan University, No. 180, Fenglin Road, Shanghai, 200032, China. jixuezou@163.com.ORCID 0000-0003-1853-2454
Shuanghai LiuDepartment of Hepatopancreatobiliary Surgery, Jiangyin People's Hospital, School of Medicine, Southeast University, No. 163, Shoushan Road, Jiangyin, 214400, Jiangsu Province, China. shuanghaimed@yeah.net.ORCID 0000-0002-4460-3757
Jiangyin People's Hospital · CNFudan University · CN

Funding

National Science Foundation of China | Young Scientists Fund 81702310National Science Foundation of China | Young Scientists Fund 81802401
6 · The paper itself

Abstract

Emerging evidence has demonstrated that alternative splicing has a vital role in regulating protein function, but how alternative splicing factors can be regulated remains unclear. We showed that the PPM1G, a protein phosphatase, regulated the phosphorylation of SRSF3 in hepatocellular carcinoma (HCC) and contributed to the proliferation, invasion, and metastasis of HCC. PPM1G was highly expressed in HCC tissues compared to adjacent normal tissues, and higher levels of PPM1G were observed in adverse staged HCCs. The higher levels of PPM1G were highly correlated with poor prognosis, which was further validated in the TCGA cohort. The knockdown of PPM1G inhibited the cell growth and invasion of HCC cell lines. Further studies showed that the knockdown of PPM1G inhibited tumor growth in vivo. The mechanistic analysis showed that the PPM1G interacted with proteins related to alternative splicing, including SRSF3. Overexpression of PPM1G promoted the dephosphorylation of SRSF3 and changed the alternative splicing patterns of genes related to the cell cycle, the transcriptional regulation in HCC cells. In addition, we also demonstrated that the promoter of PPM1G was activated by multiple transcription factors and co-activators, including MYC/MAX and EP300, MED1, and ELF1. Our study highlighted the essential role of PPM1G in HCC and shed new light on unveiling the regulation of alternative splicing in malignant transformation.

Indexed as

Disease ProgressionAlternative SplicingAnimalsCarcinoma, HepatocellularCell CycleCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansKaplan-Meier EstimateLiver NeoplasmsMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessPPM1G protein, humanProtein Phosphatase 2CSerine-Arginine Splicing FactorsSRSF3 protein, human

Identifiers

PMID34290239
PMCPMC8295330
OpenAlexW3184218303

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.