Evidence map›Paper›PMID 35346236›Full record

ArticleCell communication and signaling : CCS2022

Co-targeting WIP1 and PARP induces synthetic lethality in hepatocellular carcinoma.

Miaoqin Chen, Weikai Wang, Shiman Hu, Yifan Tong, Yiling Li, Qi Wei, Lei Yu, Liyuan Zhu, Yiran Zhu, Leiming Liu and 4 more

Open access · goldAbstract readVideo-Audio Media
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. 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

14 authors at 2 institutions in 1 country.

Miaoqin ChenLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Weikai WangLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Shiman HuLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Yifan TongDepartment of General Surgery, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Yiling LiLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Qi WeiLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Lei YuLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Liyuan ZhuLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Yiran ZhuDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Leiming LiuInstitute of Aging and Regenerative Medicine, Jinan University, Guangzhou, China.
Zhenyu JuInstitute of Aging and Regenerative Medicine, Jinan University, Guangzhou, China.
Xian WangDepartment of Medical Oncology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Hongchuan JinLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China. jinhc@zju.edu.cn.
Lifeng FengLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw Hospital, Cancer Center, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China. lffeng@zju.edu.cn.ORCID 0000-0003-4506-1213
Sir Run Run Shaw Hospital · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the most fatal cancers. Due to limited strategies for effective treatments, patients with advanced HCC have a very poor prognosis. This study aims to identify new insights in HCC to develop novel strategies for HCC management.

methodsThe role of WIP1 (wild type p53 induced protein phosphatase1) in HCC was analyzed in HCC cells, xenograft model, DEN (Diethylnitrosamine) induced mice liver cancer model with WIP1 knockout mice, and TCGA database. DNA damage was evaluated by Gene Set Enrichment Analysis, western blotting, comet assay, and Immunofluorescence.

resultsHigh expression of WIP1 is associated with the poor prognosis of patients with HCC. Genetically and chemically suppression of WIP1 drastically reduced HCC cell proliferation. Besides, WIP1 knockout retarded DEN induced mice hepato-carcinogenesis. Mechanically, WIP1 inhibition induced DNA damage by increasing H2AX phosphorylation (γH2AX). Therefore, suppression of WIP1 and PARP induced synthetic lethality in HCC in vitro and in vivo by augmenting DNA damage.

conclusionWIP1 plays an oncogenic effect in HCC development, and targeting WIP1-dependent DNA damage repair alone or in combination with PARP inhibition might be a reasonable strategy for HCC management. Video abstract.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsMicePhosphoprotein PhosphatasesPoly(ADP-ribose) Polymerase InhibitorsProtein Phosphatase 2CSynthetic Lethal MutationsPhosphoprotein PhosphatasesPoly(ADP-ribose) Polymerase InhibitorsProtein Phosphatase 2CDNA damage repairHepatocellular carcinomaPAPR inhibitorWIP1

Identifiers

PMID35346236
PMCPMC8962187
OpenAlexW4220674938

What OpenQuestion holds

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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.