Evidence map›Paper›PMID 35589951›Full record

ArticleOncogene2022

RIOK1 mediates p53 degradation and radioresistance in colorectal cancer through phosphorylation of G3BP2.

Yaqi Chen, Sha Zhou, Kairui Wan, Long Yu, Chongchong Zhao, Haiteng Deng, Qingjian Ou, Jiayi Qin, Junbo Hu, Zhenlin Hou

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-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

22 citing papers in PubMed, 34 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Yaqi Chen *GI Cancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China.
Sha Zhou *Department of Anesthesiology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China.
Kairui WanGI Cancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China.
Long YuDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China.
Chongchong ZhaoProtein Chemistry and Proteomics Facility, Tsinghua University Technology Center for Protein Research, Beijing, 100084, China.
Haiteng DengProtein Chemistry and Proteomics Facility, Tsinghua University Technology Center for Protein Research, Beijing, 100084, China.ORCID http://orcid.org/0000-0001-9496-1280
Qingjian OuDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China.
Jiayi QinDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China.
Junbo HuGI Cancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China.ORCID http://orcid.org/0000-0002-3582-999X
Zhenlin HouDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China. houzl@sysucc.org.cn.ORCID http://orcid.org/0000-0003-0650-2151
Sun Yat-sen University · CNTongji Hospital · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RIO Kinase 1 (RIOK1) is involved in various pathologies, including cancer. However, the role of RIOK1 in radioresistance of colorectal cancer (CRC) remains largely unknown. In this study, we reported that RIOK1 was overexpressed in rectal cancer tissue with weaker tumor regression after neoadjuvant chemoradiotherapy (neoCRT). Moreover, higher RIOK1 expression predicted a poor prognosis in patients with rectal cancer. Blockade of RIOK1 using Toyocamycin, a pharmacological inhibitor of RIOK1, or by knocking down its expression, decreased the resistance of CRC cells to radiotherapy in vitro and in vivo. A mechanistic study revealed that RIOK1 regulates radioresistance by suppressing the p53 signaling pathway. Furthermore, we found that RIOK1 and Ras-GAP SH3 domain binding protein 2 (G3BP2) interact with each other. RIOK1 phosphorylates G3BP2 at Thr226, which increases the activity of G3BP2. RIOK1-mediated phosphorylation of G3BP2 facilitated ubiquitination of p53 by murine double minute 2 protein (MDM2). Altogether, our study revealed the clinical significance of RIOK1 in CRC, and therapies targeting RIOK1 might alleviate the CRC tumor burden in patients.

Indexed as

Colorectal NeoplasmsRectal NeoplasmsAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorHumansMicePhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mdm2RNA-Binding ProteinsTumor Suppressor Protein p53Adaptor Proteins, Signal TransducingG3BP2 protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mdm2RIOK1 protein, humanRNA-Binding ProteinsTumor Suppressor Protein p53

Identifiers

PMID35589951
OpenAlexW4280508531

What OpenQuestion holds

Textmetadata
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.