Evidence map›Paper›PMID 38906869›Full record

ArticleCell death & disease2024

Regulator of G protein signaling 16 restrains apoptosis in colorectal cancer through disrupting TRAF6-TAB2-TAK1-JNK/p38 MAPK signaling.

Hao Shen, Jie Yuan, Dafeng Tong, Bingchen Chen, Enda Yu, Guanglei Chen, Cheng Peng, Wenjun Chang, Jifu E, Fuao Cao

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  8. World journal of gastroenterology · 2025
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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.

Hao Shen *Department of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Jie Yuan *Department of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Dafeng Tong *Department of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Bingchen ChenDepartment of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Enda YuDepartment of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Guanglei ChenDepartment of Health Management, Beidaihe Rest and Recuperation Center of PLA Joint Logistics Support Force, Qinhuangdao, China.
Cheng PengDepartment of Health Management, Beidaihe Rest and Recuperation Center of PLA Joint Logistics Support Force, Qinhuangdao, China.
Wenjun ChangDepartment of Environmental and Occupational Health, Naval Medical University, Shanghai, China. cwjcwj1976@smmu.edu.cn.
Jifu EDepartment of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China. ejifu@smmu.edu.cn.ORCID 0000-0002-4121-1731
Fuao CaoDepartment of Colorectal Surgery, The First Affiliated Hospital of Naval Medical University, Shanghai, China. caofuao@me.com.ORCID 0000-0002-3234-5041

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82272705
6 · The paper itself

Abstract

Colorectal cancer (CRC) remains a major global cause of cancer-related mortality, lacking effective biomarkers and therapeutic targets. Revealing the critical pathogenic factors of CRC and the underlying mechanisms would offer potential therapeutic strategies for clinical application. G protein signaling (RGS) protein family modulators play essential role within regulating downstream signaling of GPCR receptors, with function in cancers unclear. Our study focused on the expression patterns of RGS proteins in CRC, identifying Regulator of G protein signaling 16 (RGS16) as a prospective diagnostic and therapeutic target. Analyzing 899 CRC tissues revealed elevated RGS16 levels, correlating with clinicopathological features and CRC prognosis by immunohistochemistry (IHC) combined with microarray. We confirmed the elevated RGS16 protein level in CRC, and found that patients with RGS16-high tumors exhibited decreased disease-specific survival (DSS) and disease-free survival (DFS) compared to those with low RGS16 expression. Functional assays demonstrated that RGS16 promoted the CRC progression, knockdown of RGS16 led to significantly increased apoptosis rates of CRC in vitro and in vivo. Notably, we also confirmed these phenotypes of RGS16 in organoids originated from resected primary human CRC tissues. Mechanistically, RGS16 restrained JNK/P38-mediated apoptosis in CRC cells through disrupting the recruitment of TAB2/TAK1 to TRAF6. This study provides insights into addressing the challenges posed by CRC, offering avenues for clinical translation.

Indexed as

ApoptosisColorectal NeoplasmsMAP Kinase Kinase KinasesRGS ProteinsAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMAP Kinase Kinase Kinase 7MAP Kinase Signaling SystemMiceMice, NudeMiddle AgedAdaptor Proteins, Signal TransducingIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase Kinasesp38 Mitogen-Activated Protein KinasesRGS16 proteinRGS ProteinsTAB2 protein, humanTifab protein, humanTNF Receptor-Associated Factor 6

Identifiers

PMID38906869
PMCPMC11192724

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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.