Evidence map›Paper›PMID 40200093›Full record

ArticleCell death and differentiation2025

p53 transcriptionally activates DCP1B to suppress tumor progression and enhance tumor sensitivity to PI3K blockade in non-small cell lung cancer.

Shiqi Chen, Qian Hao, Yu Gan, Jing Tong, Chen Xiong, Quan Liao, Yang Zhang, Ting Ye, Xiang Zhou, Haiquan Chen

Abstract read
In one paragraph

Article in Cell death and differentiation, 2025. 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
–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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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.

Shiqi Chen *Department of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.ORCID 0000-0002-3543-4939
Qian Hao *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.ORCID 0000-0002-4229-7880
Yu GanDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Jing TongDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Chen XiongDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Quan LiaoDepartment of Radiation Oncology, Jiangxi Cancer Hospital, Jiangxi, 330029, China.
Yang ZhangDepartment of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Ting YeDepartment of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. yeting831011@hotmail.com.ORCID 0000-0002-4268-870X
Xiang ZhouDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. xiangzhou@fudan.edu.cn.ORCID 0000-0002-1172-7948
Haiquan ChenDepartment of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. hqchen1@yahoo.com.ORCID 0000-0001-7846-257X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81930073National Natural Science Foundation of China (National Science Foundation of China) 82173022National Natural Science Foundation of China (National Science Foundation of China) 82273098National Natural Science Foundation of China (National Science Foundation of China) 82430099National Natural Science Foundation of China (National Science Foundation of China) 82472714
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC), which accounts for approximately 85% of lung cancer patients, is characterized by its aggressive nature and poor prognosis. In this study, we identify decapping mRNA 1B (DCP1B) as a tumor suppressor gene that is transcriptionally regulated by p53. DCP1B is found to inhibit the growth and migration of NSCLC cells. Consistently, the level of DCP1B expression is decreased in NSCLC tissues, and its low expression is associated with NSCLC patients' unfavorable outcomes. Mechanistic investigations reveal that DCP1B promotes the turnover of mitogen-activated protein kinase 4 (MAPK4) mRNA, and the activation of p53 reduces the expression level of MAPK4 partially through DCP1B. Notably, overexpression of MAPK4 can drive AKT phosphorylation independent of phosphoinositide 3-kinase (PI3K), thus neutralizing the anti-tumor activity of the PI3K inhibitor in NSCLC cells. Moreover, the p53 agonist combined with the PI3K inhibitor can suppress NSCLC proliferation synergistically in vitro and in vivo. Collectively, this study not only uncovers the function and mechanism of the p53-DCP1B-MAPK4 axis in suppressing NSCLC progression but also suggests a promising combination strategy for treating NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsPhosphoinositide-3 Kinase InhibitorsTumor Suppressor Protein p53AnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudePhosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID40200093
PMCPMC12432164

What Socratic 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 Socratic graph.