Evidence map›Paper›PMID 39905234›Full record

ArticleCommunications biology2025

The PDE4DIP-AKAP9 axis promotes lung cancer growth through modulation of PKA signalling.

Yangyang Fu, Shishun Huang, Rulu Pan, Xingan Chen, Ting Liu, Rongzhe Zhang, Fangsheng Zhu, Qiwei Fang, Liyue Wu, Juji Dai and 5 more

Abstract read
In one paragraph

Article in Communications biology, 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. Article
  2. Review
  3. Article
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

15 authors.

Yangyang Fu *Division of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Shishun Huang *School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Rulu PanDepartment of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xingan ChenSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Ting LiuSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Rongzhe ZhangSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Fangsheng ZhuSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Qiwei FangSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Liyue WuSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Juji DaiDepartment of Colorectal and Anal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Ouchen WangDepartment of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Liting LuSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Xiduan WeiSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Liangxing WangDivision of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. wangliangxing@wzhospital.cn.
Xincheng LuSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. xinchenglu@yahoo.com.ORCID http://orcid.org/0000-0003-0858-7590

Funding

National Natural Science Foundation of China (National Science Foundation of China) No. 82172995National Natural Science Foundation of China (National Science Foundation of China) No. 82373065
6 · The paper itself

Abstract

Phosphodiesterase 4D interacting protein (PDE4DIP) is a Golgi/centrosome-associated protein that plays critical roles in the regulation of microtubule dynamics and maintenance of the Golgi structure. However, its biological role in human cancer remains largely unknown. In this study, we showed that PDE4DIP is overexpressed in human non-small cell lung cancer (NSCLC) tissues and that upregulated PDE4DIP expression is associated with poor prognosis in patients with lung cancer. We demonstrated that PDE4DIP knockdown inhibits NSCLC cell proliferation in vitro and tumorigenicity in vivo. We further demonstrated that PDE4DIP knockdown triggers apoptosis and cell cycle arrest in NSCLC cells by activating the Protein kinase A (PKA) /CREB signalling pathway. PDE4DIP coordinates with A-kinase anchoring proteins 9 (AKAP9) to enhance the Golgi localization and stability of PKA RIIα. Depletion of PDE4DIP mislocalizes PKA RIIα from the Golgi and leads to its degradation, thereby compromising its negative regulatory effect on PKA signalling. Overall, our findings provide novel insights into the roles of the PDE4DIP-AKAP9 complex in regulating PKA signalling and NSCLC growth and highlight PDE4DIP as a promising therapeutic target for NSCLC.

Indexed as

A Kinase Anchor ProteinsCarcinoma, Non-Small-Cell LungCyclic AMP-Dependent Protein KinasesLung NeoplasmsSignal TransductionAnimalsCell Line, TumorCell ProliferationCytoskeletal ProteinsFemaleGene Expression Regulation, NeoplasticGolgi ApparatusHumansMaleMiceMice, NudeAKAP9 protein, humanA Kinase Anchor ProteinsCyclic AMP-Dependent Protein KinasesCytoskeletal Proteins

Identifiers

PMID39905234
PMCPMC11794602

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.