Evidence map›Paper›PMID 41250149›Full record

ReviewCancer cell international2025

P21-activated kinase 4: a potent oncogene, molecular mechanisms and opportunities for targeted therapy.

Guojing Huang, Yalin Yang, Qian Luo, Xiaoqing Wang, Yifan Wang, Rong Liu, Wenting Liu, Shiwen Yan, Xiang Li

Abstract readReview
In one paragraph

Review in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Guojing Huang *Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Yalin Yang *Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Qian Luo *Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Xiaoqing Wang *Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Yifan Wang *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Yangtze University, Jingzhou, 434023, Hubei, China.
Rong LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Wenting LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Shiwen YanDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Xiang LiDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China. lixiang@zzu.edu.cn.

Funding

National Natural Science Foundation of China No.82172996
6 · The paper itself

Abstract

P21-activated kinase 4 (PAK4), recognized as a key effector protein of the Rho family of small G proteins Cell division regulatory protein 42 homologue (Cdc42) and Ras-related C3 botulinum toxin substrate 1 (Rac1), is a serine/threonine protein kinase that plays a critical role in a variety of biological processes.By analyzing the Tumour Immune Estimation Resource 2.0 (TIMER 2.0) databases, we observed that the expression level of PAK4 was significantly elevated in a wide range of tumors, and that its elevated expression level was strongly associated with poor patient prognosis. The activation of PAK4 plays an important role in promoting tumorigenesis and progression, which has been revealed by KEGG and GO analyses to play a key regulatory role in classical oncogenic signaling pathways, such as cell cycle, apoptosis, Ras signaling axis, PI3K/AKT, and P53, etc. Moreover, PAK4 plays an important function in tumor cell proliferation, migration invasion, cytoskeleton remodeling, and cell adhesion. In recent years, PAK4 has become a new target for therapeutic studies of antitumor drugs, and multiple types of PAK4 inhibitors have been gradually discovered. This review explores in detail the role of PAK4 in the following classical signaling pathways: PAK4/PI3K/AKT, PAK4/Wnt/β-catenin, PAK4/LIMK1/cofilin, and PAK4/MEK/ERK, and summarizes the PAK4-related inhibitors. The in-depth analysis of the classical pathway of carcinogenesis in this paper reveals the key role of PAK4 in cancer development and provides a theoretical basis for the development of novel PAK4 small molecule inhibitors.

Indexed as

InhibitorPAK4PrognosisRoleSignaling pathway

Identifiers

PMID41250149
PMCPMC12625063

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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.