Evidence map›Paper›PMID 41667799›Full record

ArticleScientific reports2026

PLOD2 promotes proliferation, migration and invasion of colorectal cancer cells via PI3K-AKT-GSK3β signaling pathway.

Hua Fang, Jing Zheng, Shutong Ren, Danjing Chen, Yunli Wu, Xian-E Peng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. 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

6 authors.

Hua Fang *Department of Epidemiology and Health Statistics, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.
Jing Zheng *Department of Epidemiology and Health Statistics, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.
Shutong Ren *Department of Epidemiology and Health Statistics, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.
Danjing ChenDepartment of Epidemiology and Health Statistics, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.
Yunli WuKey Laboratory of Gastrointestinal Cancer (Fujian Medical University), Ministry of Education, Fuzhou, China. wuyunli422@163.com.
Xian-E PengDepartment of Epidemiology and Health Statistics, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China. peng123456@fjmu.edu.cn.

Funding

Natural Science Foundation of Fujian Province 2023J01628Natural Science Foundation of Fujian Province 2023J06030
6 · The paper itself

Abstract

Colorectal cancer (CRC) progression critically depends on the tumor microenvironment. PLOD2, an enzyme involved in collagen biosynthesis, is highly expressed in many cancers. While it promotes CRC growth via the USP15–AKT/mTOR pathway, its role in enhancing tumor cell migration and invasion remains unclear. Our study identified a significant upregulation of PLOD2 in colorectal cancer. This upregulation was closely associated with clinical stage, lymph node metastasis, and nerve invasion in CRC. Functional assays, including CCK-8, colony formation, wound healing, and Transwell migration and invasion assays, showed that PLOD2 overexpression enhanced CRC cell proliferation, migration, and invasion, while PLOD2 silencing exerted the opposite effects. Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that PLOD2 may influence CRC progression via the PI3K-AKT signaling pathway. Co-immunoprecipitation assays demonstrated that PLOD2 was co-precipitated with PI3K, confirming their interaction. Additionally, rescue experiments showed that the PI3K inhibitor LY294002 and the agonist 740Y-P could reverse PLOD2-mediated effects on CRC cell proliferation, migration, and invasion. This study demonstrates that PLOD2 promotes the proliferation, migration, and invasion of CRC cells by interacting with PI3K to activate the PI3K-AKT-GSK3β signaling pathway.

Indexed as

Colorectal NeoplasmsGlycogen Synthase Kinase 3 betaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleNeoplasm InvasivenessGlycogen Synthase Kinase 3 betaGSK3B protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktColorectal cancerMalignant progressionMetastasisPI3K-AKT- GSK3βPLOD2

Identifiers

PMID41667799
PMCPMC12960814

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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.