Evidence map›Paper›PMID 41986490›Full record

ArticleScientific reports2026

LPCAT1 depletion inhibits colorectal cancer tumorigenesis and is associated with the ECM-receptor-interaction signaling pathway.

Liping Jiang, Sumei Xu, Jingbo Peng, Jing Yu, Huilan Wu, Wei Wu, Zhichun Huang, Jie Pan, Zhirong Tan

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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. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Liping Jiang *Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Sumei Xu *Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Jingbo PengDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Jing YuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Huilan WuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Wei WuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Zhichun HuangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China.
Jie PanClinical Research Laboratory, The Second Affiliated Hospital of University of South China, Hengyang, 421001, P.R. China.
Zhirong TanDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, P.R. China. 803119@csu.edu.cn.

Funding

Key Project Funded by Hunan Provincial Health Commission A202313018918National Natural Science Foundation of China 81974510Natural Science Foundation of Hunan Province 2021JJ30905, 2022JJ30951, 2024JJ7630
6 · The paper itself

Abstract

Colorectal cancer (CRC) has become one of the most important diseases due to its increasing morbidity and mortality. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is reported to be overexpressed in multiple cancers, but their role remains poorly understood. In this study, we explored the role of LPCAT1 in the progression of CRC and the possible underlying mechanism. Bioinformatics analysis was used to search for the association between target gene LPCAT1 and CRC. LPCAT1 expression was measured in CRC and paired para cancerous tissues. The role of LPCAT1 was investigated both in vitro and in vivo. iTRAQ-based quantitative proteomics was used to explore the mechanism of LPCAT1 in CRC progression. TCGA and GEO database analysis showed that LPCAT1 was upregulated in CRC. LPCAT1 was upregulated in CRC tissues and the IHC score was also correlated with tumor stage. The depletion of LPCAT1 not only abrogated cell proliferation, migration and invasion in vitro, but also arrested tumor growth in vivo. The proteomic results showed that differentially expressed proteins were enriched in multiple pathways after LPCAT1 knockdown, and the extracellular matrix (ECM) receptor interaction pathway was the most significant. The ECM is involved in the process by which LPCAT1 promotes CRC metastasis and invasion.

Indexed as

1-Acylglycerophosphocholine O-AcyltransferaseCarcinogenesisColorectal NeoplasmsExtracellular MatrixReceptors, Cell SurfaceSignal TransductionAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMice, NudeProteomics1-Acylglycerophosphocholine O-Acyltransferaseextracellular matrix receptorLpcat1 protein, humanReceptors, Cell SurfaceColorectal cancerECM pathwayLPCAT1Migration and invasionProteomics

Identifiers

PMID41986490
PMCPMC13243655

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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.