Evidence map›Paper›PMID 41831177›Full record

ArticleInvestigational new drugs2026

Crocetin suppresses colorectal cancer progression by targeting TGM2 and inhibiting the JAK2/STAT3 pathway.

Shuo Chen, Weijun Su, Kai Wang, Mingyue Xu, Binjie Su

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Article in Investigational new drugs, 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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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Shuo Chen *Department of Colorectal Surgery, Tianjin Union Medical Center, Tianjin, 300121, China. chenshuo19801106@126.com.
Weijun Su *School of Medicine, Nankai University, Tianjin, 300074, China.
Kai WangDepartment of Colorectal Surgery, Tianjin Union Medical Center, Tianjin, 300121, China.
Mingyue XuDepartment of Colorectal Surgery, Tianjin Union Medical Center, Tianjin, 300121, China.
Binjie SuSchool of Medicine, Nankai University, Tianjin, 300074, China.

Funding

CD66b-RAS-Cdc42 regulates the proliferation, invasion and migration-related mechanisms of PGCCs and its progeny cells 23JCZDJC01250
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is a major health threat with limited therapies for advanced stages. Crocetin, a natural compound from saffron, has broad anticancer potential, but its mechanisms in CRC are unclear.

methodsA CRC xenograft mouse model was established to evaluate the antitumor effect of crocetin. Next, transcriptomic analysis was performed to identify differentially expressed genes (DEGs) in tumor tissues of tumor-bearing mice between the crocetin treatment and control groups. Through the integration of network pharmacology, and protein-protein interaction (PPI) network analysis, potential key target genes regulated by crocetin in CRC were identified. Functional assays (e.g. CCK-8 and transwell assays) were employed to assess the biological role of crocetin and its target gene, TGM2, in CRC cells.

resultsCrocetin significantly inhibited tumor growth in HCT116-tumor-bearing mice in vivo. Transcriptomic analysis identified 2,577 DEGs in tumor tissues between the crocetin and control groups. Through integrated network pharmacology, transcriptomics, and molecular docking analyses, we identified five potential crocetin-targeted genes-ADAM17, DNMT1, MTOR, TGM2, and XRCC6-all of which showed significant downregulation following crocetin treatment. Furthermore, in vitro experiments demonstrated that crocetin notably suppressed cell viability, migration, and invasion, as well as reduced the expression of TGM2, p-JAK2, and p-STAT3 in HCT116 cells; however, the tumor-suppressive effects of crocetin were markedly abolished by TGM2 overexpression.

conclusionCollectively, crocetin could suppress CRC progression by targeting TGM2/JAK2/STAT3 signaling pathway, supporting its potential as a therapeutic agent for CRC.

Indexed as

CarotenoidsColorectal NeoplasmsJanus Kinase 2Protein Glutamine gamma Glutamyltransferase 2STAT3 Transcription FactorVitamin AAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHCT116 CellsHumansMiceMice, Inbred BALB CCarotenoidsJAK2 protein, humanJanus Kinase 2Protein Glutamine gamma Glutamyltransferase 2STAT3 protein, humanSTAT3 Transcription FactorTGM2 protein, humantrans-sodium crocetinateVitamin AColorectal cancerCrocetinJAK2/STAT3 pathwayTGM2Transcriptomics

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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.