Evidence map›Paper›PMID 41071453›Full record

ArticleDigestive diseases and sciences2026

FAM72A Promotes Colorectal Cancer Progression by Regulating Reactive Oxygen Species and Inhibiting Cellular Pyroptosis.

Guorui Ma, Guanwei Yin, Xinlin Wu, Zhiwen Yang

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Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1 citing paper in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

Guorui MaDepartment of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Guanwei YinCollege of Chemistry and Chemical Engineering of Inner Mongolia University, Hohhot, China.
Xinlin WuDepartment of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Zhiwen YangDepartment of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China. yang564027432@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsColorectal cancer (CRC) is a common malignant tumor worldwide with a complex pathogenesis and an urgent need for new molecular targets. The aim of this study was to investigate the expression of FAM72A in CRC and its potential mechanism to affect cancer cell proliferation and invasion through regulating cellular pyroptosis.

methodsThe expression of FAM72A in various cancers was analyzed by TIMER2.0 and GEPIA2 databases, and its relationship with the prognosis of CRC patients was evaluated. FAM72A was knocked down and overexpressed in CRC cell lines HCT116 and DLD1, respectively, and changes in cell proliferation and invasion ability were assessed by CCK-8, EdU, Transwell, and scratch assays. Meanwhile, the regulatory effects of FAM72A on cellular pyroptosis-associated proteins and inflammatory factors were detected by Western blotting and ELISA, and the role of ROS in FAM72A-regulated cellular pyroptosis and cancer cell behaviors was further explored by N-Acetylcysteine (NAC) intervention assay. Finally, the effect of FAM72A on tumor growth was verified by in vivo nude mouse experiments.

resultsHigh levels of FAM72A expression were observed in CRC, linking it to poor prognosis in patients. Knockdown of FAM72A significantly inhibited the proliferation, migration, and invasion of CRC cells and activated cellular pyroptosis, accompanied by the upregulation of NLRP3, Caspase-1, and GSDMD expression and the increased secretion of IL-1β and IL-18. In contrast, overexpression of FAM72A inhibited cell pyroptosis and enhanced cancer cell proliferation and invasion. NAC intervention experiments demonstrated that ROS played a critical role in FAM72A-regulated cell pyroptosis and CRC progression. Furthermore, in vivo experiments showed that knockdown of FAM72A significantly inhibited the growth of subcutaneous transplanted tumors in nude mice.

conclusionFAM72A inhibits cellular pyroptosis by decreasing ROS levels, which in turn promotes the proliferation and invasion of CRC cells, and it is expected to be a potential therapeutic target for CRC.

Indexed as

Colorectal NeoplasmsNeoplasm ProteinsPyroptosisReactive Oxygen SpeciesAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHCT116 CellsHumansMaleMiceMice, Inbred BALB CNeoplasm ProteinsReactive Oxygen SpeciesColorectal cancerFAM72APyroptosisReactive oxygen species

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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.