Evidence map›Paper›PMID 40844640›Full record

ArticleJournal of molecular histology2025

NLRP3 promotes NK cell-mediated cytotoxicity and inhibits colorectal cancer development via the NKG2D signaling pathway.

Chongyi Xu, Wei Qian, Yiqi Wu, Xiaotong Chen, Zheming Li, Daogun Xu

Abstract read
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Article in Journal of molecular histology, 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

6 authors.

Chongyi XuDepartment of proctology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University (Wenling Hospital of Traditional Chinese Medicine), No. 21, Mingyuan Road, Taiping Street, Wenling, 317500, Zhejiang, China.
Wei QianDepartment of proctology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University (Wenling Hospital of Traditional Chinese Medicine), No. 21, Mingyuan Road, Taiping Street, Wenling, 317500, Zhejiang, China.
Yiqi WuDepartment of proctology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University (Wenling Hospital of Traditional Chinese Medicine), No. 21, Mingyuan Road, Taiping Street, Wenling, 317500, Zhejiang, China.
Xiaotong ChenDepartment of proctology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University (Wenling Hospital of Traditional Chinese Medicine), No. 21, Mingyuan Road, Taiping Street, Wenling, 317500, Zhejiang, China.
Zheming LiSchool of Life Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Daogun XuDepartment of proctology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University (Wenling Hospital of Traditional Chinese Medicine), No. 21, Mingyuan Road, Taiping Street, Wenling, 317500, Zhejiang, China. 13906569665@163.com.

Funding

Ministry of Education Industry-University Co-operation Collaborative Education Project 202102242020Zhejiang Chinese Medical University Research Foundation 2021FSYYZY14
6 · The paper itself

Abstract

Colorectal cancer progression involves tumor metastasis and immune evasion, with the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome and Natural Killer Group 2D (NKG2D) signaling pathway playing key roles. Their relationship in regulating NK cell-mediated cytotoxicity and CRC progression remains unclear. This study investigates NLRP3's modulation on tumor dynamics and NK cell responses to uncover new therapeutic targets. Colon cancer situ models were used to analyze tumor development after NLRP3 overexpression (oeNLRP3) and the effects of NK-92 cells with silencing NKG2D using TUNEL, immunohistochemistry staining, flow cytometry, and molecular assays. Also, a co-culture model of HCT116 and NK-92 cells was used. Focus was on tumor metastasis, apoptosis, NK cell-mediated cytotoxicity, NLRP3 and NKG2D pathways. OeNLRP3 increased apoptosis, inhibited tumor growth and enhanced immune markers. NK cells with silencing NKG2D reversed these benefits, emphasizing the importance of the NLRP3-NKG2D axis. In HCT116 cells, oeNLRP3 boosted NK cell-mediated cytotoxicity, and apoptosis, and decreased cell migration and invasion. Elevated pro-inflammatory and pro-apoptotic protein levels indicated activated immune and apoptotic pathways. NKG2D silencing mitigated these effects. NLRP3 inhibition of tumor metastasis and apoptosis promotion in colon cancer through NKG2D modulation offers a potential therapeutic avenue. The NLRP3-NKG2D axis is critical for colorectal cancer management. These results suggest a promising target for treatment strategies and providing insights into the inflammasome's role in cancer biology. Further preclinical and clinical investigations are needed to evaluate the translational potential of this axis in developing more effective approaches for colorectal cancer management.

Indexed as

Colorectal NeoplasmsCytotoxicity, ImmunologicKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily KNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionAnimalsApoptosisCell Line, TumorCell MovementHCT116 CellsHumansMiceKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily KNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanColorectal cancerNK cellNKG2DNLRP3

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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.