Evidence map›Paper›PMID 41968633›Full record

ArticleClinical and translational medicine2026

Targeting SLC5A2 suppresses colorectal tumour development by enhancing NK cell activity through extracellular vesicle-dependent MICA/B signalling.

Jun Xiao, Jianghua Wu, Fengliu Deng, Chaoqun Liu, Yuanhang Chen, Ke Shen, Chuangyuan Wang, Wandie Lin, Weiwei Liu, Ziyan Ning and 2 more

Abstract read
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In one paragraph

Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Jun XiaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jianghua WuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Fengliu DengDepartment of Pathology &The Third Xiangya Hospital of Central South University, The Third Xiangya Hospital of Central South University, Hunan, China.
Chaoqun LiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuanhang ChenDepartment of Oncology, Xingyi People's Hospital, Guizhou, China.
Ke ShenDepartment of Pathology, The Eighth Affiliated Hospital of Southern Medical University (The First People's Hospital of Shunde, Foshan), Foshan, China.
Chuangyuan WangDepartment of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Wandie LinDepartment of Pathology & Guangdong Province Key Laboratory of Molecular Tumor Pathology, School of Basic Medical Science, Southern Medical University, Guangzhou, China.
Weiwei LiuDepartment of Pathology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Ziyan NingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rui ZhouDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0003-4263-8873
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Funding

National Natural Science Foundation of China
6 · The paper itself

Abstract

Tumour metabolic modulation represents a promising adjuvant therapeutic strategy for cancers, including colorectal cancer (CRC). Dapagliflozin, a clinically approved sodium‒glucose cotransporter 2 (SLC5A2/SGLT2) inhibitor, has attracted considerable attention, yet its functional role in CRC remains unclear. Here, we investigated the oncogenic effect of SLC5A2 on the colorectal mucosal epithelium using transgenic rats and an azoxymethane/dextran sulphate sodium (AOM/DSS)-induced tumour model. Multiple immunofluorescence and tissue microarray analyses of clinical samples revealed an inverse correlation between SLC5A2 expression and natural killer (NK) cell infiltration, highlighting the therapeutic potential of dapagliflozin for CRC treatment. Mechanistically, gene expression profiling analysis and coculture experiments demonstrated that SLC5A2 impairs NKG2D-mediated NK cell cytotoxicity. Furthermore, perforated patch‒clamp and calcium imaging revealed that SLC5A2 modulates the membrane potential and calcium influx, enhancing MHC-I-associated MICA/B secretion via extracellular vesicle (EV) formation and thereby enabling CRC cells to evade NK cell surveillance. Our findings reveal a critical oncogenic role of SLC5A2 in CRC progression and suggest dapagliflozin as a novel therapeutic option, particularly for CRC patients with metabolic comorbidities.

Indexed as

Colorectal NeoplasmsExtracellular VesiclesHistocompatibility Antigens Class IKiller Cells, NaturalAnimalsBenzhydryl CompoundsGlucosidesHumansMaleRatsRats, TransgenicSignal TransductionBenzhydryl CompoundsdapagliflozinGlucosidesHistocompatibility Antigens Class IMHC class I-related chain AMICB antigencolorectal cancerdapagliflozinextracellular vesicleMHC class I moleculessodium‒glucose cotransporter 2

Identifiers

PMID41968633
PMCPMC13071181

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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.