TRPV4 deficiency exacerbates colorectal cancer progression in mice by remodeling gut microbiota and promoting secretion of inflammatory factors

FENG Yunxuan; FENG Xiaojie; CHENG Lulu; WANG Yingjie; JIANG Jiao; XI Changqi; WANG Xiang; XU Fen; TANG Bo

doi:10.16016/j.2097-0927.202512128

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TRPV4 deficiency exacerbates colorectal cancer progression in mice by remodeling gut microbiota and promoting secretion of inflammatory factors

Basic Medicine | 更新时间：2026-03-30

- TRPV4 deficiency exacerbates colorectal cancer progression in mice by remodeling gut microbiota and promoting secretion of inflammatory factors
- Journal of Army Medical University Vol. 48, Issue 6, Pages: 722-732(2026)
- 作者机构：
  
  陆军军医大学（第三军医大学）第二附属医院消化内科，重庆
- 作者简介：
  
  TANG Bo，E-mail：botangxq@tmmu.edu.cn
- 基金信息：
  
  the General Program of National Natural Science Foundation of China(81972327)
- DOI：10.16016/j.2097-0927.202512128
  CLC： R735.3;R378;R730.231
- Received：29 December 2025，
  
  Revised：2026-01-20，
  
  Published：30 March 2026
- 稿件说明：
移动端阅览
冯韵璇，冯小洁，程璐璐，等.TRPV4缺失通过重塑肠道菌群及促进炎症因子分泌加剧小鼠结直肠癌进展［J］.陆军军医大学学报，2026，48（06）：722-732.DOI：10.16016/j.2097-0927.202512128.

FENG Y X，FENG X J，CHENG L L，et al.TRPV4 deficiency exacerbates colorectal cancer progression in mice by remodeling gut microbiota and promoting secretion of inflammatory factors［J］.J Army Med Univ，2026，48（06）：722-732.DOI：10.16016/j.2097-0927.202512128.
冯韵璇，冯小洁，程璐璐，等.TRPV4缺失通过重塑肠道菌群及促进炎症因子分泌加剧小鼠结直肠癌进展［J］.陆军军医大学学报，2026，48（06）：722-732.DOI：10.16016/j.2097-0927.202512128. DOI：

FENG Y X，FENG X J，CHENG L L，et al.TRPV4 deficiency exacerbates colorectal cancer progression in mice by remodeling gut microbiota and promoting secretion of inflammatory factors［J］.J Army Med Univ，2026，48（06）：722-732.DOI：10.16016/j.2097-0927.202512128. DOI：

摘要

目的

宿主基因可通过调控肠道菌群组成与功能，进而影响结直肠癌（colorectal cancer，CRC）的发生发展。本研究旨在探究宿主基因

TRPV4

缺失通过重塑肠道菌群及促进炎症因子分泌加剧小鼠结直肠癌的作用机制。

方法

本研究使用

TRPV4

基因敲除小鼠，构建葡聚糖硫酸钠（dextran sodium sulfate，DSS）+氧化偶氮甲烷（azoxymethane，AOM）诱导结直肠癌小鼠模型。分别将6~8周龄雄性

TRPV4

基因敲除小鼠及野生型小鼠按体质量分层后随机分为TRPV4

-/-

组与WT组（

=7），于第1周的第1天腹腔注射10 mg/kg AOM 1次；第7天起连续7 d给予含1.5% DSS饮水，恢复常规饮水2周，DSS处理循环3个周期。第6周的第1天再次腹腔注射10 mg/kg AOM 1次。监测肿瘤数量、大小、负荷、结肠长度、脾脏重量、结肠组织HE染色及病理评分、免疫组化检测增殖细胞核抗原（proliferating cell nuclear antigen，PCNA）阳性率等指标综合评估CRC发生发展程度。另将6~8周龄雄性

TRPV4

基因敲除小鼠及野生型小鼠按体质量分层后随机分为抗生素鸡尾酒（antibiotic cocktail，ABX）-TRPV4

-/-

组与ABX-WT组（

=5），ABX混合液用于耗竭肠道菌群，以评估TRPV4对CRC的影响的菌群依赖性。收集TRPV4

-/-

组（

=19）和WT组（

=21）小鼠造模前的粪便样本并进行16S rRNA测序，分析TRPV4基因对小鼠肠道菌群的影响。对小鼠结肠组织进行RNA测序，通过京都基因与基因组百科全书（Kyoto encyclopedia of genes and genomes，KEGG）分析差异表达基因的富集情况，并进行粪菌-细胞体外共孵育实验。

结果

TRPV4

-/-

组较WT组肿瘤发生率（

=0.037 9）、肿瘤负荷（

=0.000 3）、组织病理评分（

0.000 1）以及PCNA阳性率（

0.000 1）显著升高，结肠长度显著缩短（

=0.001 2）。ABX处理后，TRPV4

-/-

组与WT组在肿瘤发生率、肿瘤负荷、结肠长度、组织病理评分及PCNA阳性率等指标上均无显著差异（

0.05）。16S rRNA测序分析结果表明，

TRPV4

基因缺失显著重塑小鼠肠道菌群结构，TRPV4

-/-

与WT两组小鼠β多样性存在显著差异（

=0.001），菌群组成结构具有明显差异。结肠组织RNA-seq结果显示，TRPV4

-/-

小鼠组中有218个基因显著上调，152个基因显著下调，KEGG通路富集分析结果显示，差异表达基因显著富集于细胞因子信号通路和TNF信号通路。体外共孵育结果显示，TRPV4

-/-

小鼠粪菌组较WT小鼠粪菌组TNF-α（

0.000 1）、IL-1β（

0.000 1）和IL-23（

0.000 1）转录水平显著上调。

结论

TRPV4

基因缺失形成的肠道微生态可能通过促进机体炎症相关细胞因子的分泌从而加剧小鼠结直肠癌。

Abstract

Objective

Host genes regulate the composition and function of gut microbiota

thereby influencing the development of colorectal cancer (CRC). This study aims to investigate the mechanisms by which host gene

TRPV4

deficiency exacerbates CRC in mice through remodeling gut microbiota and promoting inflammatory cytokine secretion.

Methods

TRPV4

knockout (TRPV4

-/-

) mice were used to establish a CRC mouse model induced by dextran sodium sulfate (DSS) and azoxymethane (AOM). Male TRPV4

-/-

and wild-type mice (6 to 8 weeks old) were stratified by body weight and randomly divided into TRPV4

-/-

group (

=7) and WT group (

=7). The mouse model of CRC was established through a single intraperitoneal injection of 10 mg/kg AOM on day 1 of week 1; from day 7

drinking water containing 1.5% DSS for 7 consecutive days

followed by 2 weeks of regular water

with this DSS treatment cycle being repeated for 3 times; a second intraperitoneal injection of 10 mg/kg AOM on day 1 of week 6. CRC progression was assessed with tumor number

size

burden

colon length

spleen weight

colonic morphology (HE staining) and pathological score

and immunohistochemical detection of proliferating cell nuclear antigen (PCNA). Additionally

male TRPV4

-/-

and wild-type mice (6 to 8 weeks old) were stratified by body weight and randomly divided into antibiotic cocktail (ABX)-TRPV4

-/-

group (

=5) and ABX-WT group (

=5). The ABX mixture was used to deplete the gut microbiota to evaluate the microbiota-dependent effects of TRPV4 on CRC. Fecal samples were collected from the TRPV4

-/-

group (

=19) and WT group (

=21) before modeling

and then subjected to 16S rRNA sequencing to determine the effect of

TRPV4

gene on mouse gut microbiota. RNA sequencing was performed on mouse colonic tissue; Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was used to examine enrichment of differentially expressed genes

and fecal bacteria-cell co-incubation experiments were conducted

in vitro

Results

The TRPV4

-/-

group exhibited significantly increased tumor incidence (

=0.037 9)

tumor burden (

=0.000 3)

histopathological score (

0.000 1)

and PCNA-positive rate (

0.000 1)

and shorter colon length (

=0.001 2) compared with the WT group. After ABX treatment

no significant differences were observed between the TRPV4

-/-

group and WT group in tumor incidence

tumor burden

colon length

histopathological score

or PCNA positive rate (

0.05). 16S rRNA sequencing demonstrated that TRPV4 deficiency reshaped the gut microbiota structure

with significant differences in β diversity between the TRPV4

-/-

and WT groups (

=0.001) and distinct microbiota composition profiles. Colon tissue RNA-seq results revealed 218 significantly upregulated and 152 downregulated genes in TRPV4

-/-

mice. KEGG pathway enrichment showed that differentially expressed genes were significantly enriched in cytokine signaling pathways and TNF signaling pathways.

In vitro

co-incubation results demonstrated that the transcription levels of TNF-α (

0.000 1)

IL-1β (

0.000 1)

and IL-23 (

0.000 1) were significantly upregulated in TRPV4

-/-

microbiota-cell co-cultures.

Conclusion

The gut microecology formed by

TRPV4

deficiency may exacerbate CRC by promoting the secretion of inflammation-related cytokines.

关键词

Keywords

references

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