DUSP26 inhibits the proliferation, invasion, and migration of colorectal cancer cells by regulating fructose metabolism and epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway

XU Ting; TANG Yao; WU Jun

doi:10.11659/jjssx.07E025045

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DUSP26 inhibits the proliferation, invasion, and migration of colorectal cancer cells by regulating fructose metabolism and epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway

Digestive System Diseases | 更新时间：2026-03-17

- DUSP26 inhibits the proliferation, invasion, and migration of colorectal cancer cells by regulating fructose metabolism and epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 35, Issue 3, Pages: 191-198(2026)
- 作者机构：
  
  1.西安市第三医院消化内科,陕西西安 710018
  2.西安市第三医院普外科，陕西西安 710018
  3.西安高新医院神经内科，陕西西安 710075
- 作者简介：
- 基金信息：
- DOI：10.11659/jjssx.07E025045
  CLC： R735.3
- Received：10 July 2025，
  
  Published：25 March 2026
- 稿件说明：
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徐婷,唐尧,伍俊.DUSP26通过PI3K/AKT/mTOR通路调节果糖代谢和上皮间质转化抑制结直肠癌细胞增殖、侵袭和迁移[J].局解手术学杂志,2026,35(03):191-198.

XU Ting,TANG Yao,WU Jun.DUSP26 inhibits the proliferation, invasion, and migration of colorectal cancer cells by regulating fructose metabolism and epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(03):191-198.
徐婷,唐尧,伍俊.DUSP26通过PI3K/AKT/mTOR通路调节果糖代谢和上皮间质转化抑制结直肠癌细胞增殖、侵袭和迁移[J].局解手术学杂志,2026,35(03):191-198. DOI： 10.11659/jjssx.07E025045.

XU Ting,TANG Yao,WU Jun.DUSP26 inhibits the proliferation, invasion, and migration of colorectal cancer cells by regulating fructose metabolism and epithelial-mesenchymal transition via PI3K/AKT/mTOR pathway[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(03):191-198. DOI： 10.11659/jjssx.07E025045.

摘要

目的

探究DUSP26对结直肠癌（CRC）细胞的影响及潜在作用机制。

方法

通过Western blot和qRT-PCR检测DUSP26在CRC细胞系和正常结肠上皮细胞系NCM460中的表达水平。通过慢病毒转染构建稳定过表达DUSP26的SW480细胞株及稳定敲低DUSP26的Caco-2细胞株；采用克隆形成实验、划痕愈合实验及Transwell实验评估DUSP26对细胞增殖、迁移与侵袭能力的影响；通过Western blot检测磷脂酰肌醇3-激酶（PI3K）、蛋白激酶B（AKT）、哺乳动物雷帕霉素靶蛋白（mTOR）、果糖转运体5（GLUT5）、酮己糖激酶（KHK）、E-cadherin、N-cadherin、Vimentin及锌指转录因子Snail等蛋白表达。使用果糖培养细胞并检测细胞中果糖浓度；进一步采用PI3K激活剂740 Y-P与抑制剂LY294002进行回复验证。

结果

与NCM460细胞相比，DUSP26在CRC各细胞系中表达显著下调（

0.05）。过表达DUSP26可抑制细胞增殖、迁移和侵袭，降低p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR水平，下调GLUT5、KHK、Vimentin、N-cadherin及Snail蛋白表达，上调E-cadherin蛋白表达，并减少果糖消耗，差异均有统计学意义（

0.05）；敲低DUSP26则可逆转上述指标变化（

0.05）。激活PI3K可逆转DUSP26过表达对CRC细胞果糖代谢及转移的抑制作用，而抑制PI3K则显著增强敲低DUSP26对细胞增殖、迁移和侵袭的抑制作用（

0.05）。

结论

DUSP26在CRC中低表达，其可通过抑制PI3K/AKT/mTOR通路调控果糖代谢和上皮间质转化，从而发挥其抗肿瘤作用。

Abstract

Objective

To investigate the effect of DUSP26 on colorectal cancer （CRC） cells and its underlying mechanism.

Methods

The expression levels of DUSP26 in CRC cell lines and the normal colonic epithelial cell line NCM460 were detected by Western blot and qRT-PCR.SW480 cells with DUSP26 overexpression and Caco-2 cells with DUSP26 knockdown were constructed via lentiviral transduction. The effects of DUSP26 on cell proliferation， migration， and invasion were evaluated by colony formation assay， wound healing assay， and Transwell assay. The protein expression of phosphatidylinositol 3-kinase （PI3K）， protein kinase B （AKT）， mammalian target of rapamycin （mTOR）， glucose transporter 5 （GLUT5）， ketohexokinase （KHK）， E-cadherin， N-cadherin， Vimentin， and the zinc finger transcription factor Snail were detected by Western blot. Cells were cultured with fructose， and the fructose consumption in cells were detected. Further rescue experiments were conducted using the PI3K activator 740 Y-P and the inhibitor LY294002.

Results

Compared with NCM460 cells， DUSP26 expression was significantly downregulated in various CRC cell lines （

0.05）. Overexpression of DUSP26 inhibited cell proliferation， migration， and invasion， reduced the ratios of p-PI3K/PI3K，p-AKT/AKT and p-mTOR/mTOR， downregulated the protein expression of GLUT5， KHK， Vimentin， N-cadherin， and Snail， and upregulated E-cadherin protein expression， and decreased fructose consumption， with statistically significant differences （

0.05）. Knockdown of DUSP26 reversed the changes in the aforementioned indicators （

0.05）. Activation of PI3K counteracted the inhibitory effects of DUSP26 overexpression on fructose metabolism and metastasis in CRC cells， whereas inhibition of PI3K significantly enhanced the suppressive effects of DUSP26 knockdown on cell proliferation， migration， and invasion （

0.05）.

Conclusion

DUSP26 is lowly expressed in CRC. It exerts anti-tumor effects by inhibiting the PI3K/AKT/mTOR pathway， thereby regulating fructose metabolism and epithelial-mesenchymal transition.

关键词

Keywords

references

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