Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming

Research indicates that abnormal gut microbiota metabolism is linked to colorectal cancer (CRC) progression, but the role of microbiota-related tryptophan metabolism disruption remains unclear. Using metagenomic sequencing and targeted Trp metabolomics, our research identified that CRC patients had...

Full description

Saved in:
Bibliographic Details
Main Authors: Shizhen Zhou, Kai Wang, Jiandong Huang, Zhen Xu, Qinggang Yuan, Lixiang Liu, Zhifeng Wang, Ji Miao, Hao Wang, Tingting Wang, Wenxian Guan, Chao Ding
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Gut Microbes
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/19490976.2025.2508949
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849714389651816448
author Shizhen Zhou
Kai Wang
Jiandong Huang
Zhen Xu
Qinggang Yuan
Lixiang Liu
Zhifeng Wang
Ji Miao
Hao Wang
Tingting Wang
Wenxian Guan
Chao Ding
author_facet Shizhen Zhou
Kai Wang
Jiandong Huang
Zhen Xu
Qinggang Yuan
Lixiang Liu
Zhifeng Wang
Ji Miao
Hao Wang
Tingting Wang
Wenxian Guan
Chao Ding
author_sort Shizhen Zhou
collection DOAJ
description Research indicates that abnormal gut microbiota metabolism is linked to colorectal cancer (CRC) progression, but the role of microbiota-related tryptophan metabolism disruption remains unclear. Using metagenomic sequencing and targeted Trp metabolomics, our research identified that CRC patients had abnormal indole-3-lactic acid (ILA) levels, which were related to tumor malignancy. Exogenous ILA administration suppressed CRC development in AOM/DSS induced and xenograft mice models. Furthermore, in vitro experiments demonstrated that ILA inhibits tumor cell proliferation, migration, and anti-apoptotic capabilities. Mechanistically, ILA appears to directly occupy the phosphorylation sites of STAT3, leading to a reduction in intracellular phosphorylated STAT3 (p-STAT3) levels and the inhibition of the HK2 pathway, thereby downregulating glucose metabolism in cancer cells. Notably, this inhibition is independent of the aryl hydrocarbon receptor (AHR). In conclusion, our research findings demonstrate that alterations in tryptophan metabolism among CRC patients can influence tumor progression and reveal a novel mechanism through which ILA exerts its inhibitory effects on CRC. These findings offer new insights into the role of gut microbiota in CRC and identify potential clinical therapeutic targets.
format Article
id doaj-art-d6b2d5fbcb7a4fc5a449ddc12bbcf620
institution DOAJ
issn 1949-0976
1949-0984
language English
publishDate 2025-12-01
publisher Taylor & Francis Group
record_format Article
series Gut Microbes
spelling doaj-art-d6b2d5fbcb7a4fc5a449ddc12bbcf6202025-08-20T03:13:43ZengTaylor & Francis GroupGut Microbes1949-09761949-09842025-12-0117110.1080/19490976.2025.2508949Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogrammingShizhen Zhou0Kai Wang1Jiandong Huang2Zhen Xu3Qinggang Yuan4Lixiang Liu5Zhifeng Wang6Ji Miao7Hao Wang8Tingting Wang9Wenxian Guan10Chao Ding11Department of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, ChinaThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, China01life Institute, Shenzhen, ChinaThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, ChinaDepartment of Gastrointestinal Surgery, Xuzhou Central Hospital, Xuzhou, ChinaDepartment of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China01life Institute, Shenzhen, ChinaDepartment of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, ChinaDepartment of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, ChinaThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, ChinaDepartment of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, ChinaDepartment of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, ChinaResearch indicates that abnormal gut microbiota metabolism is linked to colorectal cancer (CRC) progression, but the role of microbiota-related tryptophan metabolism disruption remains unclear. Using metagenomic sequencing and targeted Trp metabolomics, our research identified that CRC patients had abnormal indole-3-lactic acid (ILA) levels, which were related to tumor malignancy. Exogenous ILA administration suppressed CRC development in AOM/DSS induced and xenograft mice models. Furthermore, in vitro experiments demonstrated that ILA inhibits tumor cell proliferation, migration, and anti-apoptotic capabilities. Mechanistically, ILA appears to directly occupy the phosphorylation sites of STAT3, leading to a reduction in intracellular phosphorylated STAT3 (p-STAT3) levels and the inhibition of the HK2 pathway, thereby downregulating glucose metabolism in cancer cells. Notably, this inhibition is independent of the aryl hydrocarbon receptor (AHR). In conclusion, our research findings demonstrate that alterations in tryptophan metabolism among CRC patients can influence tumor progression and reveal a novel mechanism through which ILA exerts its inhibitory effects on CRC. These findings offer new insights into the role of gut microbiota in CRC and identify potential clinical therapeutic targets.https://www.tandfonline.com/doi/10.1080/19490976.2025.2508949Indole-3-lactic acidHK2P-STAT3glycolysiscolorectal cancer
spellingShingle Shizhen Zhou
Kai Wang
Jiandong Huang
Zhen Xu
Qinggang Yuan
Lixiang Liu
Zhifeng Wang
Ji Miao
Hao Wang
Tingting Wang
Wenxian Guan
Chao Ding
Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
Gut Microbes
Indole-3-lactic acid
HK2
P-STAT3
glycolysis
colorectal cancer
title Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
title_full Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
title_fullStr Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
title_full_unstemmed Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
title_short Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming
title_sort indole 3 lactic acid suppresses colorectal cancer via metabolic reprogramming
topic Indole-3-lactic acid
HK2
P-STAT3
glycolysis
colorectal cancer
url https://www.tandfonline.com/doi/10.1080/19490976.2025.2508949
work_keys_str_mv AT shizhenzhou indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT kaiwang indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT jiandonghuang indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT zhenxu indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT qinggangyuan indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT lixiangliu indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT zhifengwang indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT jimiao indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT haowang indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT tingtingwang indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT wenxianguan indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming
AT chaoding indole3lacticacidsuppressescolorectalcancerviametabolicreprogramming