Evidence map›Paper›PMID 40700902›Full record

ArticleTranslational oncology2025

AGEs-RAGE manipulates tumor intrinsic pERK/Sp1/IL6 pathway and reprograms macrophage to promote intrahepatic cholangiocarcinoma progression.

Juan Zhang, Biyang Jing, Xiaojian Ni, Youpei Lin, Jiaomeng Pan, MaoPei Chen, Boheng Zhang, Lan Zhang, Ningling Ge, Ruyuan Deng and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

12 authors.

Juan ZhangDepartment of Hepatobiliary Oncology, Liver Cancer Institute, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai 200032, China.
Biyang JingSchool of Mathematical Sciences and Center for Statistical Science, Peking University, Beijing 100871, China.
Xiaojian NiDepartment of Biliary Surgery and Biliary Tract Disease, Biliary Tract Disease Institute and Cancer Center, Zhongshan Hospital, Fudan University, Shanghai Biliary Tract Minimal Invasive Surgery and Materials Engineering Research Center, Shanghai 200032, China.
Youpei LinDepartment of Hepatobiliary Surgery and Liver Transplantation, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Jiaomeng PanDepartment of Hepatobiliary Surgery and Liver Transplantation, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
MaoPei ChenDepartment of Hepatobiliary Oncology, Liver Cancer Institute, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai 200032, China.
Boheng ZhangDepartment of Hepatobiliary Oncology, Zhongshan Hospital, Fudan University (Xiamen Branch), Xiamen Clinical Research Center for Cancer Therapy, Clinical Research Center for Precision medicine of abdominal tumor of Fujian Province, Xiamen City, Fujian Province 361015, China.
Lan ZhangDepartment of Hepatobiliary Oncology, Liver Cancer Institute, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai 200032, China.
Ningling GeDepartment of Hepatobiliary Oncology, Liver Cancer Institute, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai 200032, China.
Ruyuan DengDepartment of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. Electronic address: deng.ruyuan@zs-hospital.sh.cn.
Xiao WangShanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao tong University School of Medicine, Shanghai 200025, PR China. Electronic address: wangxiao1976@hotmail.com.
Guohe SongDepartment of Hepatobiliary Surgery and Liver Transplantation, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China. Electronic address: docsong2013@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors often exhibit oxygen deprivation and enhanced glucose uptake, leading to glycolysis. Advanced glycation end products (AGEs) protein modifications induced by hyperglycemia-activate signaling pathways that promote cancer progression upon binding to its receptor (RAGE). In this study, AGEs-treatment enhanced the growth, invasion and migration of intrahepatic cholangiocarcinoma cells (ICC), while increasing IL-6 expression and secretion. Meanwhile, AGEs stimulated the expression of RAGE, specificity protein 1 (Sp1), and the phosphorylation of extracellular signal-regulated kinase (ERK) in a dose-dependent manner. However, these effects were attenuated by RAGE antibody blockade, RAGE knockdown, the ERK inhibitor U0126, or Sp1-specific siRNA. Furthermore, the supernatant of AGEs-treated RBE cells induced M2 polarization of THP-1 macrophages. Thus, AGEs promote ICC progression partly through the pERK/Sp1/IL-6 pathway and M2 macrophage polarization. These findings highlight underscore the role of the AGEs-RAGE axis in driving ICC progression via pERK/Sp1/IL-6 signaling.

Indexed as

Advanced glycation end productsExtracellular signal-regulated kinaseIL-6Intrahepatic cholangiocarcinomaReceptor for advanced glycation end productsSpecificity protein 1

Identifiers

PMID40700902
PMCPMC12861650

What Socratic holds

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Registered trials

None linked

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 Socratic graph.