Evidence map›Paper›PMID 42003909›Full record

ArticleInternational journal of biological sciences2026

CCT2 Orchestrates Glycolysis and Exosome-Mediated M2 Macrophage Polarization in HCC tumorigenesis.

Wing-Wa Guo, Cairang Dongzhi, Tianyin Ma, Minghe Zhang, Meng Gao, Xiaomian Li, Jitong Zhou, Xi Chen, Wenzhi He, Ming Tian and 2 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Wing-Wa GuoDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Cairang DongzhiDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Tianyin MaDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Minghe ZhangDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Meng GaoDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Xiaomian LiDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Jitong ZhouDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Xi ChenDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Wenzhi HeDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Ming TianDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Yufeng YuanDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Weijie MaDepartment of Hepatobiliary & Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with a poor prognosis, driven by metabolic reprogramming and immune evasion. The role of T-complex protein 1 subunit beta (CCT2) in HCC remains unclear. This study aimed to elucidate the function of CCT2 in HCC tumorigenesis. Methods: Bioinformatics analysis and Clinical samples investigation were integrated with Results: CCT2 directly interacts with and stabilizes the glycolytic enzyme ALDOA, as shown by co-immunoprecipitation and metabolic assays revealing increased extracellular acidification rate, glucose uptake, and lactate production in HCC cells. Genetic depletion of CCT2 suppresses tumor cell proliferation and migration Conclusions: CCT2 stabilizes ALDOA and facilitates exosome-mediated immunosuppressive signaling, thereby linking metabolic reprogramming to immune evasion in HCC and supporting its potential as a mechanistically informed therapeutic target.

Indexed as

Carcinoma, HepatocellularExosomesGlycolysisLiver NeoplasmsMacrophagesAnimalsCarcinogenesisCell Line, TumorCell ProliferationFructose-Bisphosphate AldolaseHumansMetabolic ReprogrammingMiceTumor MicroenvironmentFructose-Bisphosphate AldolaseCCT2exosomeglycolysishepatocellular carcinomamacrophage

Identifiers

PMID42003909
PMCPMC13085899

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.