Evidence map›Paper›PMID 38750462›Full record

ArticleJournal of translational medicine2024

CCT6A facilitates lung adenocarcinoma progression and glycolysis via STAT1/HK2 axis.

Shao-Kun Yu, Tao Yu, Yu-Ming Wang, Ao Sun, Jia Liu, Kai-Hua Lu

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
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  4. Chaperonin in health and disease.Molecular biomedicine · 2026
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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

6 authors.

Shao-Kun YuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Tao YuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yu-Ming WangDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Ao SunDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jia LiuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Kai-Hua LuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. lukaihua@njmu.edu.cn.

Funding

National Natural Science Foundation of China 82172708
6 · The paper itself

Abstract

backgroundChaperonin Containing TCP1 Subunit 6 A (CCT6A) is a prominent protein involved in the folding and stabilization of newly synthesized proteins. However, its roles and underlying mechanisms in lung adenocarcinoma (LUAD), one of the most aggressive cancers, remain elusive.

methodsOur study utilized in vitro cell phenotype experiments to assess CCT6A's impact on the proliferation and invasion capabilities of LUAD cell lines. To delve into CCT6A's intrinsic mechanisms affecting glycolysis and proliferation in lung adenocarcinoma, we employed transcriptomic sequencing and liquid chromatography-mass spectrometry analysis. Co-immunoprecipitation (Co-IP) and chromatin immunoprecipitation (CHIP) assays were also conducted to substantiate the mechanism.

resultsCCT6A was found to be significantly overexpressed in LUAD and associated with a poorer prognosis. The silencing of CCT6A inhibited the proliferation and migration of LUAD cells and elevated apoptosis rates. Mechanistically, CCT6A interacted with STAT1 protein, forming a complex that enhances the stability of STAT1 by protecting it from ubiquitin-mediated degradation. This, in turn, facilitated the transcription of hexokinase 2 (HK2), a critical enzyme in aerobic glycolysis, thereby stimulating LUAD's aerobic glycolysis and progression.

conclusionOur findings reveal that the CCT6A/STAT1/HK2 axis orchestrated a reprogramming of glucose metabolism and thus promoted LUAD progression. These insights position CCT6A as a promising candidate for therapeutic intervention in LUAD treatment.

Indexed as

Adenocarcinoma of LungCell ProliferationChaperonin Containing TCP-1Disease ProgressionGlycolysisHexokinaseLung NeoplasmsSTAT1 Transcription FactorApoptosisCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessSignal TransductionCCT6A protein, humanChaperonin Containing TCP-1HexokinaseHK2 protein, humanSTAT1 Transcription FactorAerobic glycolysisCCT6AHK2Lung adenocarcinomaSTAT1

Identifiers

PMID38750462
PMCPMC11094951

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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.