Evidence map›Paper›PMID 35409343›Full record

ArticleInternational journal of molecular sciences2022

Suppression of CCT3 Inhibits Tumor Progression by Impairing ATP Production and Cytoplasmic Translation in Lung Adenocarcinoma.

Shuohua Chen, Yang Tian, Anji Ju, Boya Li, Yan Fu, Yongzhang Luo

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. 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 at 1 institution in 1 country.

Shuohua ChenCancer Biology Laboratory, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Yang TianCancer Biology Laboratory, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Anji JuCancer Biology Laboratory, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Boya LiCancer Biology Laboratory, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Yan FuCancer Biology Laboratory, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Yongzhang LuoCancer Biology Laboratory, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Tsinghua University · CN

Funding

Self-Topic Fund of Tsinghua University 20191080585the Science and Technology Major Project 20181821569
6 · The paper itself

Abstract

Heat shock proteins are highly expressed in various cancers and exert critical functions in tumor progression. However, their expression patterns and functions in lung adenocarcinoma (LUAD) remain largely unknown. We identified that chaperonin-containing T-complex protein-1 subunit 3 (CCT3) was highly expressed in LUAD cells and was positively correlated with LUAD malignancy in the clinical samples. Animal studies showed that silencing CCT3 dramatically inhibited tumor growth and metastasis of LUAD. Proliferation and migration were markedly suppressed in CCT3-deficient LUAD cells. Moreover, the knockdown of CCT3 promoted apoptosis and cell cycle arrest. Mechanistically, the function of glycolysis was significantly inhibited and the total intracellular ATP levels were reduced by at least 25% in CCT3-deficient cells. In addition, the knockdown of CCT3 decreased the protein translation and led to a significant reduction in eukaryotic translation initiation factor 3 (EIF3G) protein, which was identified as a protein that interacts with CCT3. Impaired protein synthesis and cell growth in EIF3G-deficient cells were consistent with those caused by CCT3 knockdown in LUAD cells. Taken together, our study demonstrated in multiple ways that CCT3 is a critical factor for supporting growth and metastasis of LUAD, and for the first time, its roles in maintaining intracellular ATP levels and cytoplasmic translation are reported. Our novel findings provide a potential therapeutic target for lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungLung NeoplasmsAdenosine TriphosphateAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticProtein BiosynthesisAdenosine TriphosphateATP productionCCT3cytoplasmic translationgrowthlung adenocarcinomametastasis

Identifiers

PMID35409343
PMCPMC9000022
OpenAlexW4223591921

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.