Evidence map›Paper›PMID 36918801›Full record

ArticleBMC cancer2023

Integrated analyzes identify CCT3 as a modulator to shape immunosuppressive tumor microenvironment in lung adenocarcinoma.

Junfeng Huang, Bingqi Hu, Ying Yang, Huanhuan Liu, Xingyu Fan, Jing Zhou, Liwen Chen

Open access · goldFull text read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. 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

7 authors at 2 institutions in 1 country.

Junfeng Huang *Department of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China.
Bingqi Hu *Department of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China.
Ying YangDepartment of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China.
Huanhuan LiuDepartment of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China.
Xingyu FanDepartment of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China.
Jing ZhouDepartment of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China.
Liwen ChenDepartment of Laboratory Medicine, Second Hospital of Anhui Medical University, Hefei, China. chenliwen@ahmu.edu.cn.
Second Hospital of Anhui Medical University · CNAnhui Medical University · CN

Funding

Key Research and Development Program of Anhui Province 202004j07020027The Natural Science Foundation of Anhui Province 1808085MH229
6 · The paper itself

Abstract

backgroundChaperonin-containing tailless complex polypeptide 1 (TCP1) subunit 3 (CCT3) has tumor-promoting effects in lung adenocarcinoma (LUAD). This study aims to investigate the molecular mechanisms of CCT3 in LUAD oncogenesis.

methodsThe UALCAN databases, Human Protein Atlas (HPA) and The Cancer Genome Atlas (TCGA) data were used to analyze CCT3 expression in LUAD. Both the Wilcoxon rank-sum test and the regression model were used to investigate the connection between clinicopathologic characteristics of LUAD patients and CCT3 expression. The prognostic value of CCT3 was determined by Cox regression models, the Kaplan-Meier method and Nomogram prediction. Next, we identified the most related genes with CCT3 via GeneMANIA and String databases, and the association between CCT3 and infiltrated immune cells using single-sample Gene Set Enrichment Analysis (ssGSEA). CCT3-related pathway enrichment analysis was investigated by GSEA. Finally, CCT3 roles in cell proliferation and apoptosis of LUAD A549 cells was verified by siRNA (small interfering RNA) mediated CCT3 knockdown.

resultsCCT3 was upregulated in LUAD both in mRNA and protein levels. CCT3 overexpression was associated with clinicopathological characteristics including sex, smoking, T- and N-categories, pathological staging, and a poor prognosis of LUAD patients. GeneMANIA and String databases found a set of CCT3-related genes that are connected to the assembly and stability of proteins involved in proteostasis of cytoskeletal filaments, DNA repair and protein methylation. Furthermore, CCT3 was found to be positively correlated with the infiltrating Th2 cells (r = 0.442, p < 0.01) while negatively correlated with mast cells (r = -0.49, p < 0.01) and immature dendritic cells (iDCs, r = -0.401, p < 0.001) according to ssGSEA analyzes. The pathway analysis based on GSEA method showed that the cell cycle pathway, the protein export pathway, the proteasome pathway and the ribosome pathway are enriched in CCT3 high group, whereas the JAK/STAT pathway, B cell receptor pathway, T cell receptor pathway and toll like receptor pathway were enriched in CCT3 low group. Finally, CCT3 knockdown substantially inhibited proliferation while promoted apoptosis of A549 cells.

conclusionIntegrated analyzes identify CCT3 as a modulator to shape immunosuppressive tumor microenvironment in LUAD and therefore, a prognostic factor for LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsChaperonin Containing TCP-1HumansImmunosuppressive AgentsJanus KinasesPrognosisSignal TransductionSTAT Transcription FactorsTumor MicroenvironmentCCT3 protein, humanChaperonin Containing TCP-1Immunosuppressive AgentsJanus KinasesSTAT Transcription FactorsBiomarkerCCT3Immune cell infiltrationLung adenocarcinomaTCP1

Identifiers

PMID36918801
PMCPMC10012614
OpenAlexW4324142542

What Socratic holds

Textfull text, public
LicenceCC BY
measurements read28
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 Socratic graph.