ArticleBMC molecular and cell biology2022
Upregulation of CCT3 predicts poor prognosis and promotes cell proliferation via inhibition of ferroptosis and activation of AKT signaling in lung adenocarcinoma.
Article in BMC molecular and cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- The mechanism of deubiquitinase USP14 modifying HSP90AA1 to activate NRF2 signaling in lung cancer cell resistance to ferroptosis.Molecular biology reports · 2026Article
- TFCP2L1 suppresses breast cancer progression by promoting ferroptosis through direct and PI3K/AKT-mediated inhibition of GPX4.Cell death discovery · 2026Article
- Chaperonin in health and disease.Molecular biomedicine · 2026Review
- HSP70-mediated regulation of P-glycoprotein SUMOylation suppresses ferroptosis to drive thermoresistance in non-small cell lung cancer.Frontiers in immunology · 2026Article
- Expression patterns and clinical implications of chaperonin subunit 3 mRNA and protein in laryngeal squamous cell carcinoma.World journal of clinical oncology · 2025Article
- Potential involvement of the KLF2-GPX4 axis in ferroptosis during S.aureus-induced osteomyelitis.Human genomics · 2025Article
- Cervical Cancer Biomarkers in Non-Cervical Samples: Emerging Tools for Diagnosis and Prognosis.International journal of molecular sciences · 2025Review
- Advances in the study of CCT3 in malignant tumors: A review.Medicine · 2025Review
- Identification of novel ferroptosis-related biomarkers associated with the oxidative stress pathways in ischemic cardiomyopathy.International journal of cardiology. Heart & vasculature · 2025Article
- Chaperonins in Hepatocellular Carcinoma: Unveiling Their Role in Tumor Proliferation and Immune Modulation Through Multiomics Analysis.International journal of genomics · 2025Article
- Silencing CCT3 induces ferroptosis through the NOD1-NF-κB signaling pathway in bladder cancer.Scientific reports · 2024Article
- Oleic Acid Inhibits SDC4 and Promotes Ferroptosis in Lung Cancer Through GPX4/ACSL4.The clinical respiratory journal · 2024Article
- Article
- CCT3/ACTN4/TFRC axis protects hepatocellular carcinoma cells from ferroptosis by inhibiting iron endocytosis.Journal of experimental & clinical cancer research : CR · 2024Article
- [Role of Ferroptosis in Non-small Cell Lung Cancer and Progress of Traditional Chinese Medicine Intervention].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Revisiting the chaperonin T-complex protein-1 ring complex in human health and disease: A proteostasis modulator and beyond.Clinical and translational medicine · 2024Review
- SLC7A11 inhibits ferroptosis and downregulates PD-L1 levels in lung adenocarcinoma.Frontiers in immunology · 2024Article
- Regulation of ferroptosis by PI3K/Akt signaling pathway: a promising therapeutic axis in cancer.Frontiers in cell and developmental biology · 2024Review
- Regulation of Ferroptosis in Lung Adenocarcinoma.International journal of molecular sciences · 2023Review
- A potential tumor marker: Chaperonin containing TCP‑1 controls the development of malignant tumors (Review).International journal of oncology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChaperonin containing TCP1 subunit 3 (CCT3) acts as an oncogene in cancers, whereas its role and underlying mechanisms in lung adenocarcinoma (LUAD) are poorly understood. This study investigated the clinical relevance and function of CCT3 in LUAD.
methodsClinical relevance of CCT3 in LUAD and lung squamous cell carcinoma (LUSC) was analyzed based on TCGA database. qRT-PCR and Western blot were used to detect mRNA and protein expression, respectively. CCK8 and colony formation were performed to measure cell viability. PI and PI/Annexin V-FITC assay kit was used to determine cell cycle and cell death, respectively. Luciferase activity was performed to check whether CCT3 regulated slc7a11's transcription activity. Ferroptosis was determined by incubating the cells with ferroptosis and apoptosis inducer, their inhibitor and autophagy inhibitor, followed by cell viability examination.
resultsWe found that CCT3 was overexpressed in LUAD and LUSC tissues. Overexpression of CCT3 predicted the poor prognosis of LUAD patients. Loss-of-function and gain-of-function experiments demonstrated that CCT3 promoted the proliferation and colony formation of LUAD cells. In addition, CCT3 promoted cell cycle progression and suppressed slc7a11-mediated cell ferroptosis, but not apoptosis. We also found that CCT3 activated AKT. MK2206 significantly reduced the viability of CCT3 overexpressed LUAD cells, while had smaller inhibitory effect on the proliferation of control cells, suggesting that CCT3 dictates the sensitivity of LUAD cells to AKT inhibition.
conclusionOur study demonstrates that CCT3 contributes to the proliferation and growth of LUAD cells through inhibition of ferroptosis and activation of AKT.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.