Current understanding on the role of CCT3 in cancer research

Liu, Wenlou; Lu, Y. P.; Yan, Xiang; Lu, Quansheng; Sun, Yuwen; Xiao, Wei; Li, Yi‐Zhi; Zhao, Jiaqin; Li, Yuchen; Jiang, Guan

doi:10.3389/fonc.2022.961733

Cited by 10 publications

(4 citation statements)

References 65 publications

(89 reference statements)

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“…CCT3, a major subunit, plays a fundamental role in protein folding, with its gene located on chromosome 1. CCT3 is involved in regulating signaling pathways like STAT3, Wnt, and PI3K-AKT, impacting tumor cell proliferation, differentiation, and apoptosis ( Liu W. et al, 2022 ). The protein CCT3 plays a role in the ferroptosis of lung adenocarcinoma cells.…”

Section: Pi3k/akt Pathway Regulates Key Molecules Of Ferroptosismentioning

confidence: 99%

Regulation of ferroptosis by PI3K/Akt signaling pathway: a promising therapeutic axis in cancer

Su,

Peng,

Liu

2024

Front. Cell Dev. Biol.

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The global challenge posed by cancer, marked by rising incidence and mortality rates, underscores the urgency for innovative therapeutic approaches. The PI3K/Akt signaling pathway, frequently amplified in various cancers, is central in regulating essential cellular processes. Its dysregulation, often stemming from genetic mutations, significantly contributes to cancer initiation, progression, and resistance to therapy. Concurrently, ferroptosis, a recently discovered form of regulated cell death characterized by iron-dependent processes and lipid reactive oxygen species buildup, holds implications for diseases, including cancer. Exploring the interplay between the dysregulated PI3K/Akt pathway and ferroptosis unveils potential insights into the molecular mechanisms driving or inhibiting ferroptotic processes in cancer cells. Evidence suggests that inhibiting the PI3K/Akt pathway may sensitize cancer cells to ferroptosis induction, offering a promising strategy to overcome drug resistance. This review aims to provide a comprehensive exploration of this interplay, shedding light on the potential for disrupting the PI3K/Akt pathway to enhance ferroptosis as an alternative route for inducing cell death and improving cancer treatment outcomes.

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Section: Pi3k/akt Pathway Regulates Key Molecules Of Ferroptosismentioning

confidence: 99%

Regulation of ferroptosis by PI3K/Akt signaling pathway: a promising therapeutic axis in cancer

Su,

Peng,

Liu

2024

Front. Cell Dev. Biol.

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“…GC [44] PT aminoacyl-tRNA synthesis pathway [44] promotes cancer progression, poor prognosis, metastasis [44]; worse patient survival in BC [43] GARS1 Glycyl-tRNA synthetase 1 cytoplasmic and mitochondrial ARS overexpressed in tumor samples compared to adjacent normal tissues [43], displays androgen-dependent transcriptional initiation in several hormone-responsive cells, overexpressed in PCa [45] PT may deactivate ERK signaling pathway [45] worse patient survival in BC [43]; could induce tumor regression [45] LARS1 Leucyl-tRNA synthetase 1 (Editing Domain) cytoplasmic ARS overexpressed in some cancers: myeloid leukemia, pancreatic cancer, renal, cervical, skin cancer [45], lung cancer cell lines and tissues [46] PT senses intracellular leucine levels to activate mTORC1 pathway [45] lower patient survival in BC [43], promotes cell proliferation, growth [45], and migration [46] [47], associated with an increased risk of BC [45] PT impairment of AIMP1/EMAPII secretion in MCF7 cells [48] lower patient survival in BC [43], increases growth rate in hepatoma cells, induces stem cell-like features in head and neck tumors [47] PSMC6 Proteasome subunit p42/proteasome 26S subunit ATPase 6 protein catabolic process, regulation of DNA-template transcription, protein-containing complex assembly highly upregulated in LUAD [49], BC tissues, especially in luminal cancer [50] PT MTORC1_SIGNALING; REAC-TOME_REGULATION_OF_ MITOTIC_CELL_CYCLE; activation of Wnt signaling via degrading AXIN proteins [49] oncogenic effect [50], poor prognosis, silencing inhibits cell growth, migration and invasion [49] CCT2/CCTβ Chaperonin containing TCP1 Subunit 2 involved in cell cycle regulation, protein folding and binding biological processes [51] overexpressed in various tumors and cell lines, such as HER2+ BC, liver, prostate, cholecyst, lung, CRC, BC [51], glioblastoma [52] PT P53 signaling [51] worse prognosis, especially in luminal A subtype, promotes cell growth/surviv...…”

Section: Phosphoenolpyruvate Carboxykinase 1 (Pepck)mentioning

confidence: 99%

Two-Dimensional-PAGE Coupled with nLC-MS/MS-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in MCF7 Breast Cancer Cells Transfected for JTB Protein Silencing

Jayathirtha,

Jayaweera,

Whitham

et al. 2023

Molecules

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The identification of new cancer-associated genes/proteins, the characterization of their expression variation, the interactomics-based assessment of differentially expressed genes/proteins (DEGs/DEPs), and understanding the tumorigenic pathways and biological processes involved in BC genesis and progression are necessary and possible by the rapid and recent advances in bioinformatics and molecular profiling strategies. Taking into account the opinion of other authors, as well as based on our own team’s in vitro studies, we suggest that the human jumping translocation breakpoint (hJTB) protein might be considered as a tumor biomarker for BC and should be studied as a target for BC therapy. In this study, we identify DEPs, carcinogenic pathways, and biological processes associated with JTB silencing, using 2D-PAGE coupled with nano-liquid chromatography tandem mass spectrometry (nLC-MS/MS) proteomics applied to a MCF7 breast cancer cell line, for complementing and completing our previous results based on SDS-PAGE, as well as in-solution proteomics of MCF7 cells transfected for JTB downregulation. The functions of significant DEPs are analyzed using GSEA and KEGG analyses. Almost all DEPs exert pro-tumorigenic effects in the JTBlow condition, sustaining the tumor suppressive function of JTB. Thus, the identified DEPs are involved in several signaling and metabolic pathways that play pro-tumorigenic roles: EMT, ERK/MAPK, PI3K/AKT, Wnt/β-catenin, mTOR, C-MYC, NF-κB, IFN-γ and IFN-α responses, UPR, and glycolysis/gluconeogenesis. These pathways sustain cancer cell growth, adhesion, survival, proliferation, invasion, metastasis, resistance to apoptosis, tight junctions and cytoskeleton reorganization, the maintenance of stemness, metabolic reprogramming, survival in a hostile environment, and sustain a poor clinical outcome. In conclusion, JTB silencing might increase the neoplastic phenotype and behavior of the MCF7 BC cell line. The data is available via ProteomeXchange with the identifier PXD046265.

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“…CCT3, known as chaperonin containing TCP1 subunit 3(γ), is a molecular chaperone. It belongs to the chaperonin family and facilitates the folding of several proteins immediately after synthesis and restores the normal conformations of abnormal proteins [41]. In proliferating cells, high levels of protein synthesis are required for proliferation [42], requiring an increase in CCT levels for the folding of nascent proteins [43].…”

Section: Introductionmentioning

confidence: 99%

N-Acetylneuraminic Acid Inhibits Melanogenesis via Induction of Autophagy

Yoshikawa,

Maeda

2024

Cosmetics

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N-acetylneuraminic acid (Neu5Ac) is the predominant form of sialic acid present in the glossy swiftlet (Collocalia esculenta). It is also the only form of sialic acid detected in the human body. In this study, we investigated the mechanism underlying melanogenesis inhibition by Neu5Ac. We discovered that a reduction in tyrosinase protein levels led to an inhibition of melanin production by Neu5Ac. Additionally, the mRNA and protein levels of ubiquitin-specific protease (USP5) and microtubule-associated protein 1 light chain 3 (LC3)-II increased, while those of p62 decreased, indicating enhanced autophagic activity. Lysosomal cathepsin L2 protein levels also increased, and immunostaining revealed colocalization of lysosomal membrane protein (LAMP)-1 and tyrosinase. Additionally, levels of chaperonin containing T-complex polypeptide (CCT), implicated in increased autophagic flux, were elevated. Altogether, these findings suggest that tyrosinase-containing coated vesicles are transported by Neu5Ac into the autophagic degradation pathway, suppressing mature melanosome generation. This process involves increased USP5 levels preventing recognition of polyubiquitin by proteasomes. Furthermore, elevated CCT3 protein levels may enhance autophagic flux, leading to the incorporation of tyrosinase-containing coated vesicles into autophagosomes. These autophagosomes then fuse with lysosomes for cathepsin L2–mediated degradation. Thus, our findings suggest that Neu5Ac reduces tyrosinase activity and inhibits melanosome maturation by promoting selective autophagic degradation of abnormal proteins by p62.

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Current understanding on the role of CCT3 in cancer research

Cited by 10 publications

References 65 publications

Regulation of ferroptosis by PI3K/Akt signaling pathway: a promising therapeutic axis in cancer

Regulation of ferroptosis by PI3K/Akt signaling pathway: a promising therapeutic axis in cancer

Two-Dimensional-PAGE Coupled with nLC-MS/MS-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in MCF7 Breast Cancer Cells Transfected for JTB Protein Silencing

N-Acetylneuraminic Acid Inhibits Melanogenesis via Induction of Autophagy

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