Multi-Omics Analysis and Verification of the Oncogenic Value of CCT8 in Pan-Cancers.

CCT8 biomarker immune infiltration pan-cancer survival

Journal

Journal of inflammation research
ISSN: 1178-7031
Titre abrégé: J Inflamm Res
Pays: New Zealand
ID NLM: 101512684

Informations de publication

Date de publication:
2023
Historique:
received: 03 01 2023
accepted: 06 04 2023
medline: 5 6 2023
pubmed: 5 6 2023
entrez: 5 6 2023
Statut: epublish

Résumé

Chaperonin-containing TCP1 subunit 8 (CCT8) has been proved to be involved in the occurrence and development of some cancers. However, no study has reported the potential role of CCT8 in a pan-cancer manner. TIMER2.0, GEPIA2, UALCAN and Sangerbox were used to explore the expression, prognosis and methylation of CCT8. We used cBioPortal, TISIDB, SangerBox, TIMER2.0 and TISMO to investigate the genetic alteration of CCT8 and the relationship of CCT8 with molecular subtype, immune subtype, immune infiltration and immunotherapy response. CCT8-related genes were screened out through GEPIA and STRING for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. CCK-8, the colony formation assay, the wound healing assay and the Transwell assay were performed to explore the influence of CCT8 on proliferation and migration. CCT8 was highly expressed in most cancers with a poor prognosis. The expression level of CCT8, which was affected by the promoter region methylation and genetic alteration, was related to the molecular and immune subtype of cancers. Interestingly, CCT8 was positively associated with the activated CD4 T cells and type 2 T-helper cells. CCT8 played a vital role in the cell cycle and RNA transport of cancers, and it significantly inhibited the proliferation and migration of lung adenocarcinoma cells when it was knocked down. CCT8 plays an indispensable role in promoting the proliferation and migration of many cancers. CCT8 might be a biomarker of T-helper type 2 (Th2) cell infiltration and a promising therapeutic target for T-helper type 1(Th1)/Th2 imbalance.

Sections du résumé

Background UNASSIGNED
Chaperonin-containing TCP1 subunit 8 (CCT8) has been proved to be involved in the occurrence and development of some cancers. However, no study has reported the potential role of CCT8 in a pan-cancer manner.
Methods UNASSIGNED
TIMER2.0, GEPIA2, UALCAN and Sangerbox were used to explore the expression, prognosis and methylation of CCT8. We used cBioPortal, TISIDB, SangerBox, TIMER2.0 and TISMO to investigate the genetic alteration of CCT8 and the relationship of CCT8 with molecular subtype, immune subtype, immune infiltration and immunotherapy response. CCT8-related genes were screened out through GEPIA and STRING for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. CCK-8, the colony formation assay, the wound healing assay and the Transwell assay were performed to explore the influence of CCT8 on proliferation and migration.
Results UNASSIGNED
CCT8 was highly expressed in most cancers with a poor prognosis. The expression level of CCT8, which was affected by the promoter region methylation and genetic alteration, was related to the molecular and immune subtype of cancers. Interestingly, CCT8 was positively associated with the activated CD4 T cells and type 2 T-helper cells. CCT8 played a vital role in the cell cycle and RNA transport of cancers, and it significantly inhibited the proliferation and migration of lung adenocarcinoma cells when it was knocked down.
Conclusion UNASSIGNED
CCT8 plays an indispensable role in promoting the proliferation and migration of many cancers. CCT8 might be a biomarker of T-helper type 2 (Th2) cell infiltration and a promising therapeutic target for T-helper type 1(Th1)/Th2 imbalance.

Identifiants

pubmed: 37273485
doi: 10.2147/JIR.S403499
pii: 403499
pmc: PMC10238552
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2297-2315

Informations de copyright

© 2023 Gong et al.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Références

Front Immunol. 2022 May 03;13:844736
pubmed: 35592314
Cancer Cell Int. 2019 Oct 11;19:262
pubmed: 31632196
Nat Commun. 2015 Dec 04;6:8971
pubmed: 26634437
Front Immunol. 2022 Apr 04;13:849592
pubmed: 35444654
Gastroenterology. 2018 Apr;154(5):1421-1434
pubmed: 29274368
Cell Mol Immunol. 2019 Jul;16(7):634-643
pubmed: 30867582
Cell Rep. 2014 May 22;7(4):1130-42
pubmed: 24813893
Front Pharmacol. 2022 Mar 10;13:811338
pubmed: 35359851
Mol Biol Evol. 2017 Nov 1;34(11):2944-2958
pubmed: 28961875
Cancer Cell Int. 2022 Mar 3;22(1):101
pubmed: 35241075
Oncogenesis. 2021 Dec 3;10(12):84
pubmed: 34862361
Epigenomics. 2018 Mar;10(3):277-288
pubmed: 29264942
Channels (Austin). 2021 Dec;15(1):528-540
pubmed: 34424811
Pathol Res Pract. 2015 Oct;211(10):717-25
pubmed: 26304164
Science. 2015 Jan 23;347(6220):1260419
pubmed: 25613900
Oncotarget. 2018 Apr 10;9(27):19065-19078
pubmed: 29721184
Genomics. 2020 Nov;112(6):3958-3967
pubmed: 32645525
Cancer Res. 2019 Mar 15;79(6):1085-1097
pubmed: 30530503
Nature. 2012 Mar 28;483(7391):603-7
pubmed: 22460905
J Pers Med. 2021 Oct 26;11(11):
pubmed: 34834441
APMIS. 2014 Nov;122(11):1070-9
pubmed: 24862099
Biomolecules. 2022 Jun 13;12(6):
pubmed: 35740947
Cancer Cell. 2009 Aug 4;16(2):91-102
pubmed: 19647220
Front Oncol. 2013 Mar 26;3:63
pubmed: 23533029
Channels (Austin). 2021 Dec;15(1):496-506
pubmed: 34334114
Aging (Albany NY). 2021 Jul 30;13(14):17970
pubmed: 34329194
Cell. 2017 Nov 30;171(6):1437-1452.e17
pubmed: 29195078
Nucleic Acids Res. 2019 Jul 2;47(W1):W556-W560
pubmed: 31114875
Clin Dev Immunol. 2012;2012:925135
pubmed: 22474485
Int J Oncol. 2018 Jun;52(6):2021-2030
pubmed: 29620162
Front Genet. 2022 Jun 29;13:905051
pubmed: 35846134
Commun Biol. 2021 Jun 3;4(1):681
pubmed: 34083746
Science. 2007 Feb 9;315(5813):848-53
pubmed: 17289997
Front Immunol. 2021 May 03;12:669474
pubmed: 34012451
Immunity. 2018 Apr 17;48(4):812-830.e14
pubmed: 29628290
World J Surg Oncol. 2021 Nov 18;19(1):329
pubmed: 34794429
Cancer Res. 2021 Feb 15;81(4):1026-1039
pubmed: 33277366
Nature. 2020 Apr;580(7802):257-262
pubmed: 32269339
Am J Cancer Res. 2020 Jan 01;10(1):95-113
pubmed: 32064155
Nat Rev Genet. 2012 May 29;13(7):484-92
pubmed: 22641018
Nat Commun. 2013;4:2612
pubmed: 24113773

Auteurs

Lian Gong (L)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Ming Zhong (M)

Department of Nephrology, Center of Kidney and Urology, the Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, People's Republic of China.

Kai Gong (K)

Department of Clinical Medicine, Xiangnan University, Chenzhou, People's Republic of China.

Zhanwang Wang (Z)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Yong Zhong (Y)

Department of Clinical Medicine, Hubei Enshi College, Enshi, People's Republic of China.

Yi Jin (Y)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Haotian Chen (H)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Panpan Tai (P)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Xinyu Chen (X)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Aiyan Chen (A)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Ke Cao (K)

Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, 410013, People's Republic of China.

Classifications MeSH