TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways

Abstract The chaperonin tailless complex polypeptide 1 (TCP1) is a key subunit of chaperonin containing TCP1 (CCT) that regulates the folding and stability of proteins during cancer progression. Here, the prognostic significance of TCP1 was explored mainly in patients with hepatocellular carcinoma (...

Full description

Saved in:
Bibliographic Details
Main Authors: Hekun Liu, Linying Chen, Yuwen Chen, Yiyi Jin, Xiance Chen, Nengjun Ma, Fan Yang, Huixia Bi, Xinxin Wen, Shenmin Xu, Juan Chen, Yanping Lin, Yinghong Yang, Yong Wu, Yuanzhong Chen
Format: Article
Language:English
Published: Nature Portfolio 2025-04-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-07867-6
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850153545723019264
author Hekun Liu
Linying Chen
Yuwen Chen
Yiyi Jin
Xiance Chen
Nengjun Ma
Fan Yang
Huixia Bi
Xinxin Wen
Shenmin Xu
Juan Chen
Yanping Lin
Yinghong Yang
Yong Wu
Yuanzhong Chen
author_facet Hekun Liu
Linying Chen
Yuwen Chen
Yiyi Jin
Xiance Chen
Nengjun Ma
Fan Yang
Huixia Bi
Xinxin Wen
Shenmin Xu
Juan Chen
Yanping Lin
Yinghong Yang
Yong Wu
Yuanzhong Chen
author_sort Hekun Liu
collection DOAJ
description Abstract The chaperonin tailless complex polypeptide 1 (TCP1) is a key subunit of chaperonin containing TCP1 (CCT) that regulates the folding and stability of proteins during cancer progression. Here, the prognostic significance of TCP1 was explored mainly in patients with hepatocellular carcinoma (HCC) and pancreatic ductal adenocarcinoma (PDAC). We showed that TCP1 expression was significantly greater in clinically malignant tumour tissues than in normal tissues and that high TCP1 expression was associated with poor prognosis. TCP1 suppression not only decreased the proliferation and invasion of cancer cells in vitro but also inhibited tumour growth and metastasis in vivo. The underlying mechanisms were determined by ubiquitination assays and Co-IP (Co-Immunoprecipitation) experiments, and it was found that TCP1 regulated the stability of c-Myc through the RAC-alpha serine/threonine-protein kinase (AKT) /Glycogen synthase kinase 3β (GSK-3β) and extracellular regulated protein kinases (ERK) signalling pathways. Moreover, TCP1 knock-in (TCP1-KI) dramatically promoted the occurrence of diethylnitrosamine (DEN) -induced primary HCC in mice. Our results highlight the critical role of TCP1 in HCC and PDAC and reveal a novel mechanism to suppress HCC and PDAC by targeting c-Myc via the TCP1-induced promotion of the AKT/GSK-3β and ERK signalling pathways. TCP1 is able to modulate the stability of target proteins by multiple pathways, thus promoting the progression of HCC and PDAC. Our study identifies TCP1 as a prognostic novel marker and therapeutic target of HCC and PDAC.
format Article
id doaj-art-fd8964ea86d642a3ab8202c463f8e4db
institution OA Journals
issn 2399-3642
language English
publishDate 2025-04-01
publisher Nature Portfolio
record_format Article
series Communications Biology
spelling doaj-art-fd8964ea86d642a3ab8202c463f8e4db2025-08-20T02:25:41ZengNature PortfolioCommunications Biology2399-36422025-04-018111310.1038/s42003-025-07867-6TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathwaysHekun Liu0Linying Chen1Yuwen Chen2Yiyi Jin3Xiance Chen4Nengjun Ma5Fan Yang6Huixia Bi7Xinxin Wen8Shenmin Xu9Juan Chen10Yanping Lin11Yinghong Yang12Yong Wu13Yuanzhong Chen14Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityDepartment of Pathology, the First Affiliated Hospital of Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, The School of Basic Medical Sciences, Fujian Medical UniversityDepartment of Pathology, Fujian Medical University Union HospitalFujian Institute of Haematology, Fujian Key Laboratory on Haematology, Fujian Medical University Union HospitalFujian Institute of Haematology, Fujian Key Laboratory on Haematology, Fujian Medical University Union HospitalAbstract The chaperonin tailless complex polypeptide 1 (TCP1) is a key subunit of chaperonin containing TCP1 (CCT) that regulates the folding and stability of proteins during cancer progression. Here, the prognostic significance of TCP1 was explored mainly in patients with hepatocellular carcinoma (HCC) and pancreatic ductal adenocarcinoma (PDAC). We showed that TCP1 expression was significantly greater in clinically malignant tumour tissues than in normal tissues and that high TCP1 expression was associated with poor prognosis. TCP1 suppression not only decreased the proliferation and invasion of cancer cells in vitro but also inhibited tumour growth and metastasis in vivo. The underlying mechanisms were determined by ubiquitination assays and Co-IP (Co-Immunoprecipitation) experiments, and it was found that TCP1 regulated the stability of c-Myc through the RAC-alpha serine/threonine-protein kinase (AKT) /Glycogen synthase kinase 3β (GSK-3β) and extracellular regulated protein kinases (ERK) signalling pathways. Moreover, TCP1 knock-in (TCP1-KI) dramatically promoted the occurrence of diethylnitrosamine (DEN) -induced primary HCC in mice. Our results highlight the critical role of TCP1 in HCC and PDAC and reveal a novel mechanism to suppress HCC and PDAC by targeting c-Myc via the TCP1-induced promotion of the AKT/GSK-3β and ERK signalling pathways. TCP1 is able to modulate the stability of target proteins by multiple pathways, thus promoting the progression of HCC and PDAC. Our study identifies TCP1 as a prognostic novel marker and therapeutic target of HCC and PDAC.https://doi.org/10.1038/s42003-025-07867-6
spellingShingle Hekun Liu
Linying Chen
Yuwen Chen
Yiyi Jin
Xiance Chen
Nengjun Ma
Fan Yang
Huixia Bi
Xinxin Wen
Shenmin Xu
Juan Chen
Yanping Lin
Yinghong Yang
Yong Wu
Yuanzhong Chen
TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways
Communications Biology
title TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways
title_full TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways
title_fullStr TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways
title_full_unstemmed TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways
title_short TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways
title_sort tcp1 promotes the progression of malignant tumours by stabilizing c myc through the akt gsk 3β and erk signalling pathways
url https://doi.org/10.1038/s42003-025-07867-6
work_keys_str_mv AT hekunliu tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT linyingchen tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT yuwenchen tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT yiyijin tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT xiancechen tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT nengjunma tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT fanyang tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT huixiabi tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT xinxinwen tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT shenminxu tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT juanchen tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT yanpinglin tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT yinghongyang tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT yongwu tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways
AT yuanzhongchen tcp1promotestheprogressionofmalignanttumoursbystabilizingcmycthroughtheaktgsk3banderksignallingpathways