Abstract

As a substrate and major effector of the mammalian target of rapamycin complex 1 (mTORC1), the biological functions of ribosomal protein S6 kinase (S6K) have been canonically assigned for cell size control by facilitating mRNA transcription, splicing, and protein synthesis. However, accumulating evidence implies that diverse stimuli and upstream regulators modulate S6K kinase activity, leading to the activation of a plethora of downstream substrates for distinct pathobiological functions. Beyond controlling cell size, S6K simultaneously plays crucial roles in directing cell apoptosis, metabolism, and feedback regulation of its upstream signals. Thus, we comprehensively summarize the emerging upstream regulators, downstream substrates, mouse models, clinical relevance, and candidate inhibitors for S6K and shed light on S6K as a potential therapeutic target for cancers.

Details

Title
Beyond controlling cell size: functional analyses of S6K in tumorigenesis
Author
Wu, Xueji 1   VIAFID ORCID Logo  ; Xie, Wei 2   VIAFID ORCID Logo  ; Xie, Wenxuan 3 ; Wei, Wenyi 4   VIAFID ORCID Logo  ; Guo, Jianping 2   VIAFID ORCID Logo 

 Sun Yat-sen University, Department of Liver Surgery, Hepatobiliary Pancreatic Center, the First Affiliated Hospital, Guangzhou, China (GRID:grid.12981.33) (ISNI:0000 0001 2360 039X); Sun Yat-sen University, Institute of Precision Medicine, the First Affiliated Hospital, Guangzhou, China (GRID:grid.12981.33) (ISNI:0000 0001 2360 039X) 
 Sun Yat-sen University, Institute of Precision Medicine, the First Affiliated Hospital, Guangzhou, China (GRID:grid.12981.33) (ISNI:0000 0001 2360 039X) 
 Sun Yat-sen University, Department of Liver Surgery, Hepatobiliary Pancreatic Center, the First Affiliated Hospital, Guangzhou, China (GRID:grid.12981.33) (ISNI:0000 0001 2360 039X) 
 Harvard Medical School, Department of Pathology, Beth Israel Deaconess Medical Center, Boston, USA (GRID:grid.38142.3c) (ISNI:000000041936754X) 
Publication year
2022
Publication date
Jul 2022
Publisher
Springer Nature B.V.
e-ISSN
20414889
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2694117129
Copyright
© The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.