SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma

Solute carrier family 27 member 5 (SLC27A5/FATP5) is a liver-specific metabolic enzyme that plays a crucial role in fatty acid transport and bile acid metabolism. Deficiency of SLC27A5 promotes the progression of hepatocellular carcinoma (HCC) and is strongly associated with a poor prognosis. SLC27A...

Full description

Saved in:
Bibliographic Details
Main Authors: Xin Tang, Junji Tao, Yuanyuan Liu, Deao Gong, Xuefeng Shan, Kai Wang, Ni Tang
Format: Article
Language:English
Published: KeAi Communications Co., Ltd. 2025-07-01
Series:Genes and Diseases
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S235230422400285X
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850203697688084480
author Xin Tang
Junji Tao
Yuanyuan Liu
Deao Gong
Xuefeng Shan
Kai Wang
Ni Tang
author_facet Xin Tang
Junji Tao
Yuanyuan Liu
Deao Gong
Xuefeng Shan
Kai Wang
Ni Tang
author_sort Xin Tang
collection DOAJ
description Solute carrier family 27 member 5 (SLC27A5/FATP5) is a liver-specific metabolic enzyme that plays a crucial role in fatty acid transport and bile acid metabolism. Deficiency of SLC27A5 promotes the progression of hepatocellular carcinoma (HCC) and is strongly associated with a poor prognosis. SLC27A5 exhibits noncanonical functions beyond its metabolic role; however, its specific mechanisms in hepatocarcinogenesis remain elusive and are therefore investigated in this study. Immunoprecipitation-mass spectrometry analysis showed that SLC27A5-interacting proteins were significantly enriched in alternative polyadenylation (APA). RNA-sequencing data provided evidence that SLC27A5 plays a global role in regulating APA events in HCC. Mechanistically, SLC27A5 facilitates the usage of the proximal polyadenylation site of METTL14 by downregulating the expression of the APA-associated factor PABPC1, resulting in the shortening of the METTL14-3′UTR and the conversion of METTL14-UL to METTL14-US. In contrast to METTL14-UL, METTL14-US escapes the inhibitory effect of miRNA targeting, leading to increased METTL14 expression. METTL14-US upregulation by SLC27A5 suppressed the stemness of HCC. Therefore, low levels of SLC27A5 and METTL14 may serve as reliable biomarkers for identifying poor prognosis in patients with HCC. In conclusion, SLC27A5/PABPC1 inhibits HCC stemness via APA-regulated expression of METTL14, providing potential avenues for the development of novel therapeutic strategies.
format Article
id doaj-art-0dbba36e6be14e9783c9dd10dea0aa69
institution OA Journals
issn 2352-3042
language English
publishDate 2025-07-01
publisher KeAi Communications Co., Ltd.
record_format Article
series Genes and Diseases
spelling doaj-art-0dbba36e6be14e9783c9dd10dea0aa692025-08-20T02:11:26ZengKeAi Communications Co., Ltd.Genes and Diseases2352-30422025-07-0112410148810.1016/j.gendis.2024.101488SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinomaXin Tang0Junji Tao1Yuanyuan Liu2Deao Gong3Xuefeng Shan4Kai Wang5Ni Tang6Department of Infectious Diseases, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, ChinaDepartment of Infectious Diseases, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, ChinaDepartment of Infectious Diseases, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, ChinaDepartment of Infectious Diseases, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, ChinaDepartment of Pharmacy, Bishan Hospital of Chongqing Medical University, Chongqing 402760, China; Corresponding author.Department of Infectious Diseases, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China; Corresponding author.Department of Infectious Diseases, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China; Corresponding author.Solute carrier family 27 member 5 (SLC27A5/FATP5) is a liver-specific metabolic enzyme that plays a crucial role in fatty acid transport and bile acid metabolism. Deficiency of SLC27A5 promotes the progression of hepatocellular carcinoma (HCC) and is strongly associated with a poor prognosis. SLC27A5 exhibits noncanonical functions beyond its metabolic role; however, its specific mechanisms in hepatocarcinogenesis remain elusive and are therefore investigated in this study. Immunoprecipitation-mass spectrometry analysis showed that SLC27A5-interacting proteins were significantly enriched in alternative polyadenylation (APA). RNA-sequencing data provided evidence that SLC27A5 plays a global role in regulating APA events in HCC. Mechanistically, SLC27A5 facilitates the usage of the proximal polyadenylation site of METTL14 by downregulating the expression of the APA-associated factor PABPC1, resulting in the shortening of the METTL14-3′UTR and the conversion of METTL14-UL to METTL14-US. In contrast to METTL14-UL, METTL14-US escapes the inhibitory effect of miRNA targeting, leading to increased METTL14 expression. METTL14-US upregulation by SLC27A5 suppressed the stemness of HCC. Therefore, low levels of SLC27A5 and METTL14 may serve as reliable biomarkers for identifying poor prognosis in patients with HCC. In conclusion, SLC27A5/PABPC1 inhibits HCC stemness via APA-regulated expression of METTL14, providing potential avenues for the development of novel therapeutic strategies.http://www.sciencedirect.com/science/article/pii/S235230422400285XAlternative polyadenylationHepatocellular carcinomaMETTL14SLC27A5Stemness
spellingShingle Xin Tang
Junji Tao
Yuanyuan Liu
Deao Gong
Xuefeng Shan
Kai Wang
Ni Tang
SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma
Genes and Diseases
Alternative polyadenylation
Hepatocellular carcinoma
METTL14
SLC27A5
Stemness
title SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma
title_full SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma
title_fullStr SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma
title_full_unstemmed SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma
title_short SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma
title_sort slc27a5 inhibits cancer stem cells by inducing alternative polyadenylation of mettl14 in hepatocellular carcinoma
topic Alternative polyadenylation
Hepatocellular carcinoma
METTL14
SLC27A5
Stemness
url http://www.sciencedirect.com/science/article/pii/S235230422400285X
work_keys_str_mv AT xintang slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma
AT junjitao slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma
AT yuanyuanliu slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma
AT deaogong slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma
AT xuefengshan slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma
AT kaiwang slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma
AT nitang slc27a5inhibitscancerstemcellsbyinducingalternativepolyadenylationofmettl14inhepatocellularcarcinoma