SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway

Gastric cancer (GC) is a common digestive tract malignancy worldwide. N-myristoyltransferase 1 (NMT1) has been implicated in many cancers, but its association with gastric cancer remains to be clarified. Thus, this paper elucidated the role of NMT1 in GC. The NMT1 expression level in GC and normal t...

Full description

Saved in:
Bibliographic Details
Main Authors: Ping Qiu, Xing Li, Min Gong, Ping Wen, Jianbo Wen, Linfang Xu, Guiliang Wang
Format: Article
Language:English
Published: Wiley 2023-01-01
Series:Canadian Journal of Gastroenterology and Hepatology
Online Access:http://dx.doi.org/10.1155/2023/2021515
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850159573573304320
author Ping Qiu
Xing Li
Min Gong
Ping Wen
Jianbo Wen
Linfang Xu
Guiliang Wang
author_facet Ping Qiu
Xing Li
Min Gong
Ping Wen
Jianbo Wen
Linfang Xu
Guiliang Wang
author_sort Ping Qiu
collection DOAJ
description Gastric cancer (GC) is a common digestive tract malignancy worldwide. N-myristoyltransferase 1 (NMT1) has been implicated in many cancers, but its association with gastric cancer remains to be clarified. Thus, this paper elucidated the role of NMT1 in GC. The NMT1 expression level in GC and normal tissue samples as well as the relationship between NMT1 high or low expression and overall survival in GC was analyzed via GEPIA. GC cells were transfected with NMT1 or SPI1 overexpression plasmid and short hairpin RNA against NMT1 (shNMT1) or shSPI1. NMT1, SPI1, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, and mTOR levels were detected through qRT-PCR and western blot. MTT, wound healing, and transwell assays were applied to test cell viability, migration, and invasion. The binding relationship of SPI1 and NMT1 was determined through a dual-luciferase reporter assay and chromatin immunoprecipitation. NMT1 was upregulated in GC, the high level of which connected with a poor prognosis. Overexpressed NMT1 elevated viability, migration rate, and invasion rate of GC cells, whereas NMT1 knockdown leads to the opposite results. Besides, SPI1 could bind to NMT1. Overexpressed NMT1 reversed the effects of shSPI1 on decreasing viability, migration, invasion, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR in GC cells, and NMT1 knockdown reversed the effects of SPI1 overexpression on increasing viability, migration, invasion, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR. SPI1 upregulated NMT1 to facilitate the malignant behaviors of GC cells through the PI3K/AKT/mTOR pathway.
format Article
id doaj-art-ae10754d0859460eb5ce65aede7900f1
institution OA Journals
issn 2291-2797
language English
publishDate 2023-01-01
publisher Wiley
record_format Article
series Canadian Journal of Gastroenterology and Hepatology
spelling doaj-art-ae10754d0859460eb5ce65aede7900f12025-08-20T02:23:28ZengWileyCanadian Journal of Gastroenterology and Hepatology2291-27972023-01-01202310.1155/2023/2021515SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR PathwayPing Qiu0Xing Li1Min Gong2Ping Wen3Jianbo Wen4Linfang Xu5Guiliang Wang6Department of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyDepartment of GastroenterologyGastric cancer (GC) is a common digestive tract malignancy worldwide. N-myristoyltransferase 1 (NMT1) has been implicated in many cancers, but its association with gastric cancer remains to be clarified. Thus, this paper elucidated the role of NMT1 in GC. The NMT1 expression level in GC and normal tissue samples as well as the relationship between NMT1 high or low expression and overall survival in GC was analyzed via GEPIA. GC cells were transfected with NMT1 or SPI1 overexpression plasmid and short hairpin RNA against NMT1 (shNMT1) or shSPI1. NMT1, SPI1, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, and mTOR levels were detected through qRT-PCR and western blot. MTT, wound healing, and transwell assays were applied to test cell viability, migration, and invasion. The binding relationship of SPI1 and NMT1 was determined through a dual-luciferase reporter assay and chromatin immunoprecipitation. NMT1 was upregulated in GC, the high level of which connected with a poor prognosis. Overexpressed NMT1 elevated viability, migration rate, and invasion rate of GC cells, whereas NMT1 knockdown leads to the opposite results. Besides, SPI1 could bind to NMT1. Overexpressed NMT1 reversed the effects of shSPI1 on decreasing viability, migration, invasion, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR in GC cells, and NMT1 knockdown reversed the effects of SPI1 overexpression on increasing viability, migration, invasion, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR. SPI1 upregulated NMT1 to facilitate the malignant behaviors of GC cells through the PI3K/AKT/mTOR pathway.http://dx.doi.org/10.1155/2023/2021515
spellingShingle Ping Qiu
Xing Li
Min Gong
Ping Wen
Jianbo Wen
Linfang Xu
Guiliang Wang
SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway
Canadian Journal of Gastroenterology and Hepatology
title SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway
title_full SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway
title_fullStr SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway
title_full_unstemmed SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway
title_short SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway
title_sort spi1 mediates n myristoyltransferase 1 to advance gastric cancer progression via pi3k akt mtor pathway
url http://dx.doi.org/10.1155/2023/2021515
work_keys_str_mv AT pingqiu spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway
AT xingli spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway
AT mingong spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway
AT pingwen spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway
AT jianbowen spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway
AT linfangxu spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway
AT guiliangwang spi1mediatesnmyristoyltransferase1toadvancegastriccancerprogressionviapi3kaktmtorpathway