Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone

Abstract Background Chronic restraint stress (CRS) has iteratively been reported to be possibly implicated in the development of numerous cancer types. However, its role in oral squamous cell carcinoma (OSCC) has not been well elucidated. Here we intended to evaluate the role and mechanism. Methods...

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Main Authors: Shihong Luo, Huiqing Long, Fangzhi Lou, Yiyun Liu, Haiyang Wang, Juncai Pu, Ping Ji, Xin Jin
Format: Article
Language:English
Published: BMC 2024-01-01
Series:BMC Oral Health
Subjects:
Online Access:https://doi.org/10.1186/s12903-023-03787-1
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author Shihong Luo
Huiqing Long
Fangzhi Lou
Yiyun Liu
Haiyang Wang
Juncai Pu
Ping Ji
Xin Jin
author_facet Shihong Luo
Huiqing Long
Fangzhi Lou
Yiyun Liu
Haiyang Wang
Juncai Pu
Ping Ji
Xin Jin
author_sort Shihong Luo
collection DOAJ
description Abstract Background Chronic restraint stress (CRS) has iteratively been reported to be possibly implicated in the development of numerous cancer types. However, its role in oral squamous cell carcinoma (OSCC) has not been well elucidated. Here we intended to evaluate the role and mechanism. Methods The effects of CRS were investigated in xenograft models of OSCC by using transcriptome sequencing, LC–MS, ELISA and RT-PCR. Moreover, the role of CRS and ALDH3A1 on OSCC cells was researched by using Trans-well, flow cytometry, western blotting, immunofluorescence, ATP activity and OCR assay. Furthermore, immunohistochemical staining was employed to observe the cell proliferation and invasion of OSCC in xenotransplantation models. Results CRS promoted the progression of OSCC in xenograft models, stimulated the secretion of norepinephrine and the expression of ADRB2, but decreased the expression of ALDH3A1. Moreover, CRS changed energy metabolism and increased mitochondrial metabolism markers. However, ALDH3A1 overexpression suppressed proliferation, EMT and mitochondrial metabolism of OSCC cells. Conclusion Inhibition of ALDH3A1 expression plays a pivotal role in CRS promoting tumorigenic potential of OSCC cells, and the regulatory of ALDH3A1 on mitochondrial metabolism may be involved in this process.
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spelling doaj.art-62c2bddbad894578bce0095cbde584da2024-01-14T12:41:01ZengBMCBMC Oral Health1472-68312024-01-0124111310.1186/s12903-023-03787-1Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormoneShihong Luo0Huiqing Long1Fangzhi Lou2Yiyun Liu3Haiyang Wang4Juncai Pu5Ping Ji6Xin Jin7College of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityNHC Key Laboratory of Diagnosis and Treatment On Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical UniversityNHC Key Laboratory of Diagnosis and Treatment On Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical UniversityNHC Key Laboratory of Diagnosis and Treatment On Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityAbstract Background Chronic restraint stress (CRS) has iteratively been reported to be possibly implicated in the development of numerous cancer types. However, its role in oral squamous cell carcinoma (OSCC) has not been well elucidated. Here we intended to evaluate the role and mechanism. Methods The effects of CRS were investigated in xenograft models of OSCC by using transcriptome sequencing, LC–MS, ELISA and RT-PCR. Moreover, the role of CRS and ALDH3A1 on OSCC cells was researched by using Trans-well, flow cytometry, western blotting, immunofluorescence, ATP activity and OCR assay. Furthermore, immunohistochemical staining was employed to observe the cell proliferation and invasion of OSCC in xenotransplantation models. Results CRS promoted the progression of OSCC in xenograft models, stimulated the secretion of norepinephrine and the expression of ADRB2, but decreased the expression of ALDH3A1. Moreover, CRS changed energy metabolism and increased mitochondrial metabolism markers. However, ALDH3A1 overexpression suppressed proliferation, EMT and mitochondrial metabolism of OSCC cells. Conclusion Inhibition of ALDH3A1 expression plays a pivotal role in CRS promoting tumorigenic potential of OSCC cells, and the regulatory of ALDH3A1 on mitochondrial metabolism may be involved in this process.https://doi.org/10.1186/s12903-023-03787-1Chronic restraint stressALDH3A1HormoneOral squamous cell carcinomaMitochondrial metabolism
spellingShingle Shihong Luo
Huiqing Long
Fangzhi Lou
Yiyun Liu
Haiyang Wang
Juncai Pu
Ping Ji
Xin Jin
Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone
BMC Oral Health
Chronic restraint stress
ALDH3A1
Hormone
Oral squamous cell carcinoma
Mitochondrial metabolism
title Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone
title_full Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone
title_fullStr Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone
title_full_unstemmed Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone
title_short Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone
title_sort chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting aldh3a1 via stress response hormone
topic Chronic restraint stress
ALDH3A1
Hormone
Oral squamous cell carcinoma
Mitochondrial metabolism
url https://doi.org/10.1186/s12903-023-03787-1
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