Cargando…

SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) are one of the most common types of head and neck cancer, and it is urgent to find effective treatment for advanced patients. Exploring developing and progressing mechanisms of HNSCC could provide a theoretical basis to find new therapeutic t...

Descripción completa

Detalles Bibliográficos
Autores principales: Fu, You, Tian, Guocai, Zhang, Zhiyuan, Yang, Xiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8691088/
https://www.ncbi.nlm.nih.gov/pubmed/34930262
http://dx.doi.org/10.1186/s12935-021-02394-w
_version_ 1784618739964051456
author Fu, You
Tian, Guocai
Zhang, Zhiyuan
Yang, Xiao
author_facet Fu, You
Tian, Guocai
Zhang, Zhiyuan
Yang, Xiao
author_sort Fu, You
collection PubMed
description BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) are one of the most common types of head and neck cancer, and it is urgent to find effective treatment for advanced patients. Exploring developing and progressing mechanisms of HNSCC could provide a theoretical basis to find new therapeutic targets. METHODS: In our research, we performed a whole-gene expression profile microarray analysis to identify differential expression genes between squamous cell carcinoma cells and ΔNp63 alpha (ΔNp63α) knockdown cells. As a result, an important gene Synaptotagmin VII (SYT7) was screened out. RESULTS: SYT7 knockdown affected the proliferation, apoptosis and cell cycle of squamous cell carcinoma cells. The rescue experiment in vitro with ΔNp63α and SYT7 double knockdown resulted in partial reversion of ΔNp63α-induced phenotypes. This was also confirmed by experiments in vivo. CONCLUSIONS: Taken together, we found that ΔNp63α could inhibit the occurrence and progression of HNSCC throughout downregulating the expression of SYT7. Therefore, SYT7/ΔNp63α axis could be a potential therapeutic target for clinical treatment of HNSCC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-021-02394-w.
format Online
Article
Text
id pubmed-8691088
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-86910882021-12-23 SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC Fu, You Tian, Guocai Zhang, Zhiyuan Yang, Xiao Cancer Cell Int Primary Research BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) are one of the most common types of head and neck cancer, and it is urgent to find effective treatment for advanced patients. Exploring developing and progressing mechanisms of HNSCC could provide a theoretical basis to find new therapeutic targets. METHODS: In our research, we performed a whole-gene expression profile microarray analysis to identify differential expression genes between squamous cell carcinoma cells and ΔNp63 alpha (ΔNp63α) knockdown cells. As a result, an important gene Synaptotagmin VII (SYT7) was screened out. RESULTS: SYT7 knockdown affected the proliferation, apoptosis and cell cycle of squamous cell carcinoma cells. The rescue experiment in vitro with ΔNp63α and SYT7 double knockdown resulted in partial reversion of ΔNp63α-induced phenotypes. This was also confirmed by experiments in vivo. CONCLUSIONS: Taken together, we found that ΔNp63α could inhibit the occurrence and progression of HNSCC throughout downregulating the expression of SYT7. Therefore, SYT7/ΔNp63α axis could be a potential therapeutic target for clinical treatment of HNSCC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-021-02394-w. BioMed Central 2021-12-20 /pmc/articles/PMC8691088/ /pubmed/34930262 http://dx.doi.org/10.1186/s12935-021-02394-w Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Primary Research
Fu, You
Tian, Guocai
Zhang, Zhiyuan
Yang, Xiao
SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
title SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
title_full SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
title_fullStr SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
title_full_unstemmed SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
title_short SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
title_sort syt7 acts as an oncogene and a potential therapeutic target and was regulated by δnp63α in hnscc
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8691088/
https://www.ncbi.nlm.nih.gov/pubmed/34930262
http://dx.doi.org/10.1186/s12935-021-02394-w
work_keys_str_mv AT fuyou syt7actsasanoncogeneandapotentialtherapeutictargetandwasregulatedbydnp63ainhnscc
AT tianguocai syt7actsasanoncogeneandapotentialtherapeutictargetandwasregulatedbydnp63ainhnscc
AT zhangzhiyuan syt7actsasanoncogeneandapotentialtherapeutictargetandwasregulatedbydnp63ainhnscc
AT yangxiao syt7actsasanoncogeneandapotentialtherapeutictargetandwasregulatedbydnp63ainhnscc