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

You Fu1,2, Guocai Tian1,2, Zhiyuan Zhang3,4

  • 1Department of Oral and Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Jiao Tong University, 639 Zhizaoju Road, Shanghai, 200011, People's Republic of China.

Cancer Cell International
|December 21, 2021
PubMed
Abstract

Insights

Head and neck squamous cell carcinoma (HNSCC) progression is linked to Synaptotagmin VII (SYT7) expression. Targeting the SYT7/ΔNp63α axis offers a potential new therapy for HNSCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Head and neck squamous cell carcinoma (HNSCC) is a prevalent cancer requiring novel treatments for advanced stages.
  • Understanding HNSCC development mechanisms is crucial for identifying new therapeutic targets.

Purpose of the Study:

  • To investigate the role of Synaptotagmin VII (SYT7) in HNSCC progression.
  • To explore the relationship between ΔNp63 alpha (ΔNp63α) and SYT7 in HNSCC.

Main Methods:

  • Whole-gene expression profile microarray analysis was conducted to identify differentially expressed genes.
  • Gene knockdown experiments (ΔNp63α and SYT7) were performed in vitro and in vivo.

Main Results:

  • Synaptotagmin VII (SYT7) was identified as a key gene differentially expressed in HNSCC cells.
  • SYT7 knockdown significantly impacted HNSCC cell proliferation, apoptosis, and cell cycle.
  • Rescue experiments demonstrated that SYT7 downregulation partially reversed ΔNp63α-induced HNSCC phenotypes.

Conclusions:

  • ΔNp63α inhibits HNSCC occurrence and progression by downregulating SYT7 expression.
  • The SYT7/ΔNp63α axis represents a promising therapeutic target for HNSCC clinical treatment.

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.7K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.9K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.3K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.2K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
9.3K
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
5.5K