Related Experiment Video

Updated: Dec 1, 2025

Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics
11:28

Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics

Published on: May 11, 2016

8.8K

TSPAN1: A Novel Protein Involved in Head and Neck Squamous Cell Carcinoma Chemoresistance

Yoelsis Garcia-Mayea1,2, Cristina Mir1, Laia Carballo1

  • 1Biomedical Research in Cancer Stem Cells, Vall d'Hebron Research Institute (VHIR), Autonomous University of Barcelona, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.

Cancers
|November 10, 2020
PubMed

Insights

Tetraspanin-1 (TSPAN1) drives resistance to chemotherapy and metastasis in head and neck cancer. Inhibiting TSPAN1 resensitizes tumors to cisplatin and reduces cancer spread, offering a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Chemotherapy resistance and cancer stem cells (CSCs) pose significant challenges in cancer treatment.
  • Tetraspanin-1 (TSPAN1) has been identified as a potential factor in the development of drug resistance.

Purpose of the Study:

  • To investigate the role of TSPAN1 in cisplatin resistance, cancer stem cell biology, and head and neck squamous cell carcinoma (HNSCC) progression.
  • To evaluate TSPAN1 as a potential therapeutic target for HNSCC.

Main Methods:

  • Proteomic analysis to identify proteins involved in cisplatin resistance.
  • TSPAN1 depletion in HNSCC cell lines and in vivo models.
  • Assessment of proliferation, apoptosis, autophagy, and signaling pathways.
  • Immunohistochemical analysis of HNSCC patient samples.

Main Results:

  • TSPAN1 expression is elevated in cisplatin-resistant cells, CSCs, and HNSCC tumors.
  • TSPAN1 depletion reduces proliferation, induces apoptosis, inhibits autophagy, and sensitizes cells to chemotherapy.
  • TSPAN1 inhibition decreases tumor growth, proliferation, and metastasis in vivo.
  • TSPAN1 is linked to epithelial-mesenchymal transition (EMT) and phospho-SRC activation.

Conclusions:

  • TSPAN1 is an oncogenic protein promoting cisplatin resistance, EMT, and metastasis in HNSCC.
  • Targeting TSPAN1 represents a promising therapeutic strategy for HNSCC treatment.
Keywords:
HNSCCapoptosisautophagycancercancer stem cellsresistance

More Related Videos

Therapy Testing in a Spheroid-based 3D Cell Culture Model for Head and Neck Squamous Cell Carcinoma06:11

Therapy Testing in a Spheroid-based 3D Cell Culture Model for Head and Neck Squamous Cell Carcinoma

Published on: April 20, 2018

10.1K
Three-Dimensional 3D Tumor Spheroid Invasion Assay12:19

Three-Dimensional 3D Tumor Spheroid Invasion Assay

Published on: May 1, 2015

58.8K

Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.5K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
5.5K
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...
8.2K
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...
4.9K
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...
5.6K
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...
8.8K