Abstract
The discovery of a small subset of cancer cells with self-renewal properties that can give rise to phenotypically diverse tumour populations has shifted our understanding of cancer biology. Targeting cancer stem cells (CSCs) is becoming a promising therapeutic strategy in various malignancies, including head and neck squamous cell carcinoma (HNSCC). Diverse sub-populations of head and neck cancer stem cells (HNCSCs) have been identified previously using CSC specific markers, the most common being CD44, Aldehyde Dehydrogenase 1 (ALDH1), and CD133, or by side population assays. Interestingly, distinct HNCSC subsets play different roles in the generation and progression of tumours. This article aims to review the evidence for a role of specific CSCs in HNSCC tumorigenesis, invasion, and metastasis, together with resistance to treatment.
Highlights
Head and neck squamous cell carcinoma (HNSCC) is a broad term that encompasses a variety of malignancies arising in the oral cavity, nasal cavity, paranasal sinuses, pharynx, and larynx [1]
The evidence for a role of cancer stem cells (CSCs) in metastasis has been reported in association with the enhanced invasion potential of CSCs compared to non-CSCs in HNSCCs, both in vitro [9,11,12,31,32] and in vivo [15,24,35]; interestingly, it has been reported that CSCs have a decreased ability to invade as assessed via the Matrigel Invasion Assay in vitro [36]
An increased expression of certain stemness markers such as Oct4, Sox2, and Nanog has been demonstrated in radio- and chemo-resistant HNSCC cells [40,41,42] and, the CSC-like signature CD44 has been reported to be significantly correlated with an incomplete response to radio- and chemotherapy in patients with locally advanced HNSCC [43]
Summary
Head and neck squamous cell carcinoma (HNSCC) is a broad term that encompasses a variety of malignancies arising in the oral cavity, nasal cavity, paranasal sinuses, pharynx, and larynx [1]. HNSCC is a growing global burden and is the sixth most common type of cancer worldwide [1]. Cancer research in the 20th century has been dominated by the stochastic model of carcinogenesis, which proposes that all the cells in the tumour population have an equal potential in acquiring and accumulating genetic and/or epigenetic mutations in critical genes that control cell growth and differentiation. This results in the generation and selection of clone(s) with proliferative advantages, which eventually acquire the ability to invade surrounding tissues [4,5]. This article aims to review the role of CSC heterogeneity—as defined by the expression of a specific phenotype—in tumorigenesis, metastasis, and the radio-, chemo-, and immune resistance of HNSCC
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call