Abstract

Cancer stem cells (CSCs) have been identified as a little population of cancer cells, which have features as the same as the cells normal stem cells. There is enough knowledge of the CSCs responsibility for metastasis, medicine resistance, and cancer outbreak. Therefore, CSCs control possibly provides an efficient treatment intervention inhibiting tumor growth and invasion. In spite of the significance of targeting CSCs in treating cancer, few study comprehensively explored the nature of oral CSCs. It has been showed that oral CSCs are able to contribute to oral cancer progression though activation/inhibition a sequences of cellular and molecular pathways (microRNA network, histone modifications and calcium regulation). Hence, more understanding about the properties of oral cancers and their behaviors will help us to develop new therapeutic platforms. Head and neck CSCs remain a viable and intriguing option for targeted therapy. Multiple investigations suggested the major contribution of the CSCs to the metastasis, tumorigenesis, and resistance to the new therapeutic regimes. Therefore, experts in the field are examining the encouraging targeted therapeutic choices. In spite of the advancements, there are not enough information in this area and thus a magic bullet for targeting and eliminating the CSCs deviated us. Hence, additional investigations on the combined therapies against the head and neck CSCs could offer considerable achievements. The present research is a review of the recent information on oral CSCs, and focused on current advancements in new signaling pathways contributed to their stemness regulation. Moreover, we highlighted various therapeutic approaches against oral CSCs.

Highlights

  • It is widely accepted that the head and neck cancers involve above 650,000 people and 330,000 mortality each year throughout the world [1]

  • If chemotherapy and radiation treatment are combined, even though they affect the treatment of 97% of the initial-phase tumors, they just 33% affect the treatment of the advanced tumors [23]

  • Researchers demonstrated possible significant inhibition of malignant Cancer stem cells (CSCs) features or BMI1 knock-down by upregulating the miR-200c could so that ZEB1 or ZEB2 knockdown may enhance the miR-200c and suppress the BMI1 expressions in the ­Aldehyde dehydrogenase1 (ALDH1)+/CD44+ Head and neck squamous cell carcinoma (HNSCC) cells, which revealed that interactions between ZEB1/ ZEB2, BMI1, and miR-200c detected the fate of the cancer stemness in Oral squamous cell carcinoma (OSCC)

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Summary

Introduction

It is widely accepted that the head and neck cancers involve above 650,000 people and 330,000 mortality each year throughout the world [1]. Researchers demonstrated possible significant inhibition of malignant CSC features or BMI1 knock-down by upregulating the miR-200c could so that ZEB1 or ZEB2 knockdown may enhance the miR-200c and suppress the BMI1 expressions in the ­ALDH1+/CD44+ HNSCC cells, which revealed that interactions between ZEB1/ ZEB2, BMI1, and miR-200c detected the fate of the cancer stemness in OSCC. ­Ca2+ oscillation is the final outcome of Orai1mediated SOCE so that Orai would be improved in OCSCs. As suppressing Orai channel performance led to the complete shut-down of ­Ca2+ oscillation in OSCC cells, Orai1-mediated ­Ca2+ oscillation might be a potent selective target to treat oral CSCs. Other mechanisms From among the above pathways, researchers largely confirmed contribution Bmi and Notch signaling in oral cancer stemness. One of the studies on the bacterial toxin (cyto-lethal distending toxin) to an antihuman CD133 monoclonal antibody revealed inhibiting the cells proliferation while other investigation, which utilized a single-chain variable fragment targeting CD133 demonstrated remarkable diminishment in the rapid growth of the tumors in the cells and rat models [221,

Conclusion
Findings
71. Amsterdam
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