Cancer stem cell self-renewal as a therapeutic target in human oral cancer

Hu, Jinwei; Mirshahidi, Saied; Simental, Alfred; Lee, Steve C.; Filho, Pedro Andrade; Peterson, Nathaniel R.; Duerksen-Hughes, Penelope J.; Yuan, Xiangpeng

doi:10.1038/s41388-019-0800-z

Cited by 46 publications

(51 citation statements)

References 52 publications

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“…BMI1 was able to suppress the ability of oral CSCs to form cell spheres in vitro, and a BMI1 inhibitor could arrest the progression of xenograft tumours in association with a reduced proportion of CSCs. 156 All these results suggest that strategies targeting CSC self-renewal, such as BMI1 inhibition, have great potential to be combined with radiotherapy in oral cancer for better prognosis.…”

Section: Potential Therapeutics Targeting Cscs In Oral Cancermentioning

confidence: 98%

Radiotherapy targeting cancer stem cells “awakens” them to induce tumour relapse and metastasis in oral cancer

et al. 2020

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Radiotherapy is one of the most common treatments for oral cancer. However, in the clinic, recurrence and metastasis of oral cancer occur after radiotherapy, and the underlying mechanism remains unclear. Cancer stem cells (CSCs), considered the "seeds" of cancer, have been confirmed to be in a quiescent state in most established tumours, with their innate radioresistance helping them survive more easily when exposed to radiation than differentiated cancer cells. There is increasing evidence that CSCs play an important role in recurrence and metastasis post-radiotherapy in many cancers. However, little is known about how oral CSCs cause tumour recurrence and metastasis post-radiotherapy. In this review article, we will first summarise methods for the identification of oral CSCs and then focus on the characteristics of a CSC subpopulation induced by radiation, hereafter referred to as "awakened" CSCs, to highlight their response to radiotherapy and potential role in tumour recurrence and metastasis post-radiotherapy as well as potential therapeutics targeting CSCs. In addition, we explore potential therapeutic strategies targeting these "awakened" CSCs to solve the serious clinical challenges of recurrence and metastasis in oral cancer after radiotherapy.

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Section: Potential Therapeutics Targeting Cscs In Oral Cancermentioning

confidence: 98%

Radiotherapy targeting cancer stem cells “awakens” them to induce tumour relapse and metastasis in oral cancer

et al. 2020

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“…It is proposed that the existence of this small but aggressive cell population possesses a high risk of drug resistance and tumor relapse [39,40]. The CSC hypothesis posits that tumors mirror the hierarchy as normal tissues and that the CSCs are located at the apex of this hierarchical organization [41,42]. With the elevated capacity of persistent proliferation, CSCs undergo asymmetric division, leading to complicated tumor heterogeneity and resistance to chemotherapy [43].…”

Section: Emergingmentioning

confidence: 99%

mRNA modification orchestrates cancer stem cell fate decisions

Liang

Lin

et al. 2020

Mol Cancer

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Despite their small numbers, cancer stem cells play a central role in driving cancer cell growth, chemotherapeutic resistance, and distal metastasis. Previous studies mainly focused on how DNA or histone modification determines cell fate in cancer. However, it is still largely unknown how RNA modifications orchestrate cancer cell fate decisions. More than 170 distinct RNA modifications have been identified in the RNA world, while only a few RNA base modifications have been found in mRNA. Growing evidence indicates that three mRNA modifications, inosine, 5methylcytosine, and N 6 -methyladenosine, are essential for the regulation of spatiotemporal gene expression during cancer stem cell fate transition. Furthermore, transcriptome-wide mapping has found that the aberrant deposition of mRNA modification, which can disrupt the gene regulatory network and lead to uncontrollable cancer cell growth, is widespread across different cancers. In this review, we try to summarize the recent advances of these three mRNA modifications in maintaining the stemness of cancer stem cells and discuss the underlying molecular mechanisms, which will shed light on the development of novel therapeutic approaches for eradicating cancer stem cells.

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“…BMI1 + CSCs were required for 4‐NQO‐induced OSCC invasive progression and metastasis (Chen et al, ). OSCC exhibited enhanced BMI1 (Hu et al, ), and BMI1 inactivation may retard cell replication in a CDKN2‐independent manner (Kang et al, ). Conflicting correlation between lower BMI1 and higher recurrence was reported as well (Hayry et al, ).…”

Section: Histone Modifications In Osccmentioning

confidence: 99%

“…PTC‐209 reduces BMI1 expression thorough ubiquitin‐proteasomal degradation, decreases PRC1 activity and global ubiquitinated H2A, and impairs tumor growth. PTC‐209 exposure facilitated cell apoptosis, negatively regulated cell cycle progression, cell proliferation, and migration/invasiveness, and suppressed CSCs signatures, including tumorsphere formation, ALDH1 + subpopulation, and colony‐forming ability (Hu et al, ; Wang, Li, et al, ). Inhibitory effects of PTC‐209 in OSCC xenograft models were also noted (Hu et al, ; Wang, Li, et al, ).…”

Section: Histone Modifications As Therapeutic Targetsmentioning

confidence: 99%

“…PTC‐209 exposure increased chemosensitivity to CDDP (Chen et al, ; Hu et al, ; Wang, Li, et al, ) and 5‐FU (Wang, Li, et al, ). PTC‐209 plus CDDP impaired proliferating tumor cells, eradiated metastatic BMI1‐positive CSCs, and had stronger inhibitory effect on 4NQO induced OSCC tumorigenesis and invasiveness (Chen et al, ).…”

Section: Combined Treatment Of Epigenetic Regulators and Other Cancermentioning

confidence: 99%

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Histone modifications in oral squamous cell carcinoma and oral potentially malignant disorders

et al. 2019

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Oral squamous cell carcinoma (OSCC) is a common malignancy with dismal prognosis without effective therapeutic options in advanced cases. The evolution from oral potentially malignant disorders to OSCC has poorly described underlying epigenetic features. With the ability of silencing or activation of vital genes, histone modifications’ and modifiers’ potentiality for early diagnosis, prognosis predicting, and therapy in OSCC were evaluated by extensive epigenetic studies. This review investigates the roles of dysregulated histone modifications and the associated modifying enzymes in OSCC onset and progression. Also, we focus on the current advances of histone modifications as therapeutic targets and the potential value of epi‐drugs.

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Cancer stem cell self-renewal as a therapeutic target in human oral cancer

Cited by 46 publications

References 52 publications

Radiotherapy targeting cancer stem cells “awakens” them to induce tumour relapse and metastasis in oral cancer

Radiotherapy targeting cancer stem cells “awakens” them to induce tumour relapse and metastasis in oral cancer

mRNA modification orchestrates cancer stem cell fate decisions

Histone modifications in oral squamous cell carcinoma and oral potentially malignant disorders

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