BMI1'S maintenance of the proliferative capacity of laryngeal cancer stem cells

Chen, Hui; Zhou, Liang; Dou, Tonghai; Wan, Guanghua; Tang, Hui-Qing; Tian, Jie

doi:10.1002/hed.21576

Cited by 42 publications

(40 citation statements)

References 39 publications

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“…36 Prior studies showed that CD44 and CD133 had been used to isolate CSCs from multiple tumor types. 21,[37][38][39] However, in the present study, both of the cell lines presented as CD44 high , and showed only 0.53% of the SCC9-S cells expressed CD133, in contrast to 0.06% of the SCC9-N cells. With these findings in mind, a 'stemness' marker that works well in one cancer may not apply to other types of cancers.…”

Section: Discussioncontrasting

confidence: 44%

Snail overexpression induces an epithelial to mesenchymal transition and cancer stem cell-like properties in SCC9 cells

Zhu

Yang

et al. 2012

Laboratory Investigation

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Local invasiveness and distant metastasis are critical factors that contribute to oral squamous cell carcinoma-related deaths. Increasing evidence has shown that the epithelial to mesenchymal transition (EMT) is involved in cancer progression and is associated with the 'stemness' of cancer cells. Snail is a transcriptional factor that can induce EMT and preserve stem-cell function, which may induce resistance to radio-and chemotherapies in the cells. In the present study, SCC9 cells were transfected with an empty vector or a vector encoding human Snail (SCC9-S). Overexpression of Snail induced SCC9 cells to undergo EMT, in which the cells presented a fibroblast-like appearance, downregulated the epithelial markers E-cadherin and b-catenin, upregulated the mesenchymal marker vimentin, and associated with highly invasive and metastatic properties. Furthermore, the induction of EMT promoted cancer stem cell (CSC)-like characteristics in the SCC9-S cells, such as low proliferation, self-renewal, and CSC-like markers expression. These results indicate that overexpression of Snail induces EMT and promotes CSC-like traits in the SCC9 cells. Further understanding the role of Snail in cancer progression may reveal new targets for the prevention or therapy of oral cancers. Oral squamous cell carcinoma (OSCC) is the most frequent type of cancer in the oral cavity and is associated with high morbidity and poor prognosis. 1,2 Despite progress in surgery, chemotherapy, and radiotherapy, the 5-year survival rate has remained at 50-55% over the past several decades. 3 Local or regional recurrences and distant metastases have a critical role in this process, and the mechanism underlying their occurrence remains poorly understood. 2,4 During metastatic progression, tumour cells lose cell-cell adhesion, detach from the primary site, invade the basement membrane, survive and circulate in the blood vessels, leave the bloodstream, and finally colonise in a new host environment to form micrometastases. 2,5-7 A growing body of research strongly suggests that the epithelial to mesenchymal transition (EMT), which occurs normally during embryonic development, tissue remodelling, and wound healing, is a critical early event in tumour invasion and metastasis. [8][9][10] It is characterised by downregulation of epithelial markers, such as E-cadherin, and upregulation of mesenchymal markers, such as vimentin. During the process of EMT, epithelial cells acquire mesenchymal cell properties and show reduced intercellular adhesion and increased invasion. 11 The transcriptional repressor Snail, which is a zinc finger protein, first described in Drosophila melanogaster, can bind to the E-boxes in the human E-cadherin promoter and suppress its transcription. 12,13 Snail has previously been implicated in triggering EMT during embryonic development, fibrosis, and tumour progression. 14 This process also occurs in the progression of carcinomas (including oral carcinoma cells), following the downregulation of E-cadherin expression or co-expression of NB...

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Section: Discussioncontrasting

confidence: 44%

Snail overexpression induces an epithelial to mesenchymal transition and cancer stem cell-like properties in SCC9 cells

Zhu

Yang

et al. 2012

Laboratory Investigation

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“…Its knockdown resulted in inhibition of in vitro proliferative, clonogenic, invasive capacity, and in vivo tumorigenic potential of CD133+ cells through up-regulation of p16(INK4A) and p14(ARF) [57]. More importantly, BMI1 expression was demonstrated to be co-localized with CD133 in LCa specimens [52,58]. These findings suggested BMI1 as a molecular target to treat patients with LCa.…”

Section: Bmi1mentioning

confidence: 87%

“…As an initial study, Yu et al [55] demonstrated significant overexpression of oncogenic BMI1 protein,which involves in gene silencing, through chromatin modifications [55], in CD44+/CD133+ cells [34]. It was reported to be upregulated in laryngeal tumor tissue samples and CD133 positive Hep-2 cells, which provided maintenance of cell proliferation and prevented apoptosis [52,56]. Its knockdown resulted in inhibition of in vitro proliferative, clonogenic, invasive capacity, and in vivo tumorigenic potential of CD133+ cells through up-regulation of p16(INK4A) and p14(ARF) [57].…”

Section: Bmi1mentioning

confidence: 99%

See 1 more Smart Citation

Current cancer stem cell biomarkers in laryngeal cancer

Karataş¹,

Barlak²,

Şahin³

2017

The European Research Journal

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Larynx cancer (LCa), being an aggressive malignancy, is the second most commonly diagnosed malignant type of head and neck squamous cell carcinoma worldwide. Although there have been significant improvements in the detection and diagnosis of LCa in the last decades, it is still one of the considerable causes of cancer deaths and an urgent need for identification of novel biomarkers with diagnostic and prognostic significance still remains. The cancer stem cells (CSCs) resemble normal stem cells in terms of biological features and are considered to play critical roles in biological aggressiveness of tumors. Accumulating evidences have proven the existence of CSCs in various tumors including LCa and they are considered as driving force for tumor relapse, metastasis, and chemo-radioresistance. Comprehensive identification and characterization of the CSCs is of paramount importance for their further characterization to develop more effective and targeted therapeutic strategies against cancer. Here, we reviewed and summarized the most current literature to provide an insight into the functions and roles of current CSCs biomarkers in human LCa. We believe that this review will contribute to the knowledge of scientists especially working with LCa CSCs and will help understanding the significance of CSCs biomarkers implicated in LCa pathogenesis.

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“…Higher levels of CD133, have been associated with CD44+ expression in HNSCC and with Bmi1 induced proliferation in laryngeal carcinomas (Zhang et al, 2010;Chen et al, 2011;Sun et al, 2012). In fact, positive correlation of Oct-4, Nanog with an increased expression status of CD133 depicted a poorer prognosis for oral cancer patients (Chiou et al, 2008).…”

Section: Cd133mentioning

confidence: 98%