Cancer stem cell-like cells from a single cell of oral squamous carcinoma cell lines

Felthaus, Oliver; Ettl, Tobias; Gosau, Martin; Driemel, Oliver; Brockhoff, Gero; Reck, Anja; Zeitler, Katharina; Hautmann, Matthias G.; Reichert, Torsten E.; Schmalz, Gottfried; Morsczeck, Christian

doi:10.1016/j.bbrc.2011.02.084

Cited by 53 publications

(42 citation statements)

References 24 publications

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“…To date, there is no effective treatment for patients with local relapse and distant metastasis. It remains a highly lethal and disfiguring disease [1, 28]. Recent studies showed that the resistance of OSCC to conventional chemotherapy or radiation therapy might be due to the presence of CSC [28].…”

Section: Discussionmentioning

confidence: 99%

Honokiol Eliminates Human Oral Cancer Stem-Like Cells Accompanied with Suppression of Wnt/β-Catenin Signaling and Apoptosis Induction

Yao

Lai

Yeh

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Honokiol, an active compound of Magnolia officinalis, exerted many anticancer effects on various types of cancer cells. We explored its effects on the elimination of cancer stem-like side population (SP) cells in human oral squamous cell carcinoma SAS cells. The sorted SP cells possessed much higher expression of stemness genes, such as ABCG2, ABCC5, EpCAM, OCT-4, CD133, CD44, and β-catenin, and more clonogenicity as compared with the Non-SP cells. After 48 h of treatment, honokiol dose dependently reduced the proportion of SP from 2.53% to 0.09%. Apoptosis of honokiol-treated SP cells was evidenced by increased annexin V staining and cleaved caspase-3 as well as decreased Survivin and Bcl-2. Mechanistically, honokiol inhibited the CD44 and Wnt/β-catenin signaling of SP cells. The Wnt signaling transducers such as β-catenin and TCF-4 were decreased in honokiol-treated SP cells, while the β-catenin degradation promoting kinase GSK-3α/β was increased. Consistently, the protein levels of β-catenin downstream targets such as c-Myc and Cyclin D1 were also downregulated. Furthermore, the β-catenin-related EMT markers such as Slug and Snail were markedly suppressed by honokiol. Our findings indicate honokiol may be able to eliminate oral cancer stem cells through apoptosis induction, suppression of Wnt/β-catenin signaling, and inhibition of EMT.

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Section: Discussionmentioning

confidence: 99%

Honokiol Eliminates Human Oral Cancer Stem-Like Cells Accompanied with Suppression of Wnt/β-Catenin Signaling and Apoptosis Induction

Yao

Lai

Yeh

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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show abstract

“…In addition, CD44, 15 GNL3L/ nucleostemin, 16 and YBX1 17 showed higher average expression in tumors. By contrast, EpCAM, CD133 (Prominin 1), 18 and SHH expression levels showed great variability among individual cases. These molecules are expressed in tumor regions at relatively high mean levels; however, the stemness molecule expression pattern did not show a similar tendency among the cases.…”

Section: Discussionmentioning

confidence: 90%

Stem cell self-renewal factors Bmi1 and HMGA2 in head and neck squamous cell carcinoma: clues for diagnosis

Yamazaki

Mori

Yazawa

et al. 2013

Laboratory Investigation

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Head and neck squamous cell carcinoma (HNSCC) includes both morphological and functional cellular heterogeneity, as would be expected if it arose from dysregulated stem or progenitor cells as opposed to the simple clonal expansion of a mutated cell; however, stemness molecule expression levels and distribution in HNSCC remain unclear. To clarify this, stemness molecule expressions were determined in HNSCC, as well as their properties and prognosis. Two protooncogenic chromatin regulators, Bmi-1 and high-mobility-group A2 (Hmga2), were identified in 12 pair cases of HNSCC tumor regions by comparison with their non-cancerous background tissues using cDNA microarray. Both Bmi-1 and Hmga2 are known to promote stem cell self-renewal by negatively regulating the expressions of Ink4a and Arf tumor suppressors. Despite similar targets, Bmi-1 protein was expressed in an early cancerous region and HMGA2 protein was expressed in a region showing more progression. Similarly, Bmi1 expression had no significance with regard to overall survival (P ¼ 0.67), whereas HMGA2 expression was associated with decreased overall survival (P ¼ 0.05). Quantitative realtime reverse transcription polymerase chain reaction analyses also correlated with protein levels. These findings suggest that Bmi-1 is an early detection marker to distinguish cancerous from non-cancerous regions, whereas HMGA2 is presumed to be a tumor prognosis marker. Among our HNSCC analyses, these stemness molecules expressed fewer primitive rare cells in the tumor than all other cells in the tumor. HNSCC cells with high expression of stemness molecules partly behave like stem cells. Head and neck squamous cell carcinoma (HNSCC) is typically associated with virus infection, persistent chronic inflammation, and tobacco and alcohol use. Survival rates have changed in the last 40 years because of reductions in these factors; 1 however, the mortality rate remains high because advanced and recurrent locoregional control is difficult in many cases. Better understanding of the biology of HNSCC is required to define relevant targets and to develop novel therapeutic approaches. HNSCCs have both morphological and functional cellular heterogeneity, as would be expected if they arose from dysregulated stem or progenitor cells as opposed to the simple clonal expansion of a mutated cell. 2 Recently, numerous reports have shown support for the 'cancer stem cell' theory in many types of tumor, including HNSCC. 3,4,5 Acute and chronic myeloid leukemias follow the cancer stem cell model. Both tumors show robustly hematopoietic hierarchical organization in the tumor cells; 6,7 however, for solid cancers such as squamous cell carcinoma, it is not clear how generalizable the cancer stem cell model is. Not all cancer cells have the same capacity to proliferate. 8 In some cancers, most cancer cells appear to have limited ability to proliferate, while in the same tumors, stochastic minority populations of stemness molecules highly expressed in cancer as a 'stem-like cancer' retain the capacity...

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“…Accumulating evidence has shown that CSCs may not only originate from the transformation of normal stem cells but also arise from the dedifferentiation of cancer cells (22). An impressive observation has shown that CSCs exist in single cancer cell-derived cultures, which reveals the flexibility of the cancer cell status in tumors due to genomic instability in cancer cells (23,24). In addition, the dedifferentiation of cancer cells can be induced by different environmental cues, such as inflammation, hypoxia, and serum deprivation, through epigenetic or genetic regulation (25).…”

Section: Discussionmentioning

confidence: 99%

Cisplatin Selects for Multidrug-Resistant CD133+ Cells in Lung Adenocarcinoma by Activating Notch Signaling

et al. 2013

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Platinum-based chemotherapy is the first-line treatment for non-small cell lung cancer, but recurrence occurs in most patients. Recent evidence suggests that CD133 þ cells are the cause of drug resistance and tumor recurrence. However, the correlation between chemotherapy and regulation of CD133 þ cells has not been investigated methodically. In this study, we revealed that CD133 þ lung cancer cells labeled by a human CD133

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Cancer stem cell-like cells from a single cell of oral squamous carcinoma cell lines

Cited by 53 publications

References 24 publications

Honokiol Eliminates Human Oral Cancer Stem-Like Cells Accompanied with Suppression of Wnt/β-Catenin Signaling and Apoptosis Induction

Honokiol Eliminates Human Oral Cancer Stem-Like Cells Accompanied with Suppression of Wnt/β-Catenin Signaling and Apoptosis Induction

Stem cell self-renewal factors Bmi1 and HMGA2 in head and neck squamous cell carcinoma: clues for diagnosis

Cisplatin Selects for Multidrug-Resistant CD133+ Cells in Lung Adenocarcinoma by Activating Notch Signaling

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