Nanog siRNA plus Cisplatin may enhance the sensitivity of chemotherapy in esophageal cancer

Du, Yuchen; Shi, Lei‐Zhi; Wang, Tianyi; Liu, Zhiliang; Zhong-bin, Wang

doi:10.1007/s00432-012-1253-8

Cited by 23 publications

(18 citation statements)

References 27 publications

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“…Furthermore, a previous study reported that Nanog expression was associated with TNM stage and differentiation of ESCC [16]. The present study indicated that Nanog expression was associated with TRG, but not with clinical stage or OS.…”

Section: Discussionsupporting

confidence: 55%

A Retrospective Review of the Prognostic Value of ALDH-1, Bmi-1 and Nanog Stem Cell Markers in Esophageal Squamous Cell Carcinoma

et al. 2014

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Stem cell markers are upregulated in various cancers and have potential as prognostic indicators. The objective of this study was to determine the expression of three stem cell markers, aldehyde dehydrogenase 1 (ALDH-1), B cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1), and Nanog, in esophageal squamous cell carcinoma (ESCC) tissues. Immunohistochemistry was used to measure the expression of ALDH-1, Bmi-1, and Nanog in ESCC tissues from 41 patients who received pre-operative chemoradiation. We evaluated the relationship between expression of these markers, and clinicopathological features, tumor regression grade (TRG), and 5-year overall survival (OS). There were no significant associations of ALDH-1 or Bmi-1 expression with age, gender, clinical stage, and treatments (p>0.05). However, patients with Nanog-positive tumors were significantly older than those whose tumors were Nanog-negative (p = 0.033). TRG after treatment was significantly associated with expression of ALDH-1 (p = 0.001), Bmi-1 (p = 0.004), and Nanog (p<0.001). Although OS was significantly better in patients with low TRGs (p = 0.001), there were no significant correlations between ALDH-1, Bmi-1, or Nanog with OS. Expression of ALDH-1, Bmi-1, and Nanog correlated with TRG, but not OS. Further large studies are necessary to fully elucidate the prognostic value of these stem cell markers for ESCC patients.

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Section: Discussionsupporting

confidence: 55%

A Retrospective Review of the Prognostic Value of ALDH-1, Bmi-1 and Nanog Stem Cell Markers in Esophageal Squamous Cell Carcinoma

et al. 2014

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“…Given their almost identical protein sequence, currently available antibodies cannot distinguish between NANOG1 and NANOGP8 (the two proteins differ in two amino acids) and we refer to them collectively as NANOG. We focused on oesophageal squamous cell carcinomas (ESCCs) and head and neck squamous cell carcinomas (HNSCCs) for which there is evidence of NANOG expression [42][43][44] . We confirmed that NANOG expression is common in ESCCs (n ¼ 29) and HNSCCs (n ¼ 355), often with very intense and widespread staining, both in poorly differentiated and in well-differentiated carcinomas (Fig.…”

Section: Sa-2xpamentioning

confidence: 99%

“…Moreover, in the case of SOX2, which is expressed in adult stratified epithelia 18 , there is compelling evidence for its oncogenic role in human oesophageal squamous cell carcinomas (ESCCs) and mouse forestomach squamous cell carcinomas 19,54 . NANOG is also overexpressed in a number of human cancers, including ESCCs and head and neck squamous cells carcinomas (HNSCCs) 21,[42][43][44]53 . Importantly, we have found a positive association between NANOG and AURKA expression in HNSCCs, suggesting that AURKA is a target of NANOG both in normal stratified epithelia and in their derived cancers.…”

Section: A-ctr (Hi) A-ctr (Hi)mentioning

confidence: 99%

Lineage-restricted function of the pluripotency factor NANOG in stratified epithelia

et al. 2014

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NANOG is a pluripotency transcription factor in embryonic stem cells; however, its role in adult tissues remains largely unexplored. Here we show that mouse NANOG is selectively expressed in stratified epithelia, most notably in the oesophagus where the Nanog promoter is hypomethylated. Interestingly, inducible ubiquitous overexpression of NANOG in mice causes hyperplasia selectively in the oesophagus, in association with increased cell proliferation. NANOG transcriptionally activates the mitotic programme, including Aurora A kinase (Aurka), in stratified epithelia, and endogenous NANOG directly binds to the Aurka promoter in primary keratinocytes. Interestingly, overexpression of Nanog or Aurka in mice increased proliferation and aneuploidy in the oesophageal basal epithelium. Finally, inactivation of NANOG in cell lines from oesophageal or head and neck squamous cell carcinomas (ESCCs or HNSCCs, respectively) results in lower levels of AURKA and decreased proliferation, and NANOG and AURKA expression are positively correlated in HNSCCs. Together, these results indicate that NANOG has a lineage-restricted mitogenic function in stratified epithelia.

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“…Furthermore, BMI1 knockdown in oral [35], gastric [242], and colon [217] CSCs reduced their stemness and malignant properties. In addition, NANOG-siRNA transfection induced apoptosis and enhanced chemosensitivity of ESCC cells [106], similar to downregulation of SOX2 with siRNA, which reduced colony forming, drug resistance, and in vivo tumorigenicity of gastric CSCs [149]. Reports have also demonstrated that RNAi targeting LGR5 in CRC-SCs enhanced drug sensitivity of cells [202,204], while decreased their survival, proliferation [203][204][205], migration, and tumorigenic [205] abilities.…”

Section: Implications Of Cscs In Developing Targeted Therapies For DImentioning

confidence: 87%

“…In addition, BMI1 overexpression was correlated to advanced pathological stage and lymph node metastasis in ESCC and EAC [102,103]. Clinical studies have also revealed that EpCAM [95,104], ABCG2 [100], ALDH1 [96,105], NANOG [106], GLI1 [107,108], and CD24 [109] could be considered as CSC markers in ESCC, since their expression was associated with clinicopathological characteristics of tumors.…”

Section: Esophagusmentioning

confidence: 98%

Cancer stem cells in human digestive tract malignancies

2015

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Digestive tract malignancies, including oral, pharyngeal, esophageal, gastric, and colorectal cancers, are among the top 10 most common cancers worldwide. In spite of using various treatment modalities, cancer patients still suffer from recurrence and metastasis of malignant cells. Cancer stem cells (CSCs) are undifferentiated and highly proliferative malignant cells with unique properties mediated by overexpression of stemness markers, metastasis-related proteins, drug transporters, and DNA repair machinery. Due to their salient characteristics, it has been suggested that CSCs are responsible for tumor initiation, progression, invasion, recurrence, and therapy resistance. Exploring different aspects of CSC biology has fueled a great enthusiasm in designing novel therapeutic strategies to help patients. For instance, identification of markers associated with digestive tract CSCs, such as CD44, CD133, CD24, EpCAM, LGR5, ALDH1, and BMI1, has made it possible to develop more accurate diagnosis approaches. In addition, specifically targeting CSCs by their markers imposes fewer side effects and improves therapeutic outcomes. Here, we focus on the current status of CSC biology in digestive tract cancers, with emphasis on CSC markers, and review achieved progress in eradication of digestive tract CSC cells.

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Nanog siRNA plus Cisplatin may enhance the sensitivity of chemotherapy in esophageal cancer

Abstract: The present study's results suggest that detecting Nanog might be helpful for diagnosing ESCC, and Nanog siRNA combined with Cisplatin may be a feasible strategy to enhance the sensitivity of chemotherapy in patients with ESCC.

Cited by 23 publications

References 27 publications

A Retrospective Review of the Prognostic Value of ALDH-1, Bmi-1 and Nanog Stem Cell Markers in Esophageal Squamous Cell Carcinoma

A Retrospective Review of the Prognostic Value of ALDH-1, Bmi-1 and Nanog Stem Cell Markers in Esophageal Squamous Cell Carcinoma

Lineage-restricted function of the pluripotency factor NANOG in stratified epithelia

Cancer stem cells in human digestive tract malignancies

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