Clinical and biological significance of stem-like CD133+CXCR4+ cells in esophageal squamous cell carcinoma

Chen, Lu; Xu, Fan; Gu, Jie; Yuan, Yunfeng; Zhao, Guochao; Yu, Xiaofang

doi:10.1016/j.jtcvs.2015.05.030

Cited by 37 publications

(31 citation statements)

References 23 publications

(40 reference statements)

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“…Then, EIF3B antibody (Abcam, Cambridge, UK) was used to detect the expression of the related protein. Based on the measurement standard described previously [22], all cases were separated into two groups: a low expression level group for scores 0 and 1, and a high expression level group for scores 2 and 3.…”

Section: Methodsmentioning

confidence: 99%

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Eukaryotic translation initiation factor 3B accelerates the progression of esophageal squamous cell carcinoma by activating β-catenin signaling pathway

et al. 2016

Oncotarget

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IntroductionEsophageal squamous cell carcinoma (ESCC) is one of the most aggressive malignant tumors. Eukaryotic translation initiation factors 3B (EIF3B) is considered to influence tumor proliferation, invasion, apoptosis and cell cycle, which act together to promote the progression of tumors. However, the role of EIF3B in ESCC is unknown. This study aims to explore the clinical and biological role of EIF3B in ESCC.ResultsEIF3B expressions were up-regulated in both ESCC tissues and cell lines. Overexpression of EIF3B was associated with tumor depth, lymph node metastasis and advanced TNM stage. Importantly, patients with high EIF3B expression suffered shorter overall and disease-free survival. Knockdown of EIF3B could inhibit cell proliferation and invasion, promote cell apoptosis, and interfere the cell cycle in vitro. EIF3B-knockdown cells could form smaller subcutaneous tumors in vivo. Finally, we demonstrated EIF3B could activate β-catenin signaling pathway.MethodsImmunohistochemical staining and Western blot were performed to detect the EIF3B expression in ESCC patient tissues and cell lines. The association between EIF3B expression and patients’ prognosis was analyzed by Kaplan-Meier and Cox regression. Then, CCK-8, colony-formation, Transwell and wound-healing assay were performed to compare the bio-functional change after knockdown of EIF3B. Flow cytometry was applied to analyze the change of cell apoptosis and cycle induced by EIF3B knockdown. Tumor xenograft assay was done to verify the in-vitro results.ConclusionsEIF3B might serve as a novel marker for predicting prognosis of ESCC patients and as a potential therapeutic target, individually or together with other subunits of EIF3 complex.

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Section: Methodsmentioning

confidence: 99%

“…The process was applied as previously described [22]. For wound healing assay, 6-well plates were chosen for healing assay.…”

Section: Methodsmentioning

confidence: 99%

Eukaryotic translation initiation factor 3B accelerates the progression of esophageal squamous cell carcinoma by activating β-catenin signaling pathway

et al. 2016

Oncotarget

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“…Evidences including the important role of CXCL12/CXCR4 in tumor invasion and metastasis [12–13] and its strong correlation with the poor prognosis in patients with esophageal cancer [12–14] have been reported in literature. Therefore, in order to clarify the role of CXCL12/CXCR4 in the invasion and metastasis of ECSCs, we added a CXCR4 inhibitor AMD-070 to ECSCs, and observed its effect on ECSCs’ ability to invade and metastasize after incubation for 24 hours.…”

Section: Resultsmentioning

confidence: 99%

Stem cell autocrine CXCL12/CXCR4 stimulates invasion and metastasis of esophageal cancer

et al. 2017

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Esophageal cancer is one of the most common malignant tumors of the digestive tract. The greatest obstacle to the curing of esophageal cancer is its propensity to spread and metastasize. Esophageal cancer stem cells are considered the source for recurrence and metastasis of the tumors. While clinical evidence suggested that continuous up-regulation of CXCL12/CXCR4 was significantly associated with poor prognosis in patients with esophageal cancer, but the role and mechanism of CXCL12/CXCR4 in the invasion and metastasis of esophageal cancer has not been reported by far. This study found that esophageal cancer stem cells not only autocrine a great amount of CXCL12, but also high expression of its corresponding receptor CXCR4. Most importantly, the ability of esophageal cancer stem cells to spread and metastasize could be inhibited by blockage of CXCR4 with inhibitors or shRNA approaches both in vivo and in vitro studies. The important role of CXCL12 in the invasion and metastasis of esophageal cancer stem cells was also confirmed by loss-of-function and gain-of-function strategies. Mechanistically, we demonstrated that CXCL12/CXCR4 activated the ERK1/2 pathway and thereby ultimately maintained the characteristics of high-level invasion and metastasis of esophageal cancer stem cells. Taken together, our findings suggested that autocrine CXCL12/CXCR4 was one of the major mechanisms underlying the metastatic property of esophageal cancer stem cells through ERK1/2 signaling pathway, and might serve as a therapeutic target for esophageal cancer patients.

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“…Afterward, p75NTR was introduced as a marker to identify esophageal cancerous cells with self-renewal and enhanced drug resistance [76]. Further studies characterized esophageal CSCs and proposed CD44 [77][78][79][80][81], CD133, CXCR4 [82], CD90 [83], and CD15 [78] as markers for esophageal stemlike cancer cells. ALDH1 activity has also been reported as a CSC marker in ESCC and esophageal adenocarcinoma (EAC), because ALDH1 + cells were highly proliferative and chemoresistant [84,85].…”

Section: Esophagusmentioning

confidence: 99%

“…Furthermore, the expression of OCT4 and SOX2 was significantly associated with higher histological grade and poorer survival of ESCC [93,94]. In addition, expression of CD133 [82] and CD44 [79,95,96], specifically CD44v6 [97,98], was associated with clinicopathological features of ESCC and EAC, although a number of studies reported contradictive results [99][100][101]. In addition, BMI1 overexpression was correlated to advanced pathological stage and lymph node metastasis in ESCC and EAC [102,103].…”

Section: Esophagusmentioning

confidence: 99%

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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Clinical and biological significance of stem-like CD133+CXCR4+ cells in esophageal squamous cell carcinoma

Cited by 37 publications

References 23 publications

Eukaryotic translation initiation factor 3B accelerates the progression of esophageal squamous cell carcinoma by activating β-catenin signaling pathway

Eukaryotic translation initiation factor 3B accelerates the progression of esophageal squamous cell carcinoma by activating β-catenin signaling pathway

Stem cell autocrine CXCL12/CXCR4 stimulates invasion and metastasis of esophageal cancer

Cancer stem cells in human digestive tract malignancies

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