CD44 Upregulation in E-Cadherin-Negative Esophageal Cancers Results in Cell Invasion

Bras, Grégoire F. Le; Allison, Gillian L.; Richards, Nicole F.; Ansari, Shazia S.; Washington, Mary Kay; Andl, Claudia D.

doi:10.1371/journal.pone.0027063

Cited by 27 publications

(32 citation statements)

References 45 publications

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“…Le Bras et al (30) revealed that activin A increases cell invasion through CD44 upregulation following E-cadherin loss and increased CD44 expression in areas of cell invasion associated with MMP-9. In addition, activin A induced in vitro invasion of esophageal squamous cell carcinoma cells, which was accompanied by an increased MMP-2 and MMP-9 in esophageal squamous cell carcinoma cells samples (28).…”

Section: Discussionmentioning

confidence: 99%

Activin A regulates proliferation, invasion and migration in osteosarcoma cells

Jun

Fan

et al. 2015

Molecular Medicine Reports

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Activin A is a member of the TGF‑β superfamily. Previous studies have demonstrated that activin A exhibited pluripotent effects in several tumours. However, the roles of activin A signaling in osteosarcoma pathogenesis have not been previously investigated. Therefore, the present study aimed to investigate the effects of activin A on osteosarcoma cell proliferation, invasion and migration. Firstly, the expression of activin A in osteosarcoma cell lines (MG63, SaOS‑2 and U2OS) and a human osteoblastic cell line (hFOB1.19) was detected using reverse transcription quantitative polymerase chain reaction and western blotting. Activin A was upregulated in osteosarcoma cell lines compared with hFOB1.19 cells. To investigate the effects of activin A on osteosarcoma cell proliferation, invasion and migration, MG63 cells were generated in which activin A was either overexpressed or depleted. MTT staining, propidium iodide staining and a Transwell assay were used to analyze the cell cycle, proliferation, invasion and migration of MG63 cells, respectively. The results of the present study revealed that the abilities of proliferation, invasion and migration were suppressed in MG63 cells in which activin A was depleted, while they were enhanced in activin A-overexpressing cells. In conclusion, the results of the present study suggested that activin A may facilitate proliferation, invasion and migration of osteosarcoma cells, and it may therefore be a potential target for the treatment of osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

Activin A regulates proliferation, invasion and migration in osteosarcoma cells

Jun

Fan

et al. 2015

Molecular Medicine Reports

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“…However, these reports did not describe the significance of podoplanin membrane expression that we focused on in this study. We demonstrated two different evaluations, namely, intensity and localization, in the present change by which epithelial cells lose their polarity, epithelial markers, such as E-cadherin, and obtain migratory factors, such as vimentin and snail which is one of the transcription factors playing an important role in epithelial-to-mesenchymal transition (9,17,26,31,32). Vimentin expression is one of the good indicators for epithelial-to-mesenchymal transition of carcinoma, which is considered to be associated with aggressive phenotypes with invasive/ metastatic potential (16).…”

Section: Relationships Between Podoplanin Intensity and Localizationmentioning

confidence: 97%

<b>Podoplanin expression is correlated with the prognosis of lung squamous cell car</b><b>cinoma </b>

et al. 2015

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Podoplanin is a 38 kDa transmembrane protein that is involved in cell migration and cancer cell invasion. Some studies have reported that podoplanin expression was correlated with poor prognosis in lung squamous cell carcinoma (SqCC). However, there have been no clinicopathological studies of podoplanin membrane expression and localization in lung SqCC. In this study, we focused on the intensity and localization of podoplanin membrane expression, and its clinicopathological significance for lung SqCC. Strong membrane expression of podoplanin was significantly associated with lymph node metastasis, lymphatic invasion, and histological differentiation.

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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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CD44 Upregulation in E-Cadherin-Negative Esophageal Cancers Results in Cell Invasion

Cited by 27 publications

References 45 publications

Activin A regulates proliferation, invasion and migration in osteosarcoma cells

Activin A regulates proliferation, invasion and migration in osteosarcoma cells

<b>Podoplanin expression is correlated with the prognosis of lung squamous cell car</b><b>cinoma </b>

Cancer stem cells in human digestive tract malignancies

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