Transcription Regulation of E-Cadherin by Zinc Finger E-Box Binding Homeobox Proteins in Solid Tumors

Wong, Thian‐Sze; Gao, Wei; Chan, Jmm

doi:10.1155/2014/921564

Cited by 71 publications

(79 citation statements)

References 124 publications

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“…In human and murine cancer models, it was already demonstrated that ZEB1 and ZEB2 can downregulate epithelial markers such as E‐cadherin and cytokeratin . Our results support this result as we found an inverse correlation among ZEB transcription factors and E‐cadherin expression in the CMC cell lines.…”

Section: Discussionsupporting

confidence: 89%

ZEB1 and ZEB2 transcription factors are potential therapeutic targets of canine mammary cancer cells

Xavier

Cordeiro

Rochetti

et al. 2018

Vet Comparative Oncology

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Mammary tumours are the most frequent in female dogs as in women and half are malignant. Tumorigenicity and invasiveness are important acquired characteristics for the development and progression of cancers and could be regulated by transcription factors associated with epithelial-mesenchymal transition (EMT) as ZEB1, ZEB2, SNAI1, SLUG and STAT3. Thus, here, we evaluate the expression of EMT-associated transcription factors in canine mammary cancer (CMC) cell lines characterized for invasiveness and tumorigenicity to determine if these could be considered good targets for future development of therapies. Five CMC cell lines were characterized regarding their morphology, doubling time and expression of intermediate and actin filaments. In addition, gene expression of SLUG, STAT3, ZEB1, ZEB2 and CDH1, tumorigenicity and invasiveness were assessed. Two of these cells presented an epithelial-like morphology (E20 and E37) and three a mesenchymal-like morphology (M5, M25 and CF41.Mg). M25 and CF41.Mg presented higher invasiveness. Furthermore, only mesenchymal-like cells formed tumorspheres and CF41.Mg made more and larger tumorspheres. The mesenchymal-like cells are more malignant than the epithelial-like cells being the CF41.Mg the most malignant. This cell presented higher ZEB1 and ZEB2 and lower CDH1 gene expression. Finally, our results revealed that there is a positive correlation between ZEBs and the tumorsphere number and size. In conclusion, these findings support ZEB1 and ZEB2 as potential therapeutic targets for CMC cells, demonstrating a great potential of canine models for comparative and translational studies.

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Section: Discussionsupporting

confidence: 89%

ZEB1 and ZEB2 transcription factors are potential therapeutic targets of canine mammary cancer cells

Xavier

Cordeiro

Rochetti

et al. 2018

Vet Comparative Oncology

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“…ZEB2, an E-box-binding transcription factor, was involved in the tumorigenesis of various malignancies 31. Moreover, ZEB2 was reported to promote tumor cell invasion and metastasis as it could directly bind the E-cadherin promoter and strongly inhibit E-cadherin expression during EMT 32. Here, we found that knockdown of SOX2OT significantly decreased ZEB2 expression on mRNA and protein levels, whereas co-transfection with sh-SOX2OT and miR-132 inhibitor increased ZEB2 expression levels in both A549 and H1299 cells.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA Sox2 overlapping transcript (SOX2OT) promotes non-small-cell lung cancer migration and invasion via sponging microRNA 132 (miR-132)

Zhang¹,

Yang²,

Qu³

et al. 2018

OTT

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BackgroundLong noncoding RNA (lncRNA) Sox2 overlapping transcript (SOX2OT) has been reported to be upregulated in various types of cancers, including non-small-cell lung cancer (NSCLC). However, the biological role and underlying mechanism of SOX2OT activity in NSCLC remain largely unknown. This study aims to investigate the function and possible molecular mechanisms of SOX2OT in NSCLC.Materials and methodsQuantitative real-time polymerase chain reaction was used to detect SOX2OT expression, and cellular proliferation, migration, and invasion were measured using cell counting kit-8, wound healing, and Transwell invasion assays, respectively. Western blotting was used to determine protein expression. Starbase 2.0 and luciferase reporter assay were utilized to identify the molecular target of SOX2OT.ResultsHere, we discovered that SOX2OT was markedly upregulated in NSCLC tissues and cell lines. Knockdown of SOX2OT inhibited the proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) process in NSCLC cells. Moreover, we explored the regulatory mechanism of SOX2OT and found that SOX2OT directly bound microRNA 132 (miR-132) in NSCLC cells. Importantly, miR-132 inhibition partially reversed the SOX2OT knockdown-mediated inhibitory effect on cell proliferation, migration, invasion, and EMT process. We also found that SOX2OT could regulate zinc finger E-box-binding homeobox 2 (a target of miR-132) expression, which played crucial roles in tumor cell proliferation and invasion.ConclusionThese findings indicated that SOX2OT was a noncoding oncogene that exerted important regulatory functions in NSCLC via sponging miR-132 and might represent a novel strategy for overcoming this disease.

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“…E-cadherin is a tumor suppressor that mediates cell-cell adhesion and cell-extracellular matrix interactions (19). Li et al (20) revealed that the downregulation of AQP4 results in increased expression of E-cadherin in breast cancer cells, although the association between AQP9 and E-cadherin expression is unclear.…”

Section: Discussionmentioning

confidence: 99%

AQP9 promotes astrocytoma cell invasion and motility via the AKT pathway

Huang

Dai

et al. 2018

Oncol Lett

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Abstract. The aquaporin (AQP) family, which includes 13 members identified in mammalian cells, is involved in cancer development and progression. AQP9 expression is upregulated in several tumor tissue types. However, the functions of AQP9 in astrocytoma remain elusive. The present study identified that AQP9 was expressed in astrocytoma cells. AQP9 expression was silenced by transfection with small interfering RNAs and increased by transfection with a plasmid containing the AQP9 gene. Using invasion and wound-healing assays, it was revealed that the knockdown of AQP9 suppressed astrocytoma cell invasion and motility, whereas overexpression of AQP9 promoted the invasion and motility of astrocytoma cells. It was further revealed that AQP9 could induce RAC serine/threonine-protein kinase (AKT) activation and decrease E-cadherin expression in astrocytoma cells. Inhibition of the AKT pathway attenuated AQP9-mediated invasion, motility and E-cadherin expression. Taken together, the results of the present study indicated that AQP9 promoted the invasion and motility of cells via the AKT pathway. Therefore, AQP9 may represent a potential target for therapeutic use of astrocytoma.

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Transcription Regulation of E-Cadherin by Zinc Finger E-Box Binding Homeobox Proteins in Solid Tumors

Cited by 71 publications

References 124 publications

ZEB1 and ZEB2 transcription factors are potential therapeutic targets of canine mammary cancer cells

ZEB1 and ZEB2 transcription factors are potential therapeutic targets of canine mammary cancer cells

Long noncoding RNA Sox2 overlapping transcript (SOX2OT) promotes non-small-cell lung cancer migration and invasion via sponging microRNA 132 (miR-132)

AQP9 promotes astrocytoma cell invasion and motility via the AKT pathway

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