Epithelial cell adhesion molecule is overexpressed in hypopharyngeal carcinoma and suppresses the metastasis and proliferation of the disease when downregulated

Mu, Yakui; Sa, Na; Yu, Liang; Lu, Sumei; Wang, Haibo; Xu, Wei

doi:10.3892/ol.2014.2140

Cited by 7 publications

(5 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, when EpCAM expression was studied in ALL cases with respect to age, sex, and ALL subtypes, no significant difference between pediatric and adult groups was noted. Similar results have been reported in hypopharyngeal and oral squamous cell carcinoma, in which no association has been found between EpCAM expression and age and sex [ 34 , 35 ].…”

Section: Discussionsupporting

confidence: 87%

Epithelial Cell Adhesion Molecule (EpCAM) Expression Can Be Modulated via NFκB

et al. 2022

View full text Add to dashboard Cite

The epithelial cell adhesion molecule (EpCAM) is considered an essential proliferation signature in cancer. In the current research study, qPCR induced expression of EpCAM was noted in acute lymphoblastic leukemia (ALL) cases. Costunolide, a sesquiterpene lactone found in crepe ginger and lettuce, is a medicinal herb with anticancer properties. Expression of EpCAM and its downstream target genes (Myc and TERT) wasdownregulated upon treatment with costunolide in Jurkat cells. A significant change in the telomere length of Jurkat cells was not noted at 72 h of costunolide treatment. An in silico study revealed hydrophobic interactions between EpCAM extracellular domain and Myc bHLH with costunolide. Reduced expression of NFκB, a transcription factor of EpCAM, Myc, and TERT in costunolide-treated Jurkat cells, suggested that costunolide inhibits gene expression by targeting NFκB and its downstream targets. Overall, the study proposes that costunolide could be a promising therapeutic biomolecule for leukemia.

show abstract

Section: Discussionsupporting

confidence: 87%

Epithelial Cell Adhesion Molecule (EpCAM) Expression Can Be Modulated via NFκB

et al. 2022

View full text Add to dashboard Cite

show abstract

“…We further evaluated the potential associations of EpCAM+ cell percentage with various clinicopathological features of HCC patients. Consistent with previous reports on different cancer types, we discerned that EpCAM expression positively correlated with the tumour size ( P = .031) (Table ).…”

Section: Resultsmentioning

confidence: 95%

miR‐26b‐5p helps in EpCAM+cancer stem cells maintenance via HSC71/HSPA8 and augments malignant features in HCC

Khosla

Hemati

Rastogi

et al. 2019

Liver International

View full text Add to dashboard Cite

Background Targeting cancer stem cells (CSCs) in hepatocellular carcinoma (HCC) is difficult because of their similarities with normal stem cells (NSCs). EpCAM can identify CSCs from EpCAM+AFP+HCC cases, but is also expressed on NSCs. We aimed to distinguish the two using integrated protein, mRNA and miRNA profiling. Methods iTRAQ based protein profiling and Next Generation Sequencing (NGS) was performed on EpCAM+/EpCAM− cells isolated from HCC (Ep+CSC, Ep−HCC) and EpCAM+ cells from non‐cancerous/non‐cirrhotic control liver tissues (Ep+NSC). Validations were done using qRT‐PCR, flowcytometry and western blotting followed by in vitro and in vivo functional studies. Results 11 proteins were overexpressed (>3 fold) in Ep+CSCs compared to Ep−HCC and Ep+NSC cells. However, RNA‐sequencing confirmed the Ep+CSC specific up‐regulation of only HSPA8, HNRNPC, MPST and GAPDH mRNAs among these. Database search combined with miRNA profiling revealed Ep+CSC specific down‐regulation of 29 miRNAs targeting these four genes. Of these, only miR‐26b‐5p was found to target both HSPA8 and EpCAM. Validation of HSPA8 overexpression and miR‐26b‐5p down‐regulation followed by linear regression analysis established a negative correlation between the two. Functional studies demonstrated that reduced miR‐26b‐5p expression increased the spheroid formation, migration, invasion and tumourigenicity of Ep+CSCs. Furthermore, anti‐miR‐26b‐5p increased the number of Ep+CSCs with a concomitant overexpression of stemness genes and reduction of proapoptotic protein BBC3, which is a known substrate of HSPA8. Conclusion miR‐26b‐5p imparts metastatic properties and helps in maintenance of Ep+CSCs via HSPA8. Thus, miR‐26b‐5p and HSPA8 could serve as molecular targets for selectively eliminating the Ep+CSC population in human HCCs.

show abstract

“…To date, EpCAM overexpression has been indicated to be able to predict poor prognosis of the patients with renal cancer [ 19 ], breast cancer [ 8 ], prostate cancer [ 20 ], ovarian cancer [ 21 ] and hypopharyngeal cancer [ 22 ], while its prognostic value was controversial in lung cancer. Thus, we also evaluated the correlation of EpCAM level with clinicopathological parameters and patients’ prognosis in tumor samples from lung cancer patients.…”

Section: Discussionmentioning

confidence: 99%

MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer

Zhou

Wang

Liu

et al. 2015

J Exp Clin Cancer Res

View full text Add to dashboard Cite

BackgroundOverexpression of Metastasis-associated protein 1 (MTA1) in various cancer cells promotes tumor invasion and migration and predicts cancer patients’ poor prognosis. The pilot RNA-Seq data from our laboratory indicated that Epithelial cell adhesion molecule (EpCAM) was statistically reduced in MTA1-silencing cells. EpCAM has been recognized as more than a mere cell adhesion molecule and recent findings have revealed its causal role in mediating migratory and invasive capacity. Thus, this study was aimed to explore whether MTA1 was able to upregulate EpCAM expression and, consequently, modulate its effects on invasion and migration of the lung cancer cells as well as patients’ prognosis.MethodsWe checked the EpCAM expression by overexpressing or silencing MTA1 in lung cancer cells. Furthermore, these lung cancer cells with stably overexpressed or silenced MTA1 were transfected with siEpCAM or EpCAM-expressing plasmids and then subjected to western blot, invasion and migration assays. In addition, patients (n = 118) with early-stage lung cancer were enrolled in this study to confirm the correlations between MTA1 and EpCAM and pathoclinical parameters by using immunohistochemistry (IHC). All statistical analyses were performed with SPSS 20.0 statistical software.ResultsMTA1 upregulated EpCAM expression in lung cancer cell lines, and EpCAM overexpression rescued the inhibitory effects by silencing MTA1 on cell invasion and migration in vitro. What’s more, both MTA1 and EpCAM, correlated to each other, were overexpressed in lung cancer tissues and significantly correlated with their clinical stages, tumor diameters, lymph node metastasis. Multivariate analysis indicated that local advancement (p = 0.03), MTA1 overexpression (p = 0.001) and EpCAM overexpression (p = 0.045) of the lung cancer tissues remained significant in predicting unfavorable overall survival.ConclusionsWe revealed a new molecular mechanism of MTA1-mediated invasion and metastasis in lung cancer through downstream target EpCAM, and interfering with EpCAM function may be a novel therapeutic strategy for treatment of MTA1-overexpressing lung carcinoma.

show abstract

Epithelial cell adhesion molecule is overexpressed in hypopharyngeal carcinoma and suppresses the metastasis and proliferation of the disease when downregulated

Cited by 7 publications

References 23 publications

Epithelial Cell Adhesion Molecule (EpCAM) Expression Can Be Modulated via NFκB

Epithelial Cell Adhesion Molecule (EpCAM) Expression Can Be Modulated via NFκB

miR‐26b‐5p helps in EpCAM+cancer stem cells maintenance via HSC71/HSPA8 and augments malignant features in HCC

MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer

Contact Info

Product

Resources

About