Abstract
BackgroundEsophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer, with a poor prognosis. Deregulation of WNT and NOTCH signaling pathways is important in ESCC progression, which can be due to either malfunction of their components or crosstalk with other pathways. Therefore, identification of new crosstalk between such pathways may be effective to introduce new strategies for targeted therapy of cancer. A correlation study was performed to assess the probable interaction between growth factor receptors and WNT/NOTCH pathways via the epidermal growth factor receptor (EGFR) and Musashi1 (MSI1), respectively.MethodsLevels of MSI1/EGFR mRNA expression in tumor tissues from 48 ESCC patients were compared to their corresponding normal tissues using real-time polymerase chain reaction.ResultsThere was a significant correlation between EGFR and MSI1 expression (p = 0.05). Moreover, there was a significant correlation between EGFR/MSI1 expression and grade of tumor differentiation (p = 0.02).ConclusionThis study confirms a direct correlation between MSI1 and EGFR and may support the important role of MSI1 in activation of EGFR through NOTCH/WNT pathways in ESCC.
Highlights
Esophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer, with a poor prognosis
An inverse association has been shown between epidermal growth factor receptor (EGFR) expression and survival rate of ESCC patients in which higher levels of EGFR are associated with chemo-radiotherapeutic resistance and lymph node metastasis
Levels of EGFR/MSI1 mRNA expression in ESCC patients Regarding our recent publications, we have reported the role of EGFR and MSI1 in separate studies [25, 26]
Summary
Esophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer, with a poor prognosis. EGFR experiences a conformational change and induces dimerization with other ErbB/HER family receptors leading to autophosphorylation and activation of the tyrosine kinase domain [9] Several pathways such as ERK/MAPK, PI3K, and JAK/STAT can be activated to regulate cell proliferation and migration [10, 11]. MSI1 exerts its inhibitory role through competing with eIF4G to bind PABP during initiation of translation [18] It targets different RNAs such as Numb and p21WAF-1, which are involved in the NOTCH pathway and cell cycle regulation, respectively [19]. DKK3, as one of the main targets for the post-transcriptional regulation of MSI1, functions as a tumor suppressor to block proliferation through interaction with LRP5/6 [14, 22] It prevents beta-catenin transfer into the nucleus [23]. In the present study we assessed a probable mutual correlation between EGFR and MSI1 to clarify the details of interactions between WNT and NOTCH pathways and their probable effect on EGFR in ESCC patients
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