Sa1330 ECT2 PROMOTES PROLIFERATION AND METASTASIS OF ESOPHAGEAL SQUAMOUS CELL CARCINOMA VIA THE RHOA-ERK-VEGF/MMP9 SIGLING AXIS

Binyu, Sun; Liu, Fang; Gan, Bentian

doi:10.1016/j.gie.2020.03.1126

Cited by 6 publications

(6 citation statements)

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“…In addition to the suppression of MMP‐2 and MMP‐9, 50 μM of resveratrol was found to inhibit the phosphorylation of ERK and p38 (Figure 5a), thus blocking the activation of these two proteins. The activation of ERK had been reported to promote the metastasis capacity of cancer cells (Cai et al., 2020; Lv et al., 2020; Meng et al., 2020; Song et al., 2020; Sun et al., 2020) and p38 (Hong et al., 2020; Liu et al., 2019; Pan et al., 2020; Ramadoss et al., 2017; Zhang et al., 2020; Zhu et al., 2019). In addition, blocking the phosphorylation of ERK and p38 has been tested as an anti‐metastatic strategy in cancer treatment (Choi et al., 2019; Tang et al., 2018).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol inhibited the metastatic behaviors of cisplatin‐resistant human oral cancer cells via phosphorylation of ERK/p‐38 and suppression of MMP‐2/9

et al. 2021

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Cisplatin resistance is a major clinical problem in the clinical management of oral squamous cell carcinoma (OSCC) patients. Resveratrol is a natural phytoestrogen with antitumor activities. Whether resveratrol can overcome cisplatin resistance and prevent metastasis in OSCC cells is not known. In this study, we first examined the anti‐metastatic capacity of resveratrol and then explored the underlying mechanisms using a cisplatin‐resistant human OSCC cell line (CAR). The results demonstrated that at a non‐toxic dose range (25 to 75 µM), 24‐hr treatment of resveratrol was able to suppress the migration and invasion capacities of CAR cells dose dependently. Interestingly, 50 µM resveratrol treatment could significantly down‐regulate the expression of the phosphorylated forms of ERK and p‐38, in addition to those of MMP‐2 and MMP‐9. At the same time, the expression levels of phosphorylated ERK together with those unphosphorylated forms of ERK, p38, and JNK were all insignificantly altered. In conclusion, the signaling cascade for resveratrol's suppression of cisplatin‐resistant human oral cancer CAR cells was revealed and summarized. Also the rapid effectiveness in suppressing metastatic behaviors of drug‐resistant oral cancer cells of non‐toxic resveratrol might extend its application to the drug‐resistant oral cancer treatment in the near future. Practical applications Based on the evidence we provided in the study, we have proposed a model recording the possible pathway for resveratrol inhibiting the metastasis of cisplatin‐resistant oral cancer cells. We suppose this signaling pathway may work in other cancer cell lines, and can be helpful in full understanding of the drug‐resistance

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Section: Discussionmentioning

confidence: 99%

Resveratrol inhibited the metastatic behaviors of cisplatin‐resistant human oral cancer cells via phosphorylation of ERK/p‐38 and suppression of MMP‐2/9

et al. 2021

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“…ECT2 acts as an oncogene and is involved in the proliferation and metastasis of several tumors. Sun et al found that ECT2 was involved in the development of esophageal cancer through the RhoA-ERK signal pathway [ 25 ]. Zhi et al found that ECT2 promoted the proliferation of glioma cells by upregulating PTTG1 expression [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of ECT2 and COL17A1 as Potential Biomarkers for Pancreatic Cancer

Huang

et al. 2022

Disease Markers

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Background. Pancreatic cancer (PC) is a malignant tumor of the digestive tract. It presents with atypical clinical symptoms and lacks specific diagnostic indicators. This study is aimed at exploring the potential biomarkers of PC. Methods. TCGA database pancreatic cancer dataset was normalized and used to identify differentially expressed genes (DEGs). Survival, independent prognostic, and clinical correlation analyses were performed on DEGs to screen for key genes. DNA methylation, mutation, and copy number variation (CNV) analyses were used to analyze genetic variants in key genes. GSEA was performed to explore the functional enrichment of the key genes. Based on the expression of key genes, construction of a competing endogenous RNA (ceRNA) network, analysis of the tumor microenvironment (TME), and prediction of chemotherapeutic drug sensitivity were performed. Furthermore, the GEO database was used to validate the reliability of key genes. Results. Two key genes (ECT2 and COL17A1) were identified, which were highly expressed in PC. The mRNA expression of ECT2 and COL17A1 was associated with DNA methylation and CNV. The cell cycle, proteasome, and pathways in cancer were enriched in the high-COL17A1 and ECT2 groups. The TME results showed that immune scores were decreased in the high-ECT2 group. CeRNA network results showed that there were eleven miRNAs were involved in the regulation of ECT2 and COL17A1. Moreover, pRRophetic analysis showed that 20 chemotherapeutic drugs were associated with ECT2 and COL17A1 expression. Conclusions. Collectively, ECT2 and COL17A1 may be potential biomarkers for PC, providing a new direction for clinical diagnosis and treatment.

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“…In oral cancer, reducing the expression of ANLN can promote apoptosis and inhibit the proliferation, invasion and migration of cancer cells through PI3K/mTOR signal pathway [65]. ECT2 regulates the expression of vascular endothelial growth factor and MMP9 through RhoA-ERK signaling pathway, thus promoting cell proliferation, invasion, migration and tumor development [66]. ACADM can promote the EMT process of breast cancer cells and improve the migration and invasion ability of breast cancer cells [67].…”

Section: Austin Publishing Groupmentioning

confidence: 99%

Network Analysis of Differential Expression of ANLN and Its Interacting Proteins in Esophageal Squamous Cell Carcinoma

Sun,

Cao,

et al. 2023

austinjbiosensbioelectron

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Anillin (ANLN) is an actin binding protein, which was originally extracted from Drosophila melanogaster embryos. As a key regulatory factor in cytokinesis, ANLN is highly expressed in various tumors, leading to abnormal cell division and promoting the proliferation, migration, and invasion of cancer cells. At present, the role and regulatory mechanism of ANLN in human Esophageal Squamous Cell Carcinoma (ESCC) are not fully understood. The purpose of this study is to construct a Protein-Protein Interaction Network (PPIN) to reveal the characteristics of ANLN and its interacting proteins, by the integration of their expression in ESCC. The differentially expressed ANLN and its interacting proteins in ESCC were identified from our previous RNA-seq data. By constructing a specific PPI network, it was found that many differentially expressed genes/proteins may interact with ANLN. Multiple enrichment pathways of ANLN and its differentially expressed genes were explained by functional enrichment analysis, Gene Ontology (GO) analysis and KEGG pathway analysis. In addition, it is revealed that ANLN, ECT2, ACADM and PPP1R9A play an important role in the occurrence and development of ESCC, and they are proposed as new prognostic factors for ESCC. These bioinformatics analyses provide a comprehensive perspective for the role of ANLN in ESCC.

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Sa1330 ECT2 PROMOTES PROLIFERATION AND METASTASIS OF ESOPHAGEAL SQUAMOUS CELL CARCINOMA VIA THE RHOA-ERK-VEGF/MMP9 SIGLING AXIS

Cited by 6 publications

References 0 publications

Resveratrol inhibited the metastatic behaviors of cisplatin‐resistant human oral cancer cells via phosphorylation of ERK/p‐38 and suppression of MMP‐2/9

Resveratrol inhibited the metastatic behaviors of cisplatin‐resistant human oral cancer cells via phosphorylation of ERK/p‐38 and suppression of MMP‐2/9

Integrated Analysis of ECT2 and COL17A1 as Potential Biomarkers for Pancreatic Cancer

Network Analysis of Differential Expression of ANLN and Its Interacting Proteins in Esophageal Squamous Cell Carcinoma

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