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Expression data in ezrin-knockdown ec109 cells(PSE1) and control(PS)

ABSTRACT: Ezrin belongs to the ezrin¨Cradixin¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Keywords: Gene expression after RNAi

ORGANISM(S): Homo sapiens

PROVIDER: GSE6233 | GEO | 2006/11/09

SECONDARY ACCESSION(S): PRJNA97601

REPOSITORIES: GEO

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siRNA profiling of human ezrin-knockdown ec109 cells(PSE1) and control(PS)

Project description:Ezrin belongs to the ezrinÂ¨CradixinÂ¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Experiment Overall Design: he mammalian expression vector, pSUPER.neo.circular (OligoEngine), was used for expression of siRNA in EC109 cells. Briefly, two primer pairs were synthesized, one pair encoding nucleotides 274Â¨C292 (TCCACTATGTGGATAATAA) followed by a 9 base Â¡Â®Â¡Â®loopÂ¡Â¯Â¡Â¯ (TTCAAGAGA) and the inverted repeat (PSE1), and the second encoding nucleotides 265Â¨C283 (ACTTTGGCCTCCACTATGT) again followed by the loop and inverted repeat (PSE2). And pSUPER.neo vector of nonspecific siRNA was taken as negative control (PSC). The primer pairs were annealed and inserted into the BglII and HindIII sites of pSUPER.neo and transformed into JM109 competent cells (Promega). Positive clones were verified and transfected into EC109 cells using FuGENE 6 transfection reagent (Roche) according to the manufacturerÂ¡Â¯s instructions. G418 (400 Â¦Ãg/ml, Calbiochem) was added into the culture medium after 24 h. Stable G418-resistant clones were obtained in 7Â¨C9 days. The expanded cells were then used for subsequent studies.

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Expression data from DEGs in human ESCC EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C)

Project description:Expression data from different expressed genes (DEGs) in human esophageal squamous cell carcinoma (ESCC) EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C) Lysine demethylase 5C (KDM5C), a member of lncRNAs, has tumor-suppressor properties and is downregulated in the majority of malignancies. KDM5C was found to suppress some sorts of tumors through regulating epithelial mesenchymal transformation,inducing cell cycle arrest,triggering apoptosis and so on. We used microarrays to investigate the possible regulatory mechanism of KDM5C in ESCC cell line.

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Project description:Analysis of SW480 cells following knockdown of Ezrin using RNAi. Ezrin is a protein that regulate the organization of cytoskeleton. Ezrin KD SW480 was used to study the role of ezrin in colon cancer. Keywords: ezrin, colon cancer, migration

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Expression analysis of miR-139-5p mimic-treated EC109 cells

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The protein interaction of PALM2 in HEK 293T

Project description:We identify the protein interaction of PALM2 in HEK 293T. we find that PALM2 can promote the malignant behaviors of esophageal squamous cancer cell (ESCC). Focusing on the mechanism inside, we reveal that PALM2 promotes the migration of esophageal squamous cancer cells through activating it interactor, ezrin.

2023-03-08 | PXD040700 |

The impact of knocking down METTL3 and METTL14 on the gene expression profile of EC109 esophageal squamous cell carcinoma cells.

Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism.

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Prenylated PALM2 Promotes the Migration of Esophageal Squamous Cancer Cells through Activating Ezrin

Project description:Proteins containing a CAAX motif at the C-terminus can occur prenylation modification and regulate the localization and activity of a series of key regulatory proteins, including RAS superfamily members, heterotrimeric G proteins, nuclear lamina protein, and several protein kinases and phosphatases. However, studies of prenylated proteins in esophageal cancer are limited. Here, we found that paralemmin-2 (PALM2), a potential prenylated protein, was up-regulated and associated with a poor prognosis of patients, through research on large-scale proteomic data of esophageal cancer in our laboratory. The low throughput verification also showed that the expression of PALM2 in esophageal cancer tissues was higher than that in their paired normal esophageal epithelial tissues, and it was generally expressed in the membrane and cytoplasm of esophageal squamous cancer cells (ESCC). PALM2 interacted with the two subunits of farnesyl transferase (FTase), FNTA and FNTB. The FTase inhibitor weakened the membranous location of PALM2 and mutation in the CAAX motif of PALM2 (PALM2C408S) impaired its membranous localization, indicating PALM was prenylated by FTase. Overexpressed PALM2 promoted the migration of cancer cells, whereas PALM2C408S lost this ability. Mechanistically, PALM2 interacted with the N-terminal FERM domain of ezrin of Ezrin/Radixin/Moesin (ERM) family dependent on its prenylation. The mutagenesis indicated that lysine residues K253/K254/K262/K263 in ezrin’s FERM domain and cysteine residue C408 in PALM2’s CAAX motif were important for their interaction and ezrin activation. The knockout of ezrin prevented enhanced cancer cell migration by PALM2 overexpression. PALM2, depending on its prenylation, made ezrin get more membranous distribution and increased the phosphorylation of ezrin Y146 site. In summary, prenylated PALM2 promoted the migration of cancer cells through activating ezrin.

2023-03-20 | PXD040969 |

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