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alkbh, cells, cancer, wif, expression, pdac, fig, article, wnt, cell, google, scholar, pancreatic, signaling, additional, file, gemcitabine, figure, overexpression, aspc, tumor, modification, bxpc, mrna, rna, levels, mmp, mia, mice, control, cas, proliferation, protein, xenograft, paca, data, formation, qrtpcr, human, colony, wang, migration, treatment, methylation, genes, panc, quantification, analysis, cancers, invasion,

Topics {✒️}

augmented wnt/pi3k-akt signaling gemcitabine-treated patient-derived xenograft heat-induced antigen recovery treated-patient-derived xenograft poly-a-purified rna springer nature wnt/beta-catenin pathway wnt/β-catenin pathway wnt/beta-catenin signaling wnt/β-catenin signaling [27 wnt/β-catenin signaling avidin-biotin peroxidase complex considered statistically significant β-catenin protein levels kaplan-meier analysis indicating network-based methods alkbh5-mediated m6a modification gemcitabine-treated pdx model m6a-seq m6a-ip biological processes including additional information publisher β-catenin mrna transcripts privacy choices/manage cookies anti-α-catenin antibody chemo-resistance remains paraffin-embedded tissues cut genes differentially expressed mia paca-2-alkbh5 cells authors scientific editing including cell proliferation mediating methylation reversal bmc mediating wnt signaling human neuroendocrine tumors pancreatic ductal adenocarcinoma increased cell proliferation state privacy rights diminished promoter activations pancreatic cancer stem β-catenin promoter activity n6-methyladenosine mettl3 wnt signaling pathway cell proliferation program tumor growth rate cancer cell proliferation abbreviations alkbh5 pancreatic cancer cells dna damage repair bxpc-3 cells expressing cancer stem cell

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      description:Pancreatic cancer is one of the most lethal types of cancer with extremely poor diagnosis and prognosis, and chemo-resistance remains a major challenge. The dynamic and reversible N6-methyladenosine (m6A) RNA modification has emerged as a new layer of epigenetic gene regulation. qRT-PCR and IHC were applied to examine ALKBH5 levels in normal and pancreatic cancer tissues. Cancer cell proliferation and chemo-resistance were evaluated by clonogenic formation, chemosensitivity detection, and Western blotting assays. m6A-seq was performed to identify target genes. We evaluated the inhibitory effect of ALKBH5 in both in vivo and in vitro models. Here, we show that m6A demethylase ALKBH5 is downregulated in gemcitabine-treated patient-derived xenograft (PDX) model and its overexpression sensitized pancreatic ductal adenocarcinoma (PDAC) cells to chemotherapy. Decreased ALKBH5 levels predicts poor clinical outcome in PDAC and multiple other cancers. Furthermore, silencing ALKBH5 remarkably increases PDAC cell proliferation, migration, and invasion both in vitro and in vivo, whereas its overexpression causes the opposite effects. Global m6A profile revealed altered expression of certain ALKBH5 target genes, including Wnt inhibitory factor 1 (WIF-1), which is correlated with WIF-1 transactivation and mediation of the Wnt pathway. Our work uncovers the tumor suppressive and chemo-sensitizing function for ALKBH5, which provides insight into critical roles of m6A methylation in PDAC.
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      dateModified:2020-01-06T00:00:00Z
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         m6A methylation
         Chemo-resistance
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         Wnt
         Cancer Research
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      name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Department of Health Sciences, Hiroshima Shudo University, Hiroshima, Japan

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