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Gene expression profiles in GSK-3alpha Ser21Ala knock-in mouse heart

ABSTRACT: GSK-3 is a serine-threonine protein kinase and consists of two isoforms, GSK-3alpha and GSK-3beta. GSK-3alpha and GSK-3beta are inactivated by phosphorylation at Ser21 and Ser9, respectively. GSK-3alpha Ser21Ala and GSK-3beta Ser9Ala phosphorylation-resistant knock-in mice have constitutively active form of GSK-3.

ORGANISM(S): Mus musculus

PROVIDER: GSE112158 | GEO | 2019/03/11

REPOSITORIES: GEO

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Gene expression profiles in GSK-3beta Ser9Ala knock-in mouse heart

Project description:GSK-3 is a serine-threonine protein kinase and consists of two isoforms, GSK-3alpha and GSK-3beta. GSK-3alpha and GSK-3beta are inactivated by phosphorylation at Ser21 and Ser9, respectively. GSK-3alpha Ser21Ala and GSK-3beta Ser9Ala phosphorylation-resistant knock-in mice have constitutively active form of GSK-3.

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Gene expression profiles in GSK-3alpha Ser21Ala or GSK-3beta Ser9Ala knock-in mouse heart

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GSK-3alpha Promotes Oncogenic KRAS Function in Pancreatic Cancer via TAK1-TAB Stabilization and Regulation of Non-Canonical NF-kB

Project description:Mutations in KRAS occur in a variety of tumors of epithelial origin, driving the oncogenic phenotype.The NF-kB transcription factor pathway is important for oncogenic RAS to transform cells and to drive tumorigenesis in animal models. Recently TAK1, an upstream regulator of IKK which controls canonical NF-kB, was shown to be important for chemoresistance in pancreatic cancer and for regulating KRAS+ colorectal cancer cell growth and survival. Here we show that GSK-3alpha is upregulated by KRAS leading to interaction with TAK1 to stabilize the TAK1/TAB complex to promote IKK activity. Additionally, GSK-3alpha is required for promoting critical non-canonical NF-kB signaling in pancreatic cancer cells. Pharmacologic inhibition of GSK-3 suppresses growth of human pancreatic tumor explants, consistent with loss of expression of genes such as c-myc and TERT. These data identify GSK-3alpha as a key downstream effector of oncogenic RAS via its ability to coordinately regulate distinct NF-kB signaling pathways GSK-3 inhibition at 2 and 8 hours

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GSK-3A and GSK-3B knockdown in AML cell lines

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GSK-3alpha Promotes Oncogenic KRAS Function in Pancreatic Cancer via TAK1-TAB Stabilization and Regulation of Non-Canonical NF-kB

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GSK-3A and GSK-3B knockdown in AML cell lines

Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3A–specific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML.

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