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Effect of existence or depletion of LIN28B on gene expression during tumor growth of PDAC cells

ABSTRACT: To investigate the effect of existence or depletion of LIN28B in PDAC growth , we established cell lines with or without LIN28B expression. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells.Additionally, we performed the whole exome sequencing of 14837T and 15376T to compare their differences

ORGANISM(S): Mus musculus

PROVIDER: GSE217378 | GEO | 2023/09/14

REPOSITORIES: GEO

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Effect of existence or depletion of LIN28B on gene expression during tumor growth of PDAC cells

Project description:Effect of existence or depletion of LIN28B on gene expression during tumor growth of PDAC cells

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SIRT6 suppresses pancreatic cancer through control of Lin28b [miRNA-seq]

Project description:Chromatin remodeling proteins are frequently dysregulated in human cancer, yet little is known about how they control tumorigenesis. Here, we uncover an epigenetic program mediated by the NAD+-dependent histone deacetylase Sirtuin 6 (SIRT6) that is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies. SIRT6 inactivation accelerates PDAC progression and metastasis via upregulation of Lin28b, a negative regulator of the let-7 microRNA. SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment, and pronounced induction of Lin28b and downstream let-7 target genes, HMGA2, IGF2BP1 and IGF2BP3. This epigenetic program defines a distinct subset representing 30-40% of human PDAC, characterized by poor prognosis and an exquisite dependence on Lin28b for tumor growth. Thus, we identify SIRT6 as an important PDAC tumor suppressor, and uncover the Lin28b pathway as a potential therapeutic target in a molecularlydefined PDAC subset. Small RNA-Seq experiments for PLKO and shLIN28B (three replicates each) in human Panc3.27 PDAC cells to identify miRNAs modulateed by LIN28B knockdown.

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SIRT6 suppresses pancreatic cancer through control of Lin28b [ChIP-seq]

Project description:Chromatin remodeling proteins are frequently dysregulated in human cancer, yet little is known about how they control tumorigenesis. Here, we uncover an epigenetic program mediated by the NAD+-dependent histone deacetylase Sirtuin 6 (SIRT6) that is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies. SIRT6 inactivation accelerates PDAC progression and metastasis via upregulation of Lin28b, a negative regulator of the let-7 microRNA. SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment, and pronounced induction of Lin28b and downstream let-7 target genes, HMGA2, IGF2BP1 and IGF2BP3. This epigenetic program defines a distinct subset representing 30-40% of human PDAC, characterized by poor prognosis and an exquisite dependence on Lin28b for tumor growth. Thus, we identify SIRT6 as an important PDAC tumor suppressor, and uncover the Lin28b pathway as a potential therapeutic target in a molecularlydefined PDAC subset. ChIP-Seq experiments to examine H3K56ac histone modifications in murine PDAC cells that are Sirt6 wild type (WT), Sirt6 knock-out (KO), and Sirt6 KO cells engineered to express Sirt6 WT (Sirt6 KO + Sirt6 WT Restored).

2016-04-01 | E-GEOD-79503 | biostudies-arrayexpress

SIRT6 suppresses pancreatic cancer through control of Lin28b [miRNA-seq]

2016-04-01 | GSE79504 | GEO

SIRT6 suppresses pancreatic cancer through control of Lin28b [ChIP-seq]

2016-04-01 | GSE79503 | GEO

The Lin28b/Wnt5a axis drives pancreas cancer through crosstalk between cancer associated fibroblasts and tumor epithelium

Project description:Bidirectional signal transduction between tumor epithelial cells and tumor microenvironment (TME) is important for tumor development. Here we showed that Lin28b/let-7 pathway is indispensable for modulating the expression of Wnt5a in tumor epithelium, which could be secreted and then up-regulates Lin28b in cancer-associated fibroblasts (CAFs). Moreover, we demonstrated that Lin28b in CAFs promoted growth of PDAC by inducing cytokine PCSK9’s production. Using an orthotopic mouse model of PDAC, we fouind that depletion of Lin28b in CAFs reduced tumor weight, highlighting the importance of Lin28b in PDAC stromal. Thus, our study shows that the Lin28b-Wnt5a axis plays a critical role in bidirectional crosstalk between pancreatic tumor epithelium and TME and results in a pro-‍tumorigenic contexture.

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C/EBPβ-LIP regulates the let-7/Lin28b circuit to induce cancer-type metabolic reprogramming

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Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

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