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Effect of treating DLD1 organoids with either single agent MEK (cobimetinib) inhibition or APC restoration on chromatin accessibility.

ABSTRACT: We show that single agent treatment with either cobimetinib or APC restoration, results in cell plasticity.

ORGANISM(S): Homo sapiens

PROVIDER: GSE301561 | GEO | 2026/04/05

REPOSITORIES: GEO

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Effect of treating DLD1 organoids with either single agent MEK (cobimetinib) inhibition or APC restoration on chromatin accessibility.

Project description:Effect of treating DLD1 organoids with either single agent MEK (cobimetinib) inhibition or APC restoration on chromatin accessibility.

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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition or APC restoration, or combination on chromatin accessibility.

Project description:We show that single agent treatment with either divarasib (KRAS G12Ci) or APC restoration, results in cell plasticity.

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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition, TEAD inhibiton or APC restoration, or dual and triple combination on gene expression.

Project description:We have previously shown that single agent treatment with either divarasib (KRAS G12Ci) or APC restoration, results in cell plasticity. Here, we aim to evaluate the effects on combination treatment and if gene expression changes can be enhanced with TEAD inhbiiton.

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Apc restoration promotes cellular differentiation and reestablishes crypt homeostasis in colorectal cancer

Project description:The Adenomatous Polyposis Coli (APC) tumor suppressor is mutated in the vast majority of human colorectal cancers (CRC) and leads to deregulated Wnt signaling. To determine whether Apc disruption is required for tumor maintenance, we developed a mouse model of CRC whereby Apc can be conditionally suppressed using a doxycycline-regulated shRNA. Apc suppression produces adenomas in both the small intestine and colon that, in the presence of Kras and p53 mutations, can progress to invasive carcinoma. In established tumors, Apc restoration drives rapid and widespread tumor-cell differentiation and sustained regression without relapse. Tumor regression is accompanied by the re-establishment of normal crypt-villus homeostasis, such that once aberrantly proliferating cells reacquire self-renewal and multi-lineage differentiation capability. Our study reveals that CRC cells can revert to functioning normal cells given appropriate signals, and provide compelling in vivo validation of the Wnt pathway as a therapeutic target for treatment of CRC Analysis of RNA isolated from colon polyps that presented in shAPC or shAPC/Kras mice as compared to shRenilla (neutral) mouse colon mucosa

2015-06-18 | E-GEOD-67186 | biostudies-arrayexpress

Effect of treating AKPS organoids with either single agent KRAS G12C inhibition or APC restoration, or combination on chromatin accessibility.

Project description:Effect of treating AKPS organoids with either single agent KRAS G12C inhibition or APC restoration, or combination on chromatin accessibility.

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Apc restoration promotes cellular differentiation and reestablishes crypt homeostasis in colorectal cancer

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Differential RNA-seq analysis comparing APC-defective and APC-restored SW480 colorectal cancer cells

Project description:Identify genes that are differentially regulated as a consequence of restoration of full-length functional APC in a colorectal cancer cell lines.

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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition, TEAD inhibiton or APC restoration, or dual and triple combination on gene expression.

Project description:Effect of treating AKPS organoids with either single agent KRAS G12C inhibition, TEAD inhibiton or APC restoration, or dual and triple combination on gene expression.

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RNA-seq of AKP organoids over different stages of differentiation

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The effect of TGF-beta in Apc-mutated mouse intestinal organoids

Project description:Intestinal crypts isolated from Apcflox/flox; villin-CreERT mice were treated with Tamoxifen to induce the deletion of Apc. Tamoxifen-treated organoids were selected in the absence of Wnt agonists and then treated with TGF-beta. Total RNA obtained from Tamoxifen-treated, Apc-deleted intestinal organoids in the absence or presence of 3 ng/ml TGF-beta (18h).

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