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RNA-seq of KP and KPI tumor cells isolated from KP and KPI lung adenocarcinoma tumors

ABSTRACT: RNA-seq of KP and KPI tumor cells isolated from KP and KPI lung adenocarcinoma tumors

PROVIDER: PRJNA545526 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9163430_1.fastq.gz	Fastqsanger.gz
	SRR9163430_2.fastq.gz	Fastqsanger.gz
	SRR9163431_1.fastq.gz	Fastqsanger.gz
	SRR9163431_2.fastq.gz	Fastqsanger.gz
	SRR9163422_1.fastq.gz	Fastqsanger.gz

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RNA-seq of KP and KPI tumor cells isolated from KP and KPI lung adenocarcinoma tumors

Project description:RNA-seq analysis of KP and KPI lung adenocarcinoma cells. Analysis revealed activation of Wnt signaling in KPI tumor cells.

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Project description:To systematically study the functions of epigenetic genes in controlling tumor progression and regulating anti-tumor immunity, we performed a series of in vitro and in vivo epigenome-wide CRISPR screens in mouse KP lung adenocarcinoma model. We constructed an epigenetic-focused sgRNA library, established KP-Cas9-library pools, and then performed in vitro and in vivo CRISPR screens. For in vitro screens, we compared the cell pools harvested at week 4 with the cells pools harvested at week 2 to check the functions of epigenetic genes in tumor cell proliferation. For in vivo screens, we compared the IgG treated tumors in Rag1-/- mice or WT mice with the input cell pool to check the functions of epigenetic genes in tumor growth; we compared the IgG treated tumors in WT mice with the IgG treated tumors in Rag1-/- mice to check the functions of epigenetic genes in regulating anti-tumor immunity; we compared the anti-PD-1 treated tumors in WT mice with IgG treated tumors in WT mice to check the functions of epigenetic genes in modulating sensitivity to anti-PD-1 treatment.

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Project description:The model is based on publication: Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification Abstract: Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mutation; but later, most cases acquire a resistance to gefitinib. One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5–22% of gefitinib-resistant tumors. A previous study suggested that MET amplification could cause gefitinib resistance by driving ErbB3-dependent activation of the PI3K pathway. In this study, we built a mathematical model of gefitinib resistance caused by MET amplification using lung adenocarcinoma HCC827-GR (gefitinib resistant) cells. The molecular reactions involved in gefitinib resistance consisted of dimerization and phosphorylation of three molecules, EGFR, ErbB3, and MET were described by a series of ordinary differential equations. To perform a computer simulation, we quantified each molecule on the cell surface using flow cytometry and estimated unknown parameters by dimensional analysis. Our simulation showed that the number of active ErbB3 molecules is around a hundred-fold smaller than that of active MET molecules. Limited contribution of ErbB3 in gefitinib resistance by MET amplification is also demonstrated using HCC827-GR cells in culture experiments. Our mathematical model provides a quantitative understanding of the molecular reactions underlying drug resistance.

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