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Analysis of gene expression change between HCC827 SC and HCC827 shCEACAM6

ABSTRACT: Analysis of gene expression change between HCC827 SC and HCC827 shCEACAM6

PROVIDER: PRJNA1220580 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32263968_1.fastq.gz	Fastqsanger.gz
	SRR32263968_2.fastq.gz	Fastqsanger.gz
	SRR32263969_1.fastq.gz	Fastqsanger.gz
	SRR32263969_2.fastq.gz	Fastqsanger.gz

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Analysis of gene expression change between HCC827 SC and HCC827 shCEACAM6

Project description:CEACAM family proteins have been extensively studied as cell adhesion molecules, yet the biological and clinical significance of CEACAM6 remains relatively unexplored. Our research identifies a significant increase in CEACAM6 expression in lung adenocarcinoma, particularly correlating with EGFR mutation status. In EGFR-mutated lung cancer cells, CEACAM6 knockdown induced apoptosis and reduced p-ERK1/2 signaling downstream of EGFR. Treatment with EGFR-tyrosine kinase inhibitors (TKIs) decreased CEACAM6 levels, leading to TKI-resistant lung cancer cells that exhibited reduced p-ERK1/2 and increased epithelial-mesenchymal transition (EMT) characteristics. Co-immunoprecipitation assays revealed an interaction between CEACAM6 and EGFR. Although CEACAM6 expression was lost in EGFR-TKI resistant cells, its re-expression stabilized EGFR and increased sensitivity to EGFR-TKIs. TGF-? treatment, which induced EMT, also decreased CEACAM6 expression and improved EGFR-TKI resistance. Further analysis showed that EGFR-TKI resistant lung cancer cells had lower H3K27ac epigenetic modification levels at the CEACAM6 locus than EGFR-TKI sensitive cells. Treatment with HDAC1/2 inhibitors in EGFR-TKI sensitive cells reduced CEACAM6 expression, induced EMT and TGF-?-ligand/receptor gene expression, and enhanced EGFR-TKI resistance. These data highlight the crucial role of CEACAM6 in maintaining oncogenic EGFR signaling and its regulation by cytokine stimulation and epigenetic modification, influencing EGFR-TKI sensitivity. Our findings underscore CEACAM6's potential as a valuable biomarker in EGFR-driven lung adenocarcinoma and its intricate involvement in EGFR-related pathways.

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Analysis of gene expression change between Ishikawa-02 SC and Ishikawa-02 shSOX2

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Project description:We collected total RNA from both Ishikawa-02 SC and Ishikawa-02 shSOX2 and examined mRNA expression profile, comprehensively.

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Project description:To investigate the influence of TET2 knock-down in lung cancer cell line, We performed gene expression profiling analysis using data obtained from RNA-seq of HCC827 cell line and HCC827-TET2-KO cell line.

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Gene expression of HCC827 and HCC827-OR cell line [HCC827OR_RNA]

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Mutational analysis of HCC827 and HCC827-OR cell lines [HCC827OR_WES]

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Mutational analysis of HCC827 and HCC827-OR cell lines [HCC827OR_WES]

Project description:To investigate if there are new genetic mutations occurred within the HCC827 osimertinib resistant cells compared with the parental cells.

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Gene expression of HCC827 and HCC827-TET2-KO cell line [HCC827_TET2_KO_RNA]

Project description:Gene expression of HCC827 and HCC827-TET2-KO cell line [HCC827_TET2_KO_RNA]

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Project description:To investigate the abnormal gene expression in Osimertinib Resistance lung cancer cell line, We performed gene expression profiling analysis using data obtained from RNA-seq of HCC827 cell line and HCC827OR cell line.

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