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CBX8 promotes LUAD growth and metastasis through transcriptional repression of CDKN2C and SCEL

ABSTRACT: CBX8 promotes LUAD growth and metastasis through transcriptional repression of CDKN2C and SCEL

PROVIDER: PRJNA981976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24882072_1.fastq.gz	Fastqsanger.gz
	SRR24882072_2.fastq.gz	Fastqsanger.gz
	SRR24882073_1.fastq.gz	Fastqsanger.gz
	SRR24882073_2.fastq.gz	Fastqsanger.gz
	SRR24882074_1.fastq.gz	Fastqsanger.gz

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CBX8 promotes LUAD growth and metastasis through transcriptional repression of CDKN2C and SCEL

Project description:CBX8 promotes LUAD cell proliferation and migration through downregulating the expression of CDKN2C and SCEL.The mRNAs from A549 cells expressing control shRNAs or CBX8 shRNAs were extracted and subjected to RNA-seq.

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Phosphorylation of AHR by PLK1 promotes metastasis of LUAD via DIO2-TH signaling

Project description:Metastasis of Lung adenocarcinoma (LUAD) is a major cause of death in patients. Aryl hydrocarbon receptor (AHR) is an important transcription factor involved in the initiation and progression of lung cancer. Polo-like kinase 1 (PLK1), a serine/threonine kinase, is an oncogene that promotes the malignancy of multiple cancer types. Nonetheless, the interaction between these two factors and significance in lung cancer remains to be determined. Here, we demonstrate that PLK1 phosphorylates AHR at S489 in LUAD, which leads to epithelial-mesenchymal transition (EMT) and metastatic events. RNA-seq analyses show that type 2 deiodinase (DIO2) is responsible for EMT and enhanced metastatic potential. DIO2 converts tetraiodothyronine (T4) to triiodothyronine (T3), which then activates thyroid hormone signaling. In vitro and in vivo experiments demonstrate that treatment with T3 or T4 promotes the metastasis of LUAD, whereas depletion of DIO2 or deiodinase inhibitor disrupts this property. Taken together, our results identify the phosphorylation of AHR by PLK1 as a mechanism leading to the progression of LUAD and provide possible therapeutic interventions for this event.

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PRC1-CBX8 chromatin crosslinking

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A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells.

Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 ,BMI1,CBX8 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To explore a potential functional implication of PcG components in HCC, we stably transfected HepG2 cells with either vectors or constructs expressing shRNA that specifically targets EZH2, SUZ12, BMI1, or CBX8. A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. To obtain a broader understanding of the molecular network of PcG in HCC, the whole genome microarray expression profiling was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. Comparison of gene expression results from shRNA KDs of EZH2, SUZ12, BMI1 or CBX8 HepG2 cells.

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