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Identificatinon of differentially expressed genes in Docetaxel-resistant cell lines PC3 and DU145 after combination treatment with RU486 and docetaxel

ABSTRACT: Identificatinon of differentially expressed genes in Docetaxel-resistant cell lines PC3 and DU145 after combination treatment with RU486 and docetaxel

PROVIDER: PRJNA977224 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24757749_1.fastq.gz	Fastqsanger.gz
	SRR24757749_2.fastq.gz	Fastqsanger.gz
	SRR24757750_1.fastq.gz	Fastqsanger.gz
	SRR24757750_2.fastq.gz	Fastqsanger.gz
	SRR24757751_1.fastq.gz	Fastqsanger.gz

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Identificatinon of differentially expressed genes in Docetaxel-resistant cell lines PC3 and DU145 after combination treatment with RU486 and docetaxel

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Transcription Factor Network Reveals New Treatments for Prostate Cancer Docetaxel Drug Resistance

Project description:Overcoming drug resistance is critical increasing the survival rate for prostate cancer (PCa). In this study, we modeled docetaxel resistance using two PCa cell lines, DU145 and PC3. We conducted both single cell and bulk RNA sequencing. We constructed a transcription factor (TF) network for the docetaxel sensitive and resistant variants for all cell lines and sequencing methods resulting in 8 networks. We identified shared edges and nodes that represent a shared TF network for PCa that modeled the changes after acquiring drug resistance. Using this shared TF network, we identified drivers of the resistant phenotype. Interestingly, the network constructed from the bulk sequencing dataset revealed different TF drivers of resistance compared with the network constructed from the single cells. We validated the results constructed from the single cells to demonstrate the validity of the single cell sequenced TF network. We targeted GABPA (only identified in the single cell constructed network) and successfully re-sensitized both cell lines to docetaxel treatment. Additionally, we conducted connectivity map analysis to identify potential drugs that disrupt the resistant networks. We identified trichostatin A as a potential combination treatment using the single cell sequenced network. Combination treatment of trichostatin A and docetaxel, both in vitro and in vivo PCa models decreased tumor growth. These results suggest by analyzing a population of resistant cells, identification of drivers and novel treatments is possible.

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Silenced LINC01963 enhanced the chemosensitivity of prostate cancer cells to docetaxel by sponging miR-216b-5p to inhibit TrkB protein level

Project description:Long noncoding RNAs (lncRNAs) affect docetaxel chemosensitivity. However, the biological role and regulatory mechanisms of lncRNAs in docetaxel-resistant prostate cancer remain unclear. Differences in lncRNAs were evaluated by lncRNA sequencing and evaluated using quantitative real-time polymerase chain reaction, and TrkB expression was measured through Western blot analysis. Proliferation was measured using the MTS, while apoptosis and cell cycle were measured using flow cytometry. Additionally, migration and invasion were measured using transwell assays. Forty-eight female BALB/c nude mice were used for subcutaneous tumorigenicity and lung metastasis assays. We found that LINC01963 was overexpressed in the PC3-DR cells. LINC01963 silencing enhanced the chemosensitivity of PC3-DR to docetaxel and inhibited tumorigenicity and lung metastasis, while LINC01963 overexpression enhanced the chemoresistance of PC3 cells to docetaxel. It was found that LINC01963 sponges miR-216b-5p. The miR-216b-5p inhibitor reversed the suppressive effect of sh-LINC01963 on PC3-DR cell proliferation, migration, and invasion. Furthermore, miR-216b-5p can bind to the 3’-UTR of NTRK2 and inhibit TrkB protein levels. TrkB enhances docetaxel resistance in prostate cancer and reverses the effects of LINC01963 silencing and miR-216b-5p overexpression. In conclusion, silencing LINC01963 enhanced the chemosensitivity of PC3-DR to docetaxel by sponging miR-216b-5p to inhibit TrkB protein levels.

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