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NSUN5 Mediates Resistance to Doxorubicin via Upregulation of DNA Damage Repair Proteins BRCA2 and BRIP1 in Colorectal Cancer

ABSTRACT: NSUN5 Mediates Resistance to Doxorubicin via Upregulation of DNA Damage Repair Proteins BRCA2 and BRIP1 in Colorectal Cancer

PROVIDER: PRJNA1269002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR33733275_1.fastq.gz	Fastqsanger.gz
	SRR33733275_2.fastq.gz	Fastqsanger.gz
	SRR33733276_1.fastq.gz	Fastqsanger.gz
	SRR33733276_2.fastq.gz	Fastqsanger.gz

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NSUN5 Mediates Resistance to Doxorubicin via Upregulation of DNA Damage Repair Proteins BRCA2 and BRIP1 in Colorectal Cancer

Project description:Despite advancements in diagnosis and therapy, chemotherapy resistance and metastasis remain significant challenges for colorectal cancer (CRC) patients. Addressing resistance to cell death is crucial for improving cancer treatment outcomes. NOP2/Sun RNA methyltransferase 5 (NSUN5) has been implicated in cancers, but its role in chemotherapy resistance of CRC remains unclear. Herein we reveal that NSUN5 is highly expressed in CRC through bioinformatics analysis and validation using human and mice CRC tissues. High expression of NSUN5 predicted poorer disease-free survival in CRC patients. Nsun5-deficient mice exhibited reduced tumor incidence and malignancy in an AOM/DSS-induced CRC model. NSUN5 knockdown or knockout showed diminished proliferation and migration in CRC cell lines, which was reversed by NSUN5 overexpression or reintroduction. Intriguingly, overexpression of NSUN5 conferred resistance to doxorubicin, an effective chemotherapeutic agent leads to DNA damage, whereas NSUN5 deficiency increased CRC cells' sensitivity to the drug, both in vitro and in vivo. Mechanistically, NSUN5 upregulated BRCA2 and BRCA1-interacting helicase 1 (BRIP1) expression and interacted with these proteins to prevent cell death in response to DNA damage. Analysis of our local cohort and public data sets showed a positive correlation between NSUN5, BRCA2, and BRIP1 in CRC patients. Collectively, we uncover the role of NSUN5 in CRC progression from the perspective of chemotherapy resistance, potentially offering innovative insight on the clinical therapy and prognosis of CRC.

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Next Generation Sequencing Facilitates Quantitative Analysis of in 14-day-old wt, brm-1, brm-3, brip1, brip2, brip1 brip2, brip1 brip2 brm-3 and brip1 brip2 brm-1 seedlings.

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Methods: RNA from 14-day-old seedlings of wild-type, brip1, brip2, brm-3, brm-1, brip1 brip2, brip1 brip2 brm-3 and brip1 brip2 brm-1 was isolated using the RNAprep Pure Plant Kit as described above. RNAs from three biological replicates was sequenced separately at Novogene, using Illumina Hiseq X-Ten (Sequencing method: Hiseq-PE150). Results: Reads were mapped to the TAIR10 Arabidopsis genome using TopHat (Galaxy V2.1.1 in usegalaxy.org) with default settings, except that a minimum intron length of 20 bp and a maximum intron length of 4,000 bp were required (Paired-end). Then, mapped reads were assembled according to TAIR10 version of genome annotation using cufflinks (version 2.1.1) with default settings. To analyze differential expression, the assembled transcripts from three independent biological replicates in Col and other mutants were included and compared using Cuffdiff (version 2.1.1) with default settings. Conclusions: Our study represents the first detailed analysis of brip1, brip2, brip1 brip2 transcriptomes, with biologic replicates, generated by RNA-seq technology.

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NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_1.

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Project description:NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_3.

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