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Exploring the Mechanism of Resistance to vincristine in Breast Cancer Cells through Transcriptome Sequencing Technology

ABSTRACT: Exploring the Mechanism of Resistance to vincristine in Breast Cancer Cells through Transcriptome Sequencing Technology

PROVIDER: PRJNA1007740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25713380_1.fastq.gz	Fastqsanger.gz
	SRR25713380_2.fastq.gz	Fastqsanger.gz
	SRR25713381_1.fastq.gz	Fastqsanger.gz
	SRR25713381_2.fastq.gz	Fastqsanger.gz

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Exploring the Mechanism of Resistance to vincristine in Breast Cancer Cells through Transcriptome Sequencing Technology

Project description:Breast cancer has replaced lung cancer as the leading cancer globally, but various chemotherapy drugs for breast cancer are prone to generate resistance, especially in patients with distant metastases who are susceptible to multiple chemotherapy drug resistance, these always leading to treatment failure. vincristine (VCR) is an alkaloid extracted from Catharanthus roseus and is often used in combination with other chemotherapy drugs to treat various types of cancer, including breast cancer. Recently, we conducted research on the development of resistance to VCR using transcriptome sequencing technology. Firstly, we used the gradient increase of VCR concentration to produce a VCR-resistant breast cancer cell line. Mechanistically, we further extracted RNA from the VCR-resistant breast cancer cell line and sequenced the transcriptome. Further analysis showed changes in various gene expression levels in the VCR-resistant breast cancer cell line. Meanwhile, the analysis of splicing events also indicated that variable splicing events change in the VCR-resistant breast cancer cell line. Further validation showed that multiple gene expression levels, including 1L1B, were altered in the VCR-resistant breast cancer cell line, and these gene expression changes were related to VCR resistance. Our results provide a theoretical basis for exploring the mechanism of VCR resistance clinically.

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Exploring the Mechanism of TACSTD2 Causing Cisplatin Resistance

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Transcription profiling of human ALL exhibiting cross-resistance to prednisolone, vincristine, asparaginase and daunorubicinchemotherapy cross-resistance and treatment response in childhood acute lymphoblastic leukemia

Project description:Acute lymphoblastic leukemia (ALL) can be cured with combination chemotherapy in over 75% of children, but the cause of treatment failure in the remaining patients is unknown. We determined the sensitivity of ALL cells to individual antileukemic agents in 441 patients, and used a genome-wide approach to identify 45 genes differentially expressed in ALL exhibiting cross-resistance to prednisolone, vincristine, asparaginase and daunorubicin. We also identified a distinct phenotype of discordant resistance to asparaginase and vincristine and 139 genes whose expression was associated with this novel phenotype. The expression of these genes discriminated treatment outcome in two independent patient populations, identifying a subset of patients with a markedly inferior outcome (37%Â±13% 5-year DFS).

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Gene expression signatures of chemotherapy-induced neuropathy induced by vincristine

Project description:Vincristine, oxaliplatin, and cisplatin are commonly prescribed chemotherapeutic agents for the treatment of several cancer types. However, a main side-effect is chemotherapy-induced peripheral neuropathy (CIPN), which may lead to decreased quality of life, changes in chemotherapeutic treatment or even treatment cessation. Although painful symptoms associated with CIPN are faithfully recapitulated by mouse models, there is limited knowledge of how these drugs affect the expression of genes in peripheral sensory neurons. The present study carried out a transcriptomic analysis of dorsal root ganglia isolated from mice treated with vincristine, oxaliplatin, and cisplatin with a view to gain insight into the comparative pathophysiological mechanisms of CIPN. RNA-Seq using 75-nucleotide single end runs revealed 368, 295 and 256 differential expressed genes (DEGs) induced by treatment with vincristine, oxaliplatin and cisplatin, respectively. Although there were many similarities in DEGs between chemotherapeutic agents, only 5 genes were dysregulated in all groups. Cell type enrichment analysis (CTEA) and gene set enrichment analysis (GSEA) showed predominant effects on genes associated with the immune system after treatment with vincristine, while oxaliplatin treatment affected mainly neuronal genes. Treatment with cisplatin resulted in a mixed inflammatory and neuropathic gene expression signature. Only ‘regulation of transport’ and ‘response to external stimuli’ were gene ontology terms shared between all treatments. These results provide insight into the recruitment of innate and adaptive immune responses to DRG tissue and indicate enhanced neuro-inflammatory processes following administration of vincristine, oxaliplatin, and cisplatin. These gene expression signatures may provide insight into novel drug targets for treatment of CIPN.

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