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Novel long non‐coding RNA 005620 induces epirubicin resistance of triple-negative breast cancer via regulating ITGB1 expression

ABSTRACT: Novel long non‐coding RNA 005620 induces epirubicin resistance of triple-negative breast cancer via regulating ITGB1 expression

PROVIDER: PRJNA638080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11952700_1.fastq.gz	Fastqsanger.gz
	SRR11952700_2.fastq.gz	Fastqsanger.gz
	SRR11952701_1.fastq.gz	Fastqsanger.gz
	SRR11952701_2.fastq.gz	Fastqsanger.gz
	SRR11952702_1.fastq.gz	Fastqsanger.gz

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Novel long non‐coding RNA 005620 induces epirubicin resistance of triple-negative breast cancer via regulating ITGB1 expression

Project description:In this study, a total of 12 differentially expressed lncRNAs were established through lncRNA sequencing analysis. Lnc005620 is one of the novel intronic lncRNAs which is highly expressed in Epi-R MDA-MB-231. Lnc005620 is an important lncRNA that leads to the resistance of Epirubicin in triple negative breast cancer by integrin β1.

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Novel Long Noncoding RNA 005620 Induces Epirubicin Resistance in Triple-Negative Breast Cancer by Regulating ITGB1 Expression.

Project description:Triple-negative breast cancer (TNBC) is often treated with anthracyclines (e.g., epirubicin or doxorubicin), but very little is known about anthracycline resistance, especially epirubicin resistance in TNBC. To identify novel long noncoding RNAs (lncRNAs) involved in epirubicin resistance in TNBC, we established a new TNBC MDA-MB-231 cell line that was resistant to epirubicin (Epi-R). A total of 12 differentially expressed lncRNAs were identified using RNA sequencing analysis of Epi-R cells. Among these lncRNAs, we found a novel intronic lncRNA, lnc005620, was highly expressed in Epi-R cells and human TNBC tissues. Further gain- and loss-of-function studies demonstrated that lnc005620 played an oncogenic role and partially abrogated the effects of epirubicin on TNBC cells. Using iTRAQ proteomics analysis, we found that three members of the integrin family, integrin β4, integrin β1 and integrin α6, were all upregulated in Epi-R MDA-MB-231 cells. Integrin β1, encoded by the ITGB1 gene, was validated to be a downstream target of lnc005620 in Epi-R MDA-MB-231 cells. Our study demonstrates that novel lnc005620 promotes TNBC progression and chemoresistance to epirubicin via integrin β1 both in vitro and in vivo and provides a promising therapeutic target for TNBC patients in terms of enhancing the benefits of epirubicin treatment.

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Project description:Triple-negative breast cancer (TNBC) is notoriously difficult to treat due to the lack of biological targets and poor sensitivity to conventional therapies. Chemotherapy is the main clinical therapy, but the effective screening strategy for chemotherapy drugs is poorly investigated. Drug repositioning has been the center of attention in recent years attracting numerous studies. Here, we firstly found multiple common features between leukemia and TNBC by analyzing the global transcriptome profiles based on the transformed comparison data from NCI60. Therefore, we investigated the role of the classic leukemia drug thioguanine (6-TG) in TNBC cancer cells. Our results indicated that 6-TG inhibited cell proliferation and tumor cell progression by suppressing PI3K-AKT pathway via downregulating the DNA methylation level of PTEN. Moreover, apoptosis was induced via the activation of PI3K-AKT downstream TSC1 and the downregulation of methylation levels of DAXX, TNF, FADD and CASP8 etc. These findings indicated 6-TG exerts its anti-tumor effects in vitro and in vivo through regulating the DNA methylation levels of genes involved in PI3K-AKT and apoptosis pathway. Meanwhile, our study suggested that transcriptome-based drug screening has potential implications for breast cancer therapy and drug selection.

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Basal epithelial subpopulations underlie and predict chemotherapy resistance in Triple-Negative Breast Cancer

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