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Effects of iron modulation on mesenchymal stem cell-induced drug resistance in estrogen receptor-positive breast cancer

ABSTRACT: Effects of iron modulation on mesenchymal stem cell-induced drug resistance in estrogen receptor-positive breast cancer

PROVIDER: PRJNA804240 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17923000.fastq.gz	Fastqsanger.gz
	SRR17923001.fastq.gz	Fastqsanger.gz
	SRR17923002.fastq.gz	Fastqsanger.gz
	SRR17923003.fastq.gz	Fastqsanger.gz
	SRR17923004.fastq.gz	Fastqsanger.gz

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Effects of iron modulation on mesenchymal stem cell-induced drug resistance in estrogen receptor-positive breast cancer

Project description:Patients with estrogen-receptor-positive (ER+) breast cancer, the most common subtype, remain at risk for lethal metastatic disease years after diagnosis. Recurrence arises partly because tumor cells in bone marrow become resistant to estrogen-targeted therapy. Here, we utilized a co-culture model of bone marrow mesenchymal stem cells (MSCs) and ER+ breast cancer cells to recapitulate interactions of cancer cells in bone marrow niches. ER+ breast cancer cells in direct contact with MSCs acquire cancer stem-like (CSC) phenotypes with increased resistance to standard antiestrogenic drugs. We confirmed that co-culture with MSCs increased labile iron in breast cancer cells, a phenotype associated with CSCs and disease progression. Clinically approved iron chelators and in-house lysosomal iron-targeting compounds restored sensitivity to antiestrogenic therapy. These findings establish iron modulation as a mechanism to reverse MSC-induced drug resistance and suggest iron modulation in combination with estrogen-targeted therapy as a promising, translatable strategy to treat ER+ breast cancer.

2022-07-21 | GSE196312 | GEO

Effects of iron modulation on mesenchymal stem cell-induced drug resistance in estrogen receptor-positive breast cancer.

Project description:Patients with estrogen receptor-positive (ER+) breast cancer, the most common subtype, remain at risk for lethal metastatic disease years after diagnosis. Recurrence arises partly because tumor cells in bone marrow become resistant to estrogen-targeted therapy. Here, we utilized a co-culture model of bone marrow mesenchymal stem cells (MSCs) and ER+ breast cancer cells to recapitulate interactions of cancer cells in bone marrow niches. ER+ breast cancer cells in direct contact with MSCs acquire cancer stem-like (CSC) phenotypes with increased resistance to standard antiestrogenic drugs. We confirmed that co-culture with MSCs increased labile iron in breast cancer cells, a phenotype associated with CSCs and disease progression. Clinically approved iron chelators and in-house lysosomal iron-targeting compounds restored sensitivity to antiestrogenic therapy. These findings establish iron modulation as a mechanism to reverse MSC-induced drug resistance and suggest iron modulation in combination with estrogen-targeted therapy as a promising, translatable strategy to treat ER+ breast cancer.

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Estrogen-induced lncRNA, LINC02568, promotes estrogen receptor-positive breast cancer development and drug resistance through both in trans- and in cis-mechanisms

Project description:Estrogen and estrogen receptor (ER) signaling play critical roles in the development of ER-positive breast cancer, and endocrine therapy is the frontline treatment for ER-positive breast cancer patients. However, the primary and acquired resistance to endocrine therapy including tamoxifen and fulvestrant remains as the major challenge in the clinic. Here, we identified an estrogen-induced lncRNA, LINC02568, through transcriptomic analysis, which is highly expressed in ER-positive breast cancer. LINC02568 is functional important in ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo as well as endocrine therapy resistance. Mechanically, we demonstrated that LINC02568 regulates, in trans, estrogen/ERα-induced gene transcriptional activation by sponging miR-1233-5p to stabilize ESR1 mRNA in the cytoplasm. Meanwhile, LINC02568 contributes to tumor-specific pH homeostasis in breast cancer cells by regulating CA12 in cis in the nucleus. The dual functions of LINC02568 together contribute to breast cancer cell growth and tumorigenesis as well as endocrine therapy resistance. Antisense oligonucleotides (ASO) targeting LINC02568 significantly inhibits ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo as well as resensitize tamoxifen-resistant cells to tamoxifen. Furthermore, combination treatment with ASO targeting LINC02568 and tamoxifen exhibits synergistic effect on tumor growth. Taken together, our findings revealed dual mechanisms of LINC02568 in regulating ERα signaling and pH homeostasis in ER-positive breast cancer, and indicated that targeting LINC02568 might represent a potential therapeutic avenue in clinic.

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Comparison between Estrogen receptor positive and Estrogen receptor negative breast cancer samples

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Discovery dataset on tamoxifen treated Estrogen Receptor (ER) positive breast cancer patients

Project description:56 estrogen receptor positive breast cancer tissues from patients treated with tamoxifen upon recurrence (32 Good outcome vs 24 Poor outcome) have been microdissected to obtain a pure population of epithelial tumor cells. Breast tumor enriched tissues have been sonicated and proteins have been in-solution digested and analyzed via a LTQ-Orbitrap coupled online with a nano-LC system. Thermo output .RAW files were analyzed through MaxQuant (version 1.4.1.2) using the human proteome FASTA (version 2012-09, human canonical proteome) as search library.

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