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Transcriptome changes after curcumin analog treatment in HER2+ breast cancer cells

ABSTRACT: Transcriptome changes after curcumin analog treatment in HER2+ breast cancer cells

PROVIDER: PRJNA901937 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22299998_1.fastq.gz	Fastqsanger.gz
	SRR22299998_2.fastq.gz	Fastqsanger.gz
	SRR22299999_1.fastq.gz	Fastqsanger.gz
	SRR22299999_2.fastq.gz	Fastqsanger.gz

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Transcriptome changes after curcumin analog treatment in HER2+ breast cancer cells

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Transcriptomic changes induced by Curcumin loaded solid nanoparticles and radiation in breast cells

Project description:In breast cancer (BC) care, radiotherapy is considered an efficient treatment. However, approximately 90% of BC-related deaths are due to the metastatic tumor progression. Then, it is strongly desirable to improve tumors radiosensitivity using molecules with synergistic action. In this study, we developed curcumin-loaded solid nanoparticles (Cur-SLN) in order to increase curcumin bioavailability and evaluated their radiosensitizing ability in comparison to curcumin free (Cur), by using an in vitro approach on BC models. Precisely, here we analyzed the transcriptomic profiles induced by Cur-SLN treatments, in non tumorigenic MCF10A and tumorigenic MCF7 and MDA-MB-231 BC cell lines, highlighting the networks responsible of its radiosensitization ability. Curcumin loaded- SLN can be suggested in future preclinical and clinical studies to test its concomitant use during radiotherapy treatments with the double implications of being a radiosensitizing molecule against cancer cells, with a protective role against IR side effects.

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Project description:HER2-targeted therapies including antibody drug conjugates have shown great efficacy in HER2-positive breast cancer. However, resistance to treatment in part due to pre-existing HER2 heterogeneity (HET) is a significant clinical challenge and requires the use of rationally-designed combination therapies. Here we describe transcriptomic profiling of 287 biopsies from 129 patients in a phase II neoadjuvant clinical trial using a combination of T-DM1 and pertuzumab for early-stage HER2-positive breast cancer, we investigated the mechanisms driving T-DM1 resistance. In pre-treatment tumors from patients without a complete response (pCR), distinct molecular features were identified: HER2 HET tumors retained PI3K pathway activation and a basal-like phenotype, while HER2 Non-HET tumors exhibited lower PI3K pathway enrichment. T-DM1 treatment universally reduced HER2 protein expression and copy number heterogeneity while increasing PI3K pathway enrichment and luminal identity in residual tumors. Importantly, HER2 HET tumors showed minimal transcriptomic response compared to HER2 Non-HET tumors, in line with the lesser clinical response. The response to T-DM1 was not associated with hotspot PIK3CA/ERBB2 mutations but rather correlated with immune infiltration. HER2 Non-HET tumors exhibited less effective immune surveillance at baseline but became immune activated with T-DM1 treatment, while HER2 HET tumors exhibited a more immune suppressed microenvironment upon treatment. Our study highlights the multifaceted nature of T-DM1 resistance driven by HER2 heterogeneity and provides essential evidence for optimizing therapeutic strategies for these patients.

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