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Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown efficacy_UPF2 knockdown in EpCAMhi MDA-MB-231 breast cancer cell lines

ABSTRACT: Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown efficacy_UPF2 knockdown in EpCAMhi MDA-MB-231 breast cancer cell lines

PROVIDER: PRJNA657010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12447267_1.fastq.gz	Fastqsanger.gz
	SRR12447267_2.fastq.gz	Fastqsanger.gz
	SRR12447268_1.fastq.gz	Fastqsanger.gz
	SRR12447268_2.fastq.gz	Fastqsanger.gz
	SRR12447269_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown efficacy

Project description:New strategies for cancer immunotherapy are needed since most solid tumors do not respond to current approaches. Here, we used EpCAM aptamer-linked small interfering RNAs (aptamer-siRNA chimeras (AsiCs)) to knockdown genes selectively in EpCAM+ tumors with the goal of making cancers more visible to the immune system to improve anti-tumor immunity. Gene targets were chosen whose knockdown was predicted to promote tumor neoantigen expression (Upf2 and Parp1), phagocytosis and antigen presentation (Cd47), or cause tumor cell death (Mcl1). Using scRNA-seq, we showed that knocking down the four targets simutaeoulsy potently improved the anti-tumor immunity mediated T cells and macrophage/monocytes, demonstrating the immunostimulatory capacity of EpCAM-AsiCs.

2021-02-05 | GSE156214 | GEO

Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown efficacy

Project description:Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown efficacy

| PRJNA657057 | ENA

EpCAM-Aptamer Toxin Conjugates for targeting tumors

Project description:Neocarzinostatin (NCS) is an anti-tumor DNA damaging agent. Conjugating NCS with EpCAM Aptamer will direct the toxin pay loads to the EpCAM positive cancer cells as a targeted therapy We used microarrays to detail the global gene expression to understand the pathways involved in EpCAM-mediated NCS drug delivery in breast cancer cells.

2018-09-05 | GSE69160 | GEO

Preclinical targeted therapy for retinoblastoma using EpCAM Aptamer siRNA chimeras

Project description:siRNAs have played a major role in cancer drug discovery, but their potential is hampered due to off-target effects. Thus, delivery systems like RNA aptamers have been used to enhance the specific delivery of these siRNAs to cancer stem cells. We report the efficacy of three different EpCAM aptamer siRNA chimeras, which were investigated both in vitro and in vivo for their ability to reduce cancer cell progression. Using these chimeras, we demonstrated specific gene knockdown in EpCAM positive cells which ultimately led to the apoptosis. To study the efficacy of these aptamer chimeras in vivo, retinoblastoma xenografts bearing NCC Rb C 51 cells were created for the first time. Systemic administration of these aptamer chimeras reduced tumour growth to about 50%. We further investigated the central Role of PLK1 in Cancer Progression and demonstrated the anti-cancer effects of targeted EpCAM siPLK1 approach. Using SILAC-Mass spectrometry analysis, we showed that silencing PLK 1 gene can lead to p53 mediated cell cycle arrest. Thus, we establish EpCAM-siRNA chimeras as potential markers for targeted anti-cancer applications, which paves a platform for efficient second line of therapies in addition to existing chemotherapy options.

2022-03-02 | PXD008221 | Pride

Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown efficacy_UPF2 knockdown in EpCAMhi MDA-MB-231 breast cancer cell lines

Project description:Knocking down Upf2, which encodes a protein that binds to prematurely terminated mRNAs to activate NMD, has been postulated to induce tumor cell expression of neoantigens to promote tumor recognition by T cells. To investigate whether Upf2 knockdown in breast cancer generates novel mRNA isoforms, we performed bulk RNA sequencing (RNA-seq) to compare an EpCAMhi MDA-MB-231 human breast cancer cell line transfected with noncoding control or UPF2 siRNA for 72 h. Results: 222 examples of differential exon usage (DEU) within 281 genes were identified. The number and diversity of DEUs suggest that UPF2 knockdown could have caused novel alternative splicing. To test this idea, UPF2 knockdown-related transcriptional diversity was deconvoluted to identify and estimate the abundance of transcript isoforms. 42 genes with potential differential isoform usage (DIU) were identified. Collectively, our data suggest that reducing NMD activity by UPF2 knockdown may induce expression of tumor neoantigens.

2021-02-05 | GSE156185 | GEO

b1-integrin binding and lysosome targeting aptamer homes to triple-negative breast cancer in mice

Project description:Targeted therapies for triple-negative breast cancer have increased the number of available treatment options for patients. However, an optimal treatment strategy is still an unmet medical need due to the lack of targetable biomarkers and tumour heterogeneity. Aptamers have high selectivity and specificity towards target proteins. Lower molecular weight, increased stability, less immunogenicity, and rapid tissue uptake make aptamers an attractive alternative to antibodies. Attempts to develop aptamer therapeutics have shown difficulties translating in vitro results to in vivo. Aptamer GreenB1 exhibits selectivity to triple-negative MDA-MB-231 human breast cancer cell line in vitro compared to estrogen, progesterone, and glucocorticoid receptor-expressing MCF-7 human breast cancer cell line. The aptamer is rapidly internalised into cells and trafficked to lysosomes. Here, we identify 1-integrin as the target protein for GreenB1 using proximity labelling and mass spectrometry proteomics. GreenB1 homes preferentially to the tumour in the 4T1 triple-negative breast cancer mice model in vivo.

2023-08-24 | PXD034982 | Pride

Prognostic value of biomarkers EpCAM and B-crystallin is associated with lymphatic metastasis in breast cancer by iTRAQ analysis

Project description:Metastasis is responsible for the majority of deaths in a variety of cancer types, including breast cancer. Although several factors or biomarkers have been identified to predict the outcome of patients with breast cancer, few studies have been conducted to identify metastasis-associated biomarkers. Quantitative iTRAQ proteomics analysis was used to detect differentially expressed proteins between lymph node metastases and their paired primary tumor tissues from 23 patients with metastatic breast cancer. Immunohistochemistry was performed to validate the expression of two upregulated (EpCAM, FADD) and two downregulated (NDRG1, αB-crystallin) proteins in 190 paraffin-embedded tissue samples. These four proteins were further analyzed for their correlation with clinicopathological features in 190 breast cancer patients. We identified 637 differentially regulated proteins (397 upregulated and 240 downregulated) in lymph node metastases compared with their paired primary tumor tissues. Furthermore, bioinformatics analysis using GEO profiling confirmed the difference in the expression of EpCAM between metastases and primary tumors tissues. Two upregulated (EpCAM, FADD) and two downregulated (NDRG1, αB-crystallin) proteins were associated with the progression of breast cancer. Obviously, EpCAM plays a role in the metastasis of breast cancer cells to the lymph node. We further identified αB-crystallin as an independent biomarker to predict lymph node metastasis and the outcome of breast cancer patients.

2019-08-29 | PXD013931 | Pride

Immunotherapy for breast cancer using EpCAM aptamer tumor-targeted gene knockdown.

Project description:New strategies for cancer immunotherapy are needed since most solid tumors do not respond to current approaches. Here we used epithelial cell adhesion molecule EpCAM (a tumor-associated antigen highly expressed on common epithelial cancers and their tumor-initiating cells) aptamer-linked small-interfering RNA chimeras (AsiCs) to knock down genes selectively in EpCAM+ tumors with the goal of making cancers more visible to the immune system. Knockdown of genes that function in multiple steps of cancer immunity was evaluated in aggressive triple-negative and HER2+ orthotopic, metastatic, and genetically engineered mouse breast cancer models. Gene targets were chosen whose knockdown was predicted to promote tumor neoantigen expression (Upf2, Parp1, Apex1), phagocytosis, and antigen presentation (Cd47), reduce checkpoint inhibition (Cd274), or cause tumor cell death (Mcl1). Four of the six AsiC (Upf2, Parp1, Cd47, and Mcl1) potently inhibited tumor growth and boosted tumor-infiltrating immune cell functions. AsiC mixtures were more effective than individual AsiC and could synergize with anti-PD-1 checkpoint inhibition.

| S-EPMC7936362 | biostudies-literature

EpCAM expressing Hs578T cells

2010-12-02 | GSE25743 | GEO

EpCAM expressing Hs578T cells

Project description:EpCAM is frequently overexpressed in human invasive breast cancer. We reported EpCAM overexpression to be an independent prognostic marker for poor overall survival in node-positive breast cancer. We used microarrays in order to investigate changes of the transcriptome on EpCAM gene overexpression in human breast cancer cells Hs578T cells were found to express only very little EpCAM mRNA and protein in comparison to established and well characterized breast cancer cell lines such as MCF-7 or SK-BR-3. Hs578T cells were stably transfected with the EpCAM cDNA containing construct pIRESpuro3_EpCAM and the respective empty vector control.

2010-12-02 | E-GEOD-25743 | biostudies-arrayexpress

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