Analysis of cellular and exosomal miRNAs in MCF7 cells regulated by LSD1 (miRNA-Seq)
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PROVIDER: PRJNA1103812 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of exosomal miRNAs in MCF7 cells regulated by LSD1
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Project description:Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates metastasis in luminal breast cancer. Exosomes play a major role in cell-to-cell communication. Thus, the characterization of miRNAs of exosome in MCF7 cells regulated by LSD1 is imperative in clarifying intercellular signaling.
2024-03-04 | GSE212291 | GEO
Project description:Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates metastasis in luminal breast cancer. Thus, the characterization of miRNAs in MCF7 cells regulated by LSD1 is imperative in clarifying intercellular signaling.
2024-03-04 | GSE218200 | GEO
Project description:Lysine-specific demethylase 1 (LSD1), a histone demethylating enzyme, plays a crucial role in cancer metastasis. While studies have demonstrated that the knockout of LSD1 significantly enhances lung metastasis of breast cancer cells, it remains unclear whether LSD1-deficient breast cancer cells can remodel the lung microenvironment to allow metastasis. In this study, we isolated exosomes from LSD1-knockdown breast cancer cells (LSD1 KD) and investigated their effects on the formation of pre-metastatic niches. The intravenous injection of exosomes from LSD1 KD cells in mice resulted in a substantial increase in lung colonization by breast cancer cells, while treatment with exosomes derived from LSD1 KD cells decreased the expression of the tight junction proteins ZO-1 and occludin in vascular endothelial cells, leading to increased pulmonary vascular permeability. In addition, the knockdown of LSD1 reduced the expression of the circular RNA circDOCK1, which augmented the levels of miR-1270 in exosomes. Further investigation showed that miR-1270 inhibited ZO-1 expression in human umbilical vein endothelial cells, which enhanced their permeability. In conclusion, our study uncovered a novel mechanism in which the epigenetic modifier LSD1 promotes the formation of pre-metastatic niches via the regulation of exosomal miRNA.
2024-09-12 | GSE264698 | GEO
Project description:Analysis of miRNAs in MCF7 cells regulated by LSD1
| PRJNA902734 | ENA
Project description:Lysine-specific demethylase 1 (LSD1), a histone demethylating enzyme, plays a crucial role in cancer metastasis. While studies have demonstrated that the knockout of LSD1 significantly enhances lung metastasis of breast cancer cells, it remains unclear whether LSD1-deficient breast cancer cells can remodel the lung microenvironment to allow metastasis. In this study, we isolated exosomes from LSD1-knockdown breast cancer cells (LSD1 KD) and investigated their effects on the formation of pre-metastatic niches. The intravenous injection of exosomes from LSD1 KD cells in mice resulted in a substantial increase in lung colonization by breast cancer cells, while treatment with exosomes derived from LSD1 KD cells decreased the expression of the tight junction proteins ZO-1 and occludin in vascular endothelial cells, leading to increased pulmonary vascular permeability. In addition, the knockdown of LSD1 reduced the expression of the circular RNA circDOCK1, which augmented the levels of miR-1270 in exosomes. Further investigation showed that miR-1270 inhibited ZO-1 expression in human umbilical vein endothelial cells, which enhanced their permeability. In conclusion, our study uncovered a novel mechanism in which the epigenetic modifier LSD1 promotes the formation of pre-metastatic niches via the regulation of exosomal miRNA.
2024-09-12 | GSE264699 | GEO
Project description:Analysis of cellular and exosomal circRNAs in MCF7 cells regulated by LSD1 (RNA-Seq)
| PRJNA1103819 | ENA
Project description:Exosomal miRNAs from serum sequencing
| PRJNA1100526 | ENA
Project description:Metastasis accounts for almost 90% of breast cancer-related fatalities, making it frequent malignancy and the main reason of tumor mortality globally among women. A key player in breast cancer is the histone demethylase lysine-specific demethylase 1 (LSD1). We used LSD1 knockdown MCF7 and T47D cell exosomes to treat breast cancer cells for greatly increasing the invasion and migration of breast cancer cells for evaluating the impact of LSD1 on breast cancer invasion and migration. miR-1290 expression was downregulated in LSD1 knockdown MCF7 exosomes. Furthermore, miR-1290 could control NAT1 expression by looking through the database of miR-1290 target genes. These data provide fresh insights into the biology of breast cancer therapy by demonstrating how the epigenetic factor LSD1 stimulates the breast cancer cells’ invasion and migration via controlling exosomal miRNA.
2024-07-31 | GSE266982 | GEO
Project description:Introduction: Mesenchymal stem cells (MSCs) are commonly known to influence the progression of cancer due to their ability to migrate to the tumor microenvironment and interact with cancer cells. Exosomes have been found secreted by most cell types and have been shown to act as cargo carrying biomolecules including microRNA (miRNAs). Thus, understanding interaction between MSCs and cancer cells via exosomal miRNAs is crucial in determining the therapeutic role of MSC in treating breast cancer cells and relapse. Methods: Exosomes were harvested from the medium of indirect co-culture of MCF7-luminal and MDA-MB-231-basal breast cancer cells (BCCs) subtypes with adipose MSCs and profiled for miRNAs using next-generation sequencing. Results: The interaction resulted in the changes of exosomal miRNAs profiles that modulate essential signalling pathways and cell cycle arrest into dormancy via inhibition of epithelial-to-mesenchymal transition (EMT). The maintenance and induction of epithelial features in MCF7 and MDA cells have led to a positive correlation with the reduction of proliferation and metastasis as well as increased drug resistance. Overall, adipose MSCs mediated delivery of consensus miRNAs particularly miR-200 family in MCF7, miR-146a in MDA and miR-941 in both BCCs subtypes via exosomes.
2020-08-18 | GSE156380 | GEO