Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA187192 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:HMGA2, Tet1 and HOXA9 are all regulated human breast tumorigenesis. We use gene expression array analysis to identify and compare the genes regulated by HMGA2, Tet1 and/or HOXA9 in human breast cancer cells.
2013-06-03 | GSE43741 | GEO
Project description:Triple-negative breast cancer (TNBC), the most lethal breast cancer subtype, demonstrates poor prognosis due to its high rates of metastasis, recurrence, and mortality. The metastatic potential in TNBC patients serves as a critical determinant of clinical outcomes. The high mobility group AT-hook 2 (HMGA2) has emerged as a novel chromatin architectural regulator, its specific role in TNBC metastasis requires further investigation.To investigate the mechanism of HMGA2 regulation of TNBC metastasis,we performed RNA-sequencing using shNC or shHMGA2 from MDA-MB-231 cells.
2025-06-16 | GSE296619 | GEO
Project description:HMGA2 has been implicated in tumor progression. Identification of microRNAs regulated by HMGA2 helps us to understand how HMGA2 regulates tumor metastasis via its downstream target mircoRNAs and genes. Total RNA was extracted from 1833 cells with control or depleted HMGA2 expression, respectively. Exiqon miRCURY LNA 5th generation expression array was performed to identify the microRNAs regulated by HMGA2.
2014-06-01 | E-GEOD-43739 | biostudies-arrayexpress
Project description:HMGA2 has been implicated in tumor progression. Identification of microRNAs regulated by HMGA2 helps us to understand how HMGA2 regulates tumor metastasis via its downstream target mircoRNAs and genes.
2014-06-01 | GSE43739 | GEO
Project description:Previously considered “housekeeping” genes, small nucleolar RNAs (snoRNAs) are increasingly understood to have wide-ranging functions in cancer, yet their role in metastasis remains unknown. Here, we identify the snoRNA Snord67 as a regulator of lymph node (LN) metastasis in female breast cancer. Snord67 expression is enriched in LN metastases in an immune-competent mouse model of breast cancer. In an orthotopic breast cancer model, loss of Snord67 decreases LN metastasis. In a model of lymphatic metastasis, Snord67 loss decreases LN tumor growth and distant metastases. In breast cancer cell lines, Snord67 knockout results in loss of targeted 2′-O-methylation on U6 small nuclear RNA, as well as widespread changes in splicing. Together, these results demonstrate that Snord67 regulates splicing and promotes the growth of LN metastases and subsequent spread to distant metastases. SnoRNA-guided modifications of the spliceosome and regulation of splicing may represent a previously unappreciated, potentially targetable pathway in cancer.
2025-03-15 | GSE269267 | GEO
Project description:Previously considered “housekeeping” genes, small nucleolar RNAs (snoRNAs) are increasingly understood to have wide-ranging functions in cancer, yet their role in metastasis remains unknown. Here, we identify the snoRNA Snord67 as a regulator of lymph node (LN) metastasis in female breast cancer. Snord67 expression is enriched in LN metastases in an immune-competent mouse model of breast cancer. In an orthotopic breast cancer model, loss of Snord67 decreases LN metastasis. In a model of lymphatic metastasis, Snord67 loss decreases LN tumor growth and distant metastases. In breast cancer cell lines, Snord67 knockout results in loss of targeted 2′-O-methylation on U6 small nuclear RNA, as well as widespread changes in splicing. Together, these results demonstrate that Snord67 regulates splicing and promotes the growth of LN metastases and subsequent spread to distant metastases. SnoRNA-guided modifications of the spliceosome and regulation of splicing may represent a previously unappreciated, potentially targetable pathway in cancer.
2025-03-15 | GSE274590 | GEO
Project description:Previously considered “housekeeping” genes, small nucleolar RNAs (snoRNAs) are increasingly understood to have wide-ranging functions in cancer, yet their role in metastasis remains unknown. Here, we identify the snoRNA Snord67 as a regulator of lymph node (LN) metastasis in female breast cancer. Snord67 expression is enriched in LN metastases in an immune-competent mouse model of breast cancer. In an orthotopic breast cancer model, loss of Snord67 decreases LN metastasis. In a model of lymphatic metastasis, Snord67 loss decreases LN tumor growth and distant metastases. In breast cancer cell lines, Snord67 knockout results in loss of targeted 2′-O-methylation on U6 small nuclear RNA, as well as widespread changes in splicing. Together, these results demonstrate that Snord67 regulates splicing and promotes the growth of LN metastases and subsequent spread to distant metastases. SnoRNA-guided modifications of the spliceosome and regulation of splicing may represent a previously unappreciated, potentially targetable pathway in cancer.
2025-03-15 | GSE274815 | GEO
Project description:CdGAP/ARHGAP31 is a molecular target of TGFb-mediated EMT and required for Her2-positive breast cancer growth and metastasis Metastasis is the leading cause of death in breast cancer patients. The epithelial-to-mesenchymal transition (EMT) has a crucial role in metastasis and is highly critical for tumor cell dissemination. CdGAP/ARHGAP31 is highly expressed in breast cancer tissues and is associated with poor clinical outcome in breast cancer patients. CdGAP cooperates in a GAP-independent manner with the transcriptional repressor Zeb2 to function as a critical modulator of breast cancer through repression of E-cadherin transcription. In this study, we used a murine model of Her2+ breast cancer to investigate further the role of CdGAP in breast tumorigenesis. We found that CdGAP was essential for tumor formation and metastasis to the lungs in the Her2+ mouse breast cancer model. We determined that CdGAP is required for intravasation and growth at the metastatic sites. By using global gene expression approaches, we found that CdGAP depletion in Her2+ primary tumors was associated with an EMT signature, including a decreased expression of the metastatic factor claudin-2 and an increase in E-cadherin expression. In Her2+ breast cancer cells, CdGAP expression is positively regulated by the TGFb canonical pathway in a smad-dependent manner and regulates cell proliferation, migration, invasion, and adhesion. CdGAP was found to interact with the focal adhesion protein Talin and regulates focal adhesion dynamics in breast cancer cells. Collectively, CdGAP appears as a potential anti-metastatic target for the treatment of Her2+ breast cancer.
2023-07-13 | GSE167457 | GEO
Project description:S-adenosylmethionine (SAM) treatment attenuates breast cancer growth, invasion, metastasis
| PRJNA384524 | ENA
Project description:DNA hypermethylation is known to contribute to the formation of cancer. However, DNA hypomethylation has received far less attention and the factors controlling the balance between hypo and hypermethylation and its impact on tumorigenesis remains unclear. Triple negative breast cancer (TNBC), a subtype of breast cancer that does not overexpress the hormone receptors or HER2/NEU, is one of the most hypomethylated cancers observed. Importantly, TNBCs are often a therapeutic challenge because of advanced presentation and lack of targeted therapies. TET1 is a DNA demethylase that regulates DNA methylation, hydroxymethylation and gene expression. We found that TET1 is specifically overexpressed in TNBC, where it is associated with hypomethylation and a worse overall survival. Further, we uncover an intricate network connecting TET1 expression to maintaining activation of cancer specific pathways, including PI3K, EGFR and PDGF. In TET1 KO cells, we observed reduced phospho-4EBP1 and decreased expression of genes in the PI3K pathway, suggesting loss of PI3K-mTOR activity is concomitant with loss of TET1. Additionally, TET1 KO cells have reduced cellular proliferation and migration. Our work establishes TET1 as an oncogene that contributes to the aberrant hypomethylation observed in cancer and suggests TET1 could serve as a novel druggable target for therapeutic intervention.
2018-06-26 | GSE100483 | GEO