Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA187192 | ENA |
REPOSITORIES: ENA
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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
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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 | GSE274815 | 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.
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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:The transcription regulator High Mobility Group AT-Hook 2 (HMGA2) plays an important role in many types of cancers, but the molecular mechanisms are not fully elucidated. We found by knock-down studies that HMGA2 controls expression of ATF4 and the enzymes in the serine synthesis pathway in triple negative breast cancer cells, and that HMGA2 expression correlates with poor clinical outcome in ER negative breast cancers. Furthermore, we found that the metabolism was dysregulated in cells with reduced HMGA2 expression, which affected their response to mitochondrial stressors and to changed carbon sources. Altogether, our findings demonstrate that HMGA2 is a regulator of serine biosynthesis and metabolism, consistent with the well-known role of HMGA2 as a regulator of proliferation, epithelial-mesenchymal transition and stemness.
2019-12-31 | GSE118857 | GEO
Project description:S-adenosylmethionine (SAM) treatment attenuates breast cancer growth, invasion, metastasis
| PRJNA384524 | ENA