Project description:To investigate and determine the role of EPIC1 overexpression in cancer cells, we established EPIC1 overexpressing MCF7 stable cells.
Project description:Methylated DNA binding protein 2 (MBD2) has been shown to bind specific methylated promoters and suppress transcription. Here we systematically investigate MBD2 suppression by overexpressing MBD2 in MCF-10A cells and generating gene expression profiles of overexpressing cells and normal MCF-10A cells.
Project description:In an integrated analysis of long noncoding RNA (lncRNA) epigenetic alterations in 6475 tumor samples and 781 cancer cell lines, we characterized the epigenetic landscape for 1,006 epigenetically activated and 1,117 epigenetically silenced lncRNAs across 20 cancer types. Combining bioinformatics analyses and functional validation, we identified epigenetically induced lncRNA 1 (EPIC1) as a potential oncogene. EPIC1 is epigenetically activated in 15 cancer types and correlated with poor survival of breast cancer. In EPIC1 hypermethylated cancer cell lines, its expression can be induced by demethylating agent in a time- and dose-dependent manner. Knockdown of EPIC1 inhibits MYC targets expression, leads to cell cycle arrest, inhibits colony formation, and decreases cancer cell growth in vitro and in vivo. Mechanistically, EPIC1 directly interacts with MYC 148-220 aa region through its 5’ end. Overexpression of EPIC1 increases MYC targets expression and promotes cell proliferation, which can be abolished by the MYC knockdown.
Project description:Methylated DNA binding protein 2 (MBD2) has been shown to bind specific methylated promoters and suppress transcription. Here we systematically investigate MBD2 suppression by overexpressing MBD2 in MCF-10A cells and generating gene expression profiles of overexpressing cells and normal MCF-10A cells. MCF-10A cells were infected with MBD2 lentivirus in order to increase MBD2 expression. Total RNA was extracted from both infected and non-infected cells and hybridized to Affymetrix gene expression microarrays. Three technical replicates were hybridized for infected and non-infected cells.
Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer. Breast cancer MCF-7 cells (MCF-V5) overexpressing ANXA1 were cultured for RNA extraction and hybridization on Affymetrix miRNA microarrays. These were compared against the control, which were MCF-7 cells (MCF-EV) carrying an empty expression vector. Expression analyses were carried out in triplicates
Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer.
Project description:To investigate and determine the function of EPIC1 in cancer cells, we knockdown EPIC1 in Hs578T, A2780, and A2780cis cells using siRNA.
Project description:Human EMT PCR array Real-time quantitative PCR analysis of human EMT genes in PCR array data for expression of EMT genes in MCF-7 cells, upon treatment with exosomes released from TSP5-overexpressing human primary adipocytes (ND; ABM-007), compared to exosomes released from matched control adipocytes transduced with control lentiviral vector [Data S5] PCR array data for expression of EMT genes in MCF-7 cells after treating with TSP5 overexpressing cells' exosomes