Project description:Analysis of human triple-negative breast cancer cells (TNBCs) which have high NF-kB activity. Proteins derived from NF-κB target genes might be molecular targets for cancer therapy. Results provide new insights into tumor proliferation mechanisms.
Project description:This SuperSeries is composed of the following subset Series: GSE21719: Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (miRNA study) GSE21832: Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (gene expression) Refer to individual Series
Project description:Analysis of human triple-negative breast cancer cells (TNBCs) which have high NF-kB activity. Proteins derived from NF-κB target genes might be molecular targets for cancer therapy. Results provide new insights into tumor proliferation mechanisms. Exp. 1: Mock MDA-MB-436 cells vs. MDA-MB-436 cells infected with Adenovirus-IkBaSR; Exp. 2: MDA-MB-436 cells infected with Adenovirus-GFP vs. MDA-MB-436 cells infected with Adenovirus-IkBaSR.
Project description:EZH2 has been studied most extensively in the context of PRC2-dependent gene repression. Paradoxically, accumulating evidence indicates non-canonical functions for EZH2 in cancer contexts including promoting gene expression in triple negative breast cancer (TNBC) cells through interactions with the transcription factor NF-kB. We define a genomic profile of EZH2 and NF-kB factor RelA, RelB, and NFKB2/p52 co-localization and positive regulation of a subset of NF-kB targets and genes associated with oncogenic functions in TNBC, which is enriched in patient datasets. We demonstrate interaction between EZH2 and RelA requiring the recently identified EZH2 transactivation domain (TAD), which mediates EZH2 recruitment to and activation of certain NF-kB-dependent genes, and supports downstream stemness phenotypes in TNBC cells. Interestingly, EZH2-NF-kB positive regulation of genes and stemness does not require PRC2. This study provides new insight into pro-oncogenic regulatory functions for EZH2 in breast cancer through PRC2-independent, and NF-kB-dependent regulatory mechanisms.
Project description:Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (gene expression)
Project description:The high-throughput sequencing technology was performed after the treatment of human triple negative breast cancer cells MDA-MB-231 with the active compound D16 designed and synthesized by ourselves, to explore the expression of genes related to cell proliferation, adhesion, migration and invasion of human triple negative breast cancer cells MDA-MB-231 after the treatment of the active compound Changes to explore the effect of active compounds on the proliferation and motility of triple breast breast cancer cells and to find an interesting target gene, CKAP2.
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.
Project description:The high-throughput sequencing technology was performed after the treatment of human triple negative breast cancer cells MDA-MB-231 and BT549 with Lespedeza bicolor root extracted by ourselves, to explore the expression of genes related to cell proliferation, adhesion, migration and invasion of human triple negative breast cancer cells MDA-MB-231 and BT549 after the treatment of Lespedeza bicolor root changes, and to find an interesting target gene.
Project description:Twenty-four triple-negative breast cancer and 14 adjacent normal tissues were collected from breast cancer patients during surgeries at National Taiwan University Hospital (NTUH, Taipei, Taiwan). All triple-negative breast cancer samples were invasive ductal carcinomas (IDC) and were negative in immunohistochemical statuses of ER, PR, and HER2 receptors, as confirmed by professional pathologists. Treatment procedure of all patients followed the National Comprehensive Cancer Network (NCCN) guideline. All samples were neoadjuvant-free and were collected before systemic chemotherapy treatments. Written informed consent was obtained from all patients who participated in this study. Using human tissues for research in this study was approved by the institutional review board at NTUH. A novel set of 25-miRNA signature identified in this study was able to effectively distinguish between triple-negative breast cancer and adjacent normal tissues. Moreover, we documented the first evidence of seven polycistronic miRNA clusters preferentially harboring deregulated miRNA genes in triple-negative breast cancer.
