Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549 microRNA expression profiles were conpared between the luminal group and the TNBC group
Project description:Transgelin is a protein which has been described as a marker of several cancers. Interestingly, the literature describes both up- and down-regulation of transgelin in the tumor in comparison with non-tumor tissue. The mechanisms of transgelin function in cancer are considerably unknown. Transgelin is abundant especially in smooth muscle cells. It is associated with actin stress fibers. These contractile structures participate among others in cell motility, adhesion or morphology. We focused on transgelin function in breast cancer. Initially, we studied transgelin role in cell migration in the breast cancer cell lines BT 549 and PMC 42. Using xCELLigence system we reached opposite results in two cell lines. Transgelin silencing increased and decreased migration of PMC 42 and BT 549 cells, respectively. To further clarify these contradictory results, we performed an experiment to quantify proteomic changes after transgelin silencing in these two cell lines using quantitative proteomics (iTRAQ-2DLC-MS/MS). Our results confirmed transgelin function in the migration of BT 549 cells and suggested transgelin role in apoptosis and small molecule biochemistry in PMC 42 cells.
Project description:The aim was to identify genes that were commonly influenced by a siRNA targeting PRKCD in breast cancer cell lines. MDA-MB-468 and BT-549 breast cancer cell lines were treated with control siRNA or siRNA targeting PRKCD. Three samples in each group were analyzed.
Project description:The goal for this experiment was to analyze how knockdown of homeobox transcription factor Meox1 altered functional and mechanist biology of p53 and PTEN deficient triple negative breast cancer in vitro cell lines of claudin-low BT-549 and basal-like MDA-MB-468.
Project description:We analysed aquired chemotherapeutic resistance of two different triple negative breast cancer cell lines BT-549 (Doxorubicin resistance) and MDA-MB-468 (5-Fluorouracil) by comparing the proteome of the parental cell line with the resistant cell line.
Project description:The MUC1-C protein evolved in mammals for adaptation of barrier tissues to loss of homeostasis. Prolonged activation of MUC1-C in settings of chronic inflammation promotes lineage plasticity, epigenetic reprogramming and the cancer stem cell (CSC) state. The effects of MUC1-C on the metabolism of CSCs remain unexplored. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of BT-549 spheroid cultures with and without knockdown of MUC1 to examine the effects of MUC1 on CSC renewal and metbolic states.
Project description:Polyphyllin D (PD) is the active component from an Asian traditional medicinal herb Paris polyphylla, and has been found to hold significant anticancer activity in vivo or in vitro. However, the mechanism through which PD exerts its anticancer effects in triple-negative breast cancer (TNBC) remains unclear. Our study was presented to evaluate the anticancer effect and the potential mechanisms of PD in two TNBC cell lines, namely BT-549 and MBA-MB-231. Through comprehensively comparing the liquid chromatography-tandem mass spectrometry (LC-MS/MS) data of PD-treated and -untreated BT-549 and MBA-MB-231 cells, we found PD could activate oxidative phosphorylation pathway in BT-549 cells and inhibit spliceosome function in MDA-MB-231 cells, suggesting that the anticancer effect of PD may be cell type-specificity dependent. Moreover, we found that nodal modulator 2/3 (NOMO2/3) were down-regulated both in PD-treated BT-549 and MBA-MB-231 cells, suggesting NOMO2/3 may be the potential target of PD. Whether NOMO2/3 are the upstream modulators of oxidative phosphorylation pathway and Spliceosome need further validation. In conclusion, a comprehensive proteomics study was performed on PD-treated or untreated TNBC cells, revealing the anticancer mechanisms of PD.
Project description:BT-549 cells were treated with thymoquinone for 6 h and chromatin immune-precipitation (ChIP) was performed using anti- MBD1 antibody (Abcam, USA). Anti-MBD1 could precipitate specific genomic region, which are methylated. The ChIP products were sequenced by library construction and bioinformatics analysis. The gene ontology (GO) analysis for multiple pathways was performed. The genomic methylated regions affected by TQ treatment were identified.
Project description:Here, we examined the therapeutic utility of EC359 in improving the therapeutic efficacy of HDACi in TNBC models. BT-549 cells were treated with vehicle (DMSO), EC359, HDACi(Vorinostat), EC359+HDACi and the RNA was isolated and utilized for RNA-seq analysis. Our results demonstrated that the beneficial effect of the EC359+HDACi involves regulation of multiple genes that involved in several pathways including apoptosis, metabolism and cell cycle.
