Project description:Long non-coding Rnas (lncRNAs) can act as oncogenes or tumor suppressors to regulate cancer development. We found that CYP1B1-AS1 was down-regulated in breast cancer tissues and correlated with the prognosis of patients. Lentiviral vectors were used to overexpress CYP1B1-AS1 in MCF7 cells, and the target proteins bound to CYP1B1-AS1 were detected by pulldown assay and mass spectrometry. The function of CYP1B1-AS1 is unknown. Our study revealed the molecular mechanism of CYP1B1-AS1 inhibiting breast cancer proliferation in breast cancer, and provided a new strategy for the treatment of breast cancer targeting lncRNA.
Project description:We recently showed that inactivation of the WASF3/WAVE3 gene in breast cancer cells results in loss of cell motility and invasion in vitro and metastasis in vivo. To obtain a better understanding of molecular mechanisms of action of WASF3, we have established the stable WASF3 overexpressing T47D cells using lentiviral infect system. We used miRNA microarrays to detail the global programme of miRNA expression after overexpression of WASF3 and identified distinct classes of up or down-regulated metastmir associated with breast cancer cell migration and motility invasion
Project description:The exact role of prolactin on breast cancer still remains unclear. Clues supportive or unsurpportive for prolactin to be cancer driver are confusing. To clarify the role of autocrine prolactin of breast cancer cells on cancer development, we construct T47D cells overexpressing prolactin.
Project description:We silenced FAM83H-AS1 shRNAs in cell line MCF7 carried a ~75% silencing compared to thenegative control (NC). We evaluated the role of FAM83H-AS1 on oncogenic phenotypes in the MCF7 breast cancer cell line model. The knockdown of FAM83H-AS1 was achieved with ~75% of silencing efficiency. A complete transcriptomic analysis after silencing of FAM83H-AS1 revealed an impact on the global expression.
Project description:To gain new insight into the resistance to hormonal therapy in breast cancer, we generated a tamoxifen-resistant human breast cancer cell line T47D-TR by exposing estrogen-sensitive cell line T47D to increasing concentrations of 4-hydroxy tamoxifen (4-OHT) and identified its resistance with different ways. What we interested is the underlying mechanisms of breast cancer tamoxifen resistance which was not reported yet.Here, we detect the RNA sequence of both the two cell lines hoping to find some evidence.
Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist
Project description:AS1 and AS2 encode MYB related protein and AS2-domain containing protein, respectively and may regulate transcription. These genes are involved in the determination of axes of leaves of Arabidopsis thaliana. To know the gene regulation in the leaf development, expression profile among wild-type, as1 and as2 mutants and AS2 overexpression plants were compaired. shoot apices from as1-1, as2-1, AS2 overexpressing, and wild type embryos
Project description:The PI3Kalpha-specific inhibitor Alpelisib (BYL719) has been approved for the treatment of metastatic ER+/HER2- breast cancer patients in combination with Fulvestrant. After initial response, patients develop drug resistance and disease relapses. In order to identify signalling pathways contributing to the acquired resistance to BYL719 in breast cancer, we generated BYL719-resistant T47D cells and used them together with the parental cells to perform label-free quantitative phosphoproteomics.
