Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells.Three independent experiments were performed.
Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression.
Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells. Three independent experiments were performed. p53-/- Rbf/f vs p53-/- Rbâf/âf Ptenâf/âf primary prostate cells. Four independent experiments were performed.
Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression.
Project description:The absence of the Rb tumor suppressor gene changes levels/activities of transcription factors (e.g., E2F and p53) which alter gene expression patterns, related to cell cycle control and cellular response to DNA damage. Cisplatin is a genotoxic chemotherapeutic agent and wildtype or Rb null cells have different sensitivities to cisplatin-induced cytotoxicity. We used microarrays to compare global profiles of gene expression and distinct responses of wildtype and Rb null MEFs in response to cisplatin. Experiment Overall Design: Primary wildtype or Rb null MEFs were generated from embryos at embryonic day 13.5 and cultured to passage 2. Wildtype or Rb null MEFs were either untreated or treated with 16 microM cisplatin for 24 hours prior to harvest and RNA extraction. Four different RNA samples (wildtype or Rb-/- MEFs, untreated or cisplatin-treated) were used for hybridization in triplate to Affimatrix Chips. Then, the total of 12 hybridizations were divided into 4 subseries: UT-Rb, UT-WT, CP-Rb, CP-Wt, and each subseries contained three samples (hybridization 1-3 or a-c).
Project description:We found that Rb inactivation induces sphere-forming activity under 3D culture condition in primary soft tissue sarcoma cells derived from p53 null mice. To elucidate molecular mechanism, we employed microRNA array as a discovery platform to identify miRNAs correlated with Rb-depeltion induced sphere-forming cells. To enrich sphere-forming cells and make the culture condition equivalent to that of parental cells (Primary cells), we replated sphere-forming cells on normal dishes (Rb shRNA Secondary cells), and obtained total RNA soon after replating.
Project description:To identify the downstream molecules that mediate PIM1 induced aggressive prostate cancer cells, p53 and Rb-deficient mouse prostate epithelial cells were transduced with PIM1 lentivirus and performed a gene expression profile microarray.
Project description:The absence of the Rb tumor suppressor gene changes levels/activities of transcription factors (e.g., E2F and p53) which alter gene expression patterns, related to cell cycle control and cellular response to DNA damage. Cisplatin is a genotoxic chemotherapeutic agent and wildtype or Rb null cells have different sensitivities to cisplatin-induced cytotoxicity. We used microarrays to compare global profiles of gene expression and distinct responses of wildtype and Rb null MEFs in response to cisplatin. Keywords: genotype and cisplatin treatment
