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 investigate the role of lncRNA FAM83H-AS1 in breast cancer, we used shRNA to silence FAM83H-AS1 in MDA-MB-468 cells and performed RNA-seq analysis.
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:Our study suggested that FAM83H-AS1 was a potential oncogenic driver due to chromosome 8q24 amplification in lung adenocarcinoma. To investigate the molecular mechanism of FAM83H-AS1, we performed high-thoughput RNA sequencing (RNA-Seq) assays after the silence of FAM83H-AS1 in A549 cell lines.
Project description:We generated Fam83h-deficient mice (Fam83hem2(IMPC)Ccpcz, Fam83h-/-) and mice lacking a part of N-terminal CK1-binding domain (Fam83h∆87/∆87). Co-IP with anti-FAM83H antibody has confirmed the FAM83H–CK1 interaction in Fam83hwt/wt samples, which was absent in Fam83h-/- lysates. Additionally, samples from Fam83hΔ87/Δ87 mice were less likely to show FAM83H–CK1 interaction. Similarly, when CK1a antibody was used for pull downs, FAM83H–CK1 interaction was observed in Fam83hwt/wt lysates , but not in Fam83h-/- and Fam83hΔ87/Δ87 samples.
Project description:Truncation mutations in family with sequence similarity, member H (FAM83H) gene cause autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI). The aim of this study was to explore the effects of truncated FAM83H on enamel development. High throughput RNA-sequencing was used to detect the dysregulated signaling pathways in Fam83h-mutated LS8 cells. According to mRNA-sequencing, pathway related to cell adhesion was the most notably clustered in Fam83h-mutated cells. Immunofluorescence analysis further revealed decreased protein expression of desmoglein 3, a component of desmosomes, in Fam83h-mutated cells.