Project description:To further explore the potential molecular mechanisms of NCK1-AS1 in CC cells,Human Transcriptome Array 2.0 analysis was performed to investigate the differential gene expression profiles between NCK1-AS1 knockdown group and control group in CaSki cells.
Project description:To further explore the molecular mechanism of DLEU2 in CC cells, RNA sequencing analysis was performed to investigate the differential gene expression profiles between DLEU2 knockdown group and comtrol group in CaSki cells.
Project description:Microarry based whole genome expression analysis was done for the more tumorigenic CaSki spheroids cultures and the less tumorigenic CaSki adherent cultures to identify signaling mechanisms that vary between the two populations. Subsequent to this, an independent array was done to characterize the differences in gene expression between the cancer stem cell-like Lin-CD66+ and the bulk Lin- CD66- cells isolated from primary human cervical carcinomas. The second array was custom-designed and had genes implicated in stemness, epithelial differentiation, signaling pathways implicated in stemness (Notch and Wnt) and cell cylce-regulation. Microarray analysis of CaSki cell line grown as spheroids and adherent conditions
Project description:circCDKN2B-AS1 is significantly upregulated circRNA in HPV16 positive cervical cancer tissues comprared with both HPV16 positive and HPV16 negative normal cervical tissues.So we chose it for further study.To explore the mRNA expression profiles following circCDKN2B-AS1 knockdown, we performed RNA sequencing analysis in SiHa cells with or without circCDKN2B-AS1 knockdown.We performed RNA sequencing in two pairs of RNA samples of SiHa cells with or without circCDKN2B-AS1 knockdown.
Project description:Purpose: According to the previous analysis results of gene regulation in fetal heart tissues with tetralogy of Fallot (ToF), we constructed the ceRNA mediated network driven by lncRNAs using a causal inference framework based on the expression correlations and validated miRNA-lncRNA/mRNA evidences. Totally 4 lncRNAs were identified as hub lncRNAs in the network, and FGD5-AS1 was focused for further loss-of-function investigation. Methods: The specific shRNAs against FGD5-AS1 (sh-FGD5-AS1) as well as the corresponding negative control (sh-NC) were constructed along with lentiviral vector respectively. Then the CCC-HEH-2 human cardiac myocytes cell lines were infected with lentivirus and followed puromycin treatment for several days. The knockdown efficiencies of the FGD5-AS1 expression were validated by qPCR. Genome-wide RNA expression of control and knockdown CCC-HEH-2 cell lines were observed using RNA-Seq. Conclusions: Knockdown of this lncRNA interferes with glutamate receptor activity and metalloendopeptidase inhibitor activity. The expression of abundant CHD genes with |fold change| ≥ 2 was validated with qPCR. These results indicate that FGD5-AS1 plays an important role in CHD genes regulation networks.
Project description:We discovered that USP30-AS1 is significantly upregulated in breast cancer tissues and is closely associated with the cell proliferation signaling pathway. Knockdown of USP30-AS1 notably inhibits cell proliferation in MDA-MB-231 breast cancer cells. USP30-AS1 inhibits the expression of the cell cycle inhibitor p21.
Project description:Microarry based whole genome expression analysis was done for the more tumorigenic CaSki spheroids cultures and the less tumorigenic CaSki adherent cultures to identify signaling mechanisms that vary between the two populations. Subsequent to this, an independent array was done to characterize the differences in gene expression between the cancer stem cell-like Lin-CD66+ and the bulk Lin- CD66- cells isolated from primary human cervical carcinomas. The second array was custom-designed and had genes implicated in stemness, epithelial differentiation, signaling pathways implicated in stemness (Notch and Wnt) and cell cylce-regulation.
Project description:The oncogenic transcription factor (c-)Myc is overexpressed in a variety of cancers including subtypes of B cell lymphoma. Here we study long noncoding (lnc)RNAs regulated by Myc, arguing that these lncRNAs may be involved in the very strong effect of Myc on cell proliferation. Using multiple in vitro models and taking into account the kinetics of the response to Myc as well as Myc binding sites we defined two Myc-induced and four Myc-repressed lncRNA candidates. Expression levels of the top Myc-induced lncRNA KTN1-AS1 are low in normal B cell subsets and strongly increased in multiple Myc-positive lymphoma cell lines. In addition, primary lymphoma cases stratified by high or low Myc expression show the expected KTN1-AS1 expression differences. Knockdown of KTN1-AS1 severely impaired the cell growth of multiple Burkitt lymphoma cell lines. Gene expression analysis showed that KTN1-AS1 knockdown affects >300 genes genome wide with a strong enrichment of Myc-target genes involved in metabolism and biosynthesis. In line with this finding, KTN1-AS1 depletion in B cell lymphoma cells caused a substantial decrease of Myc transcript and protein. Thus, our data indicates that KTN1-AS1 overexpression in lymphoma may reinforce high Myc expression at the transcriptional level to activate gene expression programs supporting the high metabolic rate present in lymphoma cells. In conclusion, we identified a novel positive feedback loop between c-Myc and KTN1-AS1 in B cell lymphoma cells. LncRNAs such as KTN1-AS1, that regulate important oncogenic factors in specific cell types, may open new ways to cancer therapy.