The alterations of gene expression profiling induced by ts-ARFGEF1 knockdown in MCF-7 cells
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PROVIDER: PRJNA805506 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of high-throughput transcriptome sequencing (RNA-seq) data often observed numerous 'non-co-linear' (NCL) transcripts, which may originate from genetic rearrangements (gene fusion) indicated the importance of fusion events and circRNAs in carcinogenesis; however, the role of ts-RNAs remains largely uninvestigated. Here we developed a hybrid sequencing pipeline ("NCLscan-hybrid"), which integrated different types of short (Illumina-based) and extra-long (PacBio-based) RNA-seq data to eliminate potential false positives from experimental artifacts, fusion events, and circRNAs. We applied NCLscan-hybrid to investigate of ts-RNAs in human breast cancer, the most malignant tumors diagnosed in women worldwide. Through multiple experimental validation steps, we confirmed that the intragenic ts-RNA, ts-ARFGEF1, was highly expressed in breast cancer cells but absent in normal breast cells. Furthermore, we experimentally validated that ts-ARGEF1 can contribute to cell proliferation and apoptosis. Analysis of xenograft in nude mice showed that disruption of ts-ARFGEF1 expression can significantly attenuate tumor growth. Microarray analysis revealed that ts-ARFGEF1 knockdown could trigger PERK/ATF4/CHOP signaling pathway, implying the function of ts-ARFGEF1 in ER homeostasis. Taken together, our findings provide an in-depth view of the true complexity of intragenic NCL events and, for the first time, show further insight into the potential roles of intragenic ts-RNAs in tumor cell development.
2022-02-12 | GSE196514 | GEO
Project description:Analysis of high-throughput transcriptome sequencing (RNA-seq) data often observed numerous 'non-co-linear' (NCL) transcripts, which may originate from genetic rearrangements (gene fusion) indicated the importance of fusion events and circRNAs in carcinogenesis; however, the role of ts-RNAs remains largely uninvestigated. Here we developed a hybrid sequencing pipeline ("NCLscan-hybrid"), which integrated different types of short (Illumina-based) and extra-long (PacBio-based) RNA-seq data to eliminate potential false positives from experimental artifacts, fusion events, and circRNAs. We applied NCLscan-hybrid to investigate of ts-RNAs in human breast cancer, the most malignant tumors diagnosed in women worldwide. Through multiple experimental validation steps, we confirmed that the intragenic ts-RNA, ts-ARFGEF1, was highly expressed in breast cancer cells but absent in normal breast cells. Furthermore, we experimentally validated that ts-ARGEF1 can contribute to cell proliferation and apoptosis. Analysis of xenograft in nude mice showed that disruption of ts-ARFGEF1 expression can significantly attenuate tumor growth. Microarray analysis revealed that ts-ARFGEF1 knockdown could trigger PERK/ATF4/CHOP signaling pathway, implying the function of ts-ARFGEF1 in ER homeostasis. Taken together, our findings provide an in-depth view of the true complexity of intragenic NCL events and, for the first time, show further insight into the potential roles of intragenic ts-RNAs in tumor cell development.
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Project description:To detect full-length transcript of ts-ARFGEF1 in MCF-7 cell [captureRNA]
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Project description:The ts-p53 E285K protein is a rare p53 mutant with temperature-sensitive (ts) loss of function characteristics. In cancer cells, which express ts-p53 E285K intrinsically, endogenous wild type p53 activity is reconstituted by appropriate cultivation temperature (permissive condition). At non-appropriate cultivation temperature (restrictive condition) this p53 mutant is inactive. The present study took advantage of this mechanism and employed IPH-926 lobular breast cancer cells and BT-474 ductal breast cancer cells, which both harbor endogenous ts-p53 E285K, for the transcriptional profiling of p53-responsive genes. This new approach eliminated the need for genetic modification or cytotoxic stimulation to achive a p53 response in the cells being investigated . Three subseqent passages of IPH-926 lobular breast cancer cells (harboring ts-p53 E285K) were seeded into two parallel culture dishes each and were allowed to adopt to restrictive and permissive condition for 24 h before analysis on Affymetrix U133 Plus 2.0 microarrays. Subsequently, this experiment was repeated with BT-474 ductal breast cancer cells (also harboring ts-p53 E285K). To gate out non-specific temperature effects, the same experiment was also performed with MCF-7 breast cancer cells (harboring wt p53). Probe sets differentially expressed at restrictive versus permissive condition in MCF-7 were considered as non-specifically regulated. These probe sets were excluded from the final statistical analysis of IPH-926 and BT-474 expression data. response to restored p53 activity
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Project description:NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.
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Project description:NMNAT1 is a nuclear enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NMNAT1 knockdown on gene expression in MCF-7 breast cancer cells.
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