Transcriptomes analysis for the regulation of Z36 induced autophagy in HeLa cell death
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ABSTRACT:
PROVIDER: PRJNA533543 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8926590_1.fastq.gz | Fastqsanger.gz | |||
| SRR8926590_2.fastq.gz | Fastqsanger.gz | |||
| SRR8926581_1.fastq.gz | Fastqsanger.gz | |||
| SRR8926581_2.fastq.gz | Fastqsanger.gz | |||
| SRR8926591_1.fastq.gz | Fastqsanger.gz |
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Project description:Z36 is a small molecule that induces Beclin1-dependent autophagy and autophagic cell death in HeLa cells. This is different from the typical autophagy induced by Rapamycin, which plays a protective role for cells. To gain insights into the regulation of autophagy in cell death by Z36, high-throughput RNA-sequencing were performed on HeLa cells treated with DMSO (as control), Z36 and Rapamycin. Two biological replaces were collected for each of the three conditions. The sequencing generated more than 30 million reads for each sample. RNA-seq data showed that there were about 3000 DEGs with over 2 folds changes (|log2 (fold change)| > 1 & P value < 0.05) in Z36 treated cells versus those of DMSO. On the contrary, there were only 200 DEGs for cells treated with Rapamycin. Noteworthily, expression levels of autophagic genes were significantly changed in Z36 treated cells, and the change pattern was different from Rapamycin treated ones. 8 of the ATG genes were up-regulated for more than 2 folds (log2 > 1) after Z36 treatment, while Rapa only caused small changes for the ATG genes, with the highest log2 change of 0.7. These study indicate that Z36 leads to significant modulation of a large number of genes at transcriptional level.
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Project description:Background: Successful treatment of oesophageal cancer is hampered by recurrent drug resistant disease. We have previously demonstrated the importance of apoptosis and autophagy for the recovery of oesophageal cancer cells following drug treatment. When apoptosis (with autophagy) is induced, these cells are chemosensitive and will not recover following chemotherapy treatment. In contrast, when cancer cells exhibit only autophagy and limited Type II cell death, they are chemoresistant and recover following drug withdrawal. Methods: MicroRNA (miRNA) expression profiling of an oesophageal cancer cell line panel was used to identify miRNAs that were important in the regulation of apoptosis and autophagy. The effects of miRNA overexpression on cell death mechanisms and recovery were assessed in the chemoresistant (autophagy inducing) KYSE450 oesophageal cancer cells. Results: MiR-193b was the most differentially expressed miRNA between the chemosensitive and chemoresistant cell lines with higher expression in chemosensitive apoptosis inducing cell lines. Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. The critical mRNA targets of miR-193b are unknown but target prediction and siRNA data analysis suggest that it may mediate some of its effects through stathmin 1 regulation. Apoptosis was not involved in the enhanced cytotoxicity. Overexpression of miR- 193b in these cells induced autophagic flux and non-apoptotic cell death. Conclusion: These results highlight the importance of miR-193b in determining oesophageal cancer cell viability and demonstrate an enhancement of chemotoxicity that is independent of apoptosis induction.
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Project description:Transcription factors can affect autophagy activity by promoting or inhibiting the expression of autophagy and lysosomal related genes. As a zinc finger family DNA-binding protein, ZKSCAN3 has been reported to function as a transcriptional repressor of autophagy, silencing of which can induced autophagy and promoted lysosome biogenesis in cancer cells. However, the studies in Zkscan 3 knockout mice showed that the deficiency of Zkscan3 did not induce autophagy and in-crease lysosome biogenesis. In order to further explore the role of ZKSCAN3 in the transcriptional regulation of autophagy in human cells, we generated ZKSCAN3 knockout HK-2 and Hela cells by CRISPR/Cas9 system and analyzed the differences in gene expression between ZKSCAN3 deleted cells and non-deleted cells through fluorescence quantitative PCR, Western blot and transcriptome sequencing, with special attention to the differences in gene expression of autophagy and lysosomal biogenesis. We found that ZKSCAN3 is not an essential regulator of autophagic or lysosomal gene expression, as the absence ZKSCAN3 had no significantly effect on the expression of autophagy or lysosomal genes.
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Project description:The newly sinthesized compound RZ2 induces cell death to human cancer cells. To obtain insights into its mechanism of action, the effects on autophagy and apoptosis were examined. Global perturbations in genome-wide RNA expression of HeLa cells treated with RZ2 were measured by gene expression microarray. Confluent cultures of HeLa cells were treated with 5 μM RZ2 or the vehicle (DMSO) for 24 hours, followed by RNA preparation and hybridization to a GeneChip PrimeView Human Gene Expression Array (Affymetrix)
2015-05-19 | E-GEOD-51948 | biostudies-arrayexpress
Project description:Serine protease inhibitor Kazal type 3 (Spink3) is a trypsin inhibitor in the pancreas. Spink3-/- pancreatic acinar cells are dead with excessive autophagy at birth (p0.5). To prove the role of nonapoptotic cell death with autophagy, we generated by transgenic technology the pancreas of Spink3-/-;XKI/+ mice contained both normal and dying acinar cells with autophagy. In this new mouse model, chronic inflammation occurred in the pancreas, indicating that some signals from nonapoptotic dead cell induce chronic inflammation in the pancreas.
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Project description:Autophagy to apoptosis switching event is an unexplored area. We were interested to explore the gene expression profile at this juncture. Our Microarray data emphasized that among all eNOS and p62 genes were markedly induced. In fuctional level eNOS expression activates mTORC1 followed by inhibition of autophagy. This ultimately allowed accumulation of p62 . Intraccellular accumulation of p62 sequestered unfolded toxic protein aggregates in mitochondria and ER resulting in to impaired redox regulation. Intraccelular ROS generation further sensitized cells for apoptosis and tilted autophagic response to apoptosis. Cells were treated with Tunicamycin as an inducer of both autophagy and apoptosis. At early stage of Tunicamycin treatment 24h , prostate cancer cell PC3 showed activation of autophagic process where apoptosis was not evident. Sustained ER stress with Tunicamycin induced late apoptoisis at 72h of treatment. Hence we isolated total RNA from Untreated cells, cells with Tunicamycin treatment after 24h and 72h. Further the RNA were used to perform whole genome microarray to analyze the gene expression profile at autophagy and apoptosis juncture. The selected genes were also validated by qPCR and western bot. Morover RNAi study were implemented to evaluate the signaling crosstalk at the juncture of autophagy and apoptosis.
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