Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136572 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fluorinated rhodacyanines induce apoptosis via mitochondrial damage and cell cycle arrest
| PRJNA1056264 | ENA
Project description:miR-34c inhibits Dicer/Pten double knockout mouse serous epithelial cancer cell proliferation by inducing cell cycle arrest and apoptosis. We found that miR-34c had a more dramatic effect on inhibiting tumor cell viability than let-7b. The action of miR-34c induced tumor cell cycle arrest in G1 phase and apoptosis and was accompanied with the regulation of key genes involved in cell proliferation and cell cycle G1/S transition. miR-34c suppressed the expression of EZH2 and MYBL2, which may transcriptionally and functionally activate CDKN1C. Total RNA was extracted from DKO tumor cell lines transfected with miR-34c (n=3) and control miRNA (n=3).
2014-10-03 | E-GEOD-57493 | biostudies-arrayexpress
Project description:miR-34c inhibits Dicer/Pten double knockout mouse serous epithelial cancer cell proliferation by inducing cell cycle arrest and apoptosis. We found that miR-34c had a more dramatic effect on inhibiting tumor cell viability than let-7b. The action of miR-34c induced tumor cell cycle arrest in G1 phase and apoptosis and was accompanied with the regulation of key genes involved in cell proliferation and cell cycle G1/S transition. miR-34c suppressed the expression of EZH2 and MYBL2, which may transcriptionally and functionally activate CDKN1C.
2014-10-03 | GSE57493 | GEO
Project description:The goal was to assess global gene expression changes in primary human bronchial epithelial cells exposed to environmental tobacco smoke (ETS) condensate. ETS-C was standardized by HPLC analysis and two timepoints of exposure in two different donor bronchial epithelial cell populations were assessed. These findings demonstrate that even short exposure (4.5 h) to ETS is sufficient to induce a stress response, as reflected by decreased antioxidant levels, induced HSP family members, and modulation of the family of glutathione metabolism enzymes in primary human lung cells. Upon longer exposures (48 h) with ETS-condensate, bronchial epithelial cells arrest at the G2/M phase of the cell cycle. Taken together, these data support a stress-induced state in primary human bronchial epithelial cells that culminates in cell cycle arrest. Keywords: time course, comparative, stress response
2006-12-25 | GSE4234 | GEO
Project description:: FTY720 (Fingolimod) is an immunosuppressive drug approved by FDA for Multiple Sclerosis (MS), that has gained attention as anti-cancer drug, thanks to its ability to disrupt the binding between the onco-protein SET and the tumor- suppressor phosphatase PP2A. We investigated FTY720 induced phospho-proteomic changes on acute myeloid leukemia cell lines carrying KMT2A-transocations. The phospho-proteomic data indicated that FTY720 treatment resulted in the down-regulation of phospho-sites associated to protein serine/threonine kinase activity, chromatin organisation and transcription. The findings support the hypothesis of a feedback loop between SET, PP2A and MYC, whereby FTY720 re-activates PP2A with an overall inhibitory effect on MYC, resulting in cell cycle arrest and apoptosis.
2024-01-26 | PXD038288 | Pride
Project description:HDAC9-mediated Epithelial Cell Cycle Arrest in G2/M Contributes to Kidney Fibrosis
| PRJNA897857 | ENA
Project description:Chronic hypoxia inhibits apoptosis and cell cycle arrest in cancer cells, leading to cell survival, proliferation and angiogenesis. The mechanism for anti-apoptosis and cell proliferation in hypoxic cancer cells is still elusive. Here, we showed that hypoxia inactivates Runt-related transcription factor 3 (RUNX3), which is known to play as a tumor suppressor to induce apoptosis and cell cycle arrest in various cancers. RUNX3 is methylated under hypoxic conditions at lysines (K) 129 and 171 through its interaction with methyltranferase G9a. Gene expression profiling revealed that the mutations of K129 and 171 in RUNX3 induced the expression of genes related to apoptosis and cell cycle arrest under hypoxic conditions, indicating critical roles of the RNUX methylation in anti-apoptosis and cell proliferation. Moreover, K129 and 171 mutants, compared to G9a or G9a+RUNX3 control, showed significant reduction in apoptotic ability and tumor progression in xenograft models. Therefore, G9a-dependent methylation of RUNX3 is a novel target to inhibit cell proliferation and anti-apoptosis under hypoxic conditions during tumorigenesis.
2020-11-02 | GSE81693 | GEO
Project description:p53 is a transcription factor that plays a critical role in cancer prevention. However, the mechanisms by which p53 exerts its tumor-suppressive function is still unclear. While PUMA/BBC3 and NOXA/PMAIP1 are known to be important in p53-dependent apoptosis, and p21/CDKN1A is crucial for p53-dependent cell-cycle arrest, we demonstrate that zebrafish lacking puma, noxa, and p21 do not show a predisposition to cancer. This suggests that additional p53 transcriptional targets are sufficient for its tumor suppressive function. Contrary to the prevailing belief that p21 is the key regulator of p53-dependent cell-cycle arrest, we provide evidence that p53 can still induce cell-cycle arrest in the absence of p21, following DNA damage or loss of mdm2 (p53 activation in the absence of stress). This implies the involvement of other p53 transcriptional targets in mediating p53-dependent cell-cycle arrest. Since p53 tumor suppression is conserved across multiple vertebrate species, we conducted a cross-species comparative analysis of p53-dependent transcriptional profiles to identify a conserved set of 136 p53-upregulated transcripts. Our analysis stresses the importance of ortholog to paralog analysis across species, since in many cases the paralog but not ortholog in differing species is p53 dependent. Additionally, we performed a CRISPR/Cas9 G0 “crispant” screen in a genetic background lacking mdm2, puma, noxa, and p21 to identify key components involved in p53-dependent cell-cycle arrest. Our findings revealed that ccng1, fbxw7, and foxo3b play an important role in this process.
2025-06-16 | GSE288667 | GEO
Project description:p53 is a transcription factor that plays a critical role in cancer prevention. However, the mechanisms by which p53 exerts its tumor-suppressive function is still unclear. While PUMA/BBC3 and NOXA/PMAIP1 are known to be important in p53-dependent apoptosis, and p21/CDKN1A is crucial for p53-dependent cell-cycle arrest, we demonstrate that zebrafish lacking puma, noxa, and p21 do not show a predisposition to cancer. This suggests that additional p53 transcriptional targets are sufficient for its tumor suppressive function. Contrary to the prevailing belief that p21 is the key regulator of p53-dependent cell-cycle arrest, we provide evidence that p53 can still induce cell-cycle arrest in the absence of p21, following DNA damage or loss of mdm2 (p53 activation in the absence of stress). This implies the involvement of other p53 transcriptional targets in mediating p53-dependent cell-cycle arrest. Since p53 tumor suppression is conserved across multiple vertebrate species, we conducted a cross-species comparative analysis of p53-dependent transcriptional profiles to identify a conserved set of 136 p53-upregulated transcripts. Our analysis stresses the importance of ortholog to paralog analysis across species, since in many cases the paralog but not ortholog in differing species is p53 dependent. Additionally, we performed a CRISPR/Cas9 G0 “crispant” screen in a genetic background lacking mdm2, puma, noxa, and p21 to identify key components involved in p53-dependent cell-cycle arrest. Our findings revealed that ccng1, fbxw7, and foxo3b play an important role in this process.
2025-06-16 | GSE288666 | GEO