ZBTB16 inhibits DNA replication and induces cell cycle arrest by targeting WDHD1 transcription in lung adenocarcinoma [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1095489 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28532002_1.fastq.gz | Fastqsanger.gz | |||
| SRR28532002_2.fastq.gz | Fastqsanger.gz | |||
| SRR28532003_1.fastq.gz | Fastqsanger.gz | |||
| SRR28532003_2.fastq.gz | Fastqsanger.gz |
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Project description:Lung adenocarcinoma is a malignant tumor with high morbidity and mortality. ZBTB16 plays a double role in various tumors; however, the potential mechanism of ZBTB16 in the pathophysiology of lung adenocarcinoma has yet to be elucidated. We herein observed a decreased expression of ZBTB16 mRNA and protein in lung adenocarcinoma and a significantly increased DNA methylation level of ZBTB16 in patients with lung adenocarcinoma. Analysis of public databases and patients’ clinical data indicated a close association between ZBTB16 and patient survival. Ectopic expression of ZBTB16 in lung adenocarcinoma cells significantly inhibited cell proliferation, invasion, and migration. It also induced cell cycle arrest in the S phase. Meanwhile, mitotic catastrophe was induced, and DNA damage and apoptosis occurred. In line with these findings, the overexpression of ZBTB16 in xenograft mice resulted in the inhibition of tumor growth. Comprehensive analysis showed that WDHD1 was a potential target for ZBTB16. The overexpression of both isoforms of WDHD1 significantly reversed the ZBTB16-mediated inhibition of lung adenocarcinoma proliferation and cell cycle. These studies suggest that ZBTB16 impedes the progression of lung adenocarcinoma by interfering with WDHD1 transcription, making it a potential novel therapeutic target in the management of lung adenocarcinoma.
2024-04-24 | GSE263036 | GEO
Project description:Lung adenocarcinoma is a malignant tumor with high morbidity and mortality. ZBTB16 plays a double role in various tumors; however, the potential mechanism of ZBTB16 in the pathophysiology of lung adenocarcinoma has yet to be elucidated. We herein observed a decreased expression of ZBTB16 mRNA and protein in lung adenocarcinoma and a significantly increased DNA methylation level of ZBTB16 in patients with lung adenocarcinoma. Analysis of public databases and patients’ clinical data indicated a close association between ZBTB16 and patient survival. Ectopic expression of ZBTB16 in lung adenocarcinoma cells significantly inhibited cell proliferation, invasion, and migration. It also induced cell cycle arrest in the S phase. Meanwhile, mitotic catastrophe was induced, and DNA damage and apoptosis occurred. In line with these findings, the overexpression of ZBTB16 in xenograft mice resulted in the inhibition of tumor growth. Comprehensive analysis showed that WDHD1 was a potential target for ZBTB16. The overexpression of both isoforms of WDHD1 significantly reversed the ZBTB16-mediated inhibition of lung adenocarcinoma proliferation and cell cycle. These studies suggest that ZBTB16 impedes the progression of lung adenocarcinoma by interfering with WDHD1 transcription, making it a potential novel therapeutic target in the management of lung adenocarcinoma.
2024-04-25 | GSE263037 | GEO
Project description:ZBTB16 inhibits DNA replication and induces cell cycle arrest by targeting WDHD1 transcription in lung adenocarcinoma [RNA-seq]
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Project description:In order to determine the effects of cell cycle and cell cycle arrest on DNA methylation, whole genome bisulfite sequencing was performed on primary fibroblasts sorted based on DNA content and Ki67.
2017-02-03 | GSE68657 | GEO
Project description:The inhibitory effects of metformin have been observed in many types of cancer. However, its effect on human salivary gland carcinoma is unknown. The effect of metformin alone or in combination with pp242 (an mTOR inhibitor) on salivary adenocarcinoma cells growth were determined in vitro and in vivo. We found that metformin suppressed HSY cell growth in vitro in a time and dose dependent manner associated with a reduced expression of MYC onco-protein, and the same inhibitory effect of metformin was also confirmed in HSG cells. In association with the reduction of MYC onco-protein, metformin significantly restored p53 tumor suppressor gene expression. The distinctive effects of metformin and PP242 on MYC reduction and P53 restoration suggested that metformin inhibited cell growth through a different pathway from PP242 in salivary carcinoma cells. Furthermore, the anti-tumor efficacy of metformin was confirmed in vivo as indicated by the increases of tumor necrosis and reduced proliferation in xenograft tumors from metformin treated group. For the first time, the inhibitory effect of metformin on human salivary gland tumor cells was documented. Moreover, metformin inhibitory effects were enhanced by mTOR inhibitor suggesting that metformin and mTOR inhibitor utilize distinctive signaling pathways to suppress salivary tumor growth.
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Project description:Recent genomic studies suggest that a single gene is involved in multiple diseases, however it is unclear what mechanism destined for different diseases by a single gene. Mutations of ZBTB16 are associated with autism spectrum disorder (ASD) and schizophrenia (SCZ), but how ZBTB16 fates ASD or SCZ are unknown. Here we show the deletion of Zbtb16 in mice leads to both ASD- and SCZ-like behaviors such as social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we carried out histological studies and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in the prefrontal cortex (PFC) of Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia as well as developmental defects in oligodendrocytes and neocortical myelination in the PFC of Zbtb16 KO mice. Using a genomics approach, we identified the Zbtb16-transcriptome that includes genes involved in both ASD and SCZ pathophysiology and neocortical maturation such as neurogenesis and myelination. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ respectively. Our study provides insight into the differential role of the single gene ZBTB16 in ASD and SCZ.
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Project description:Glucocorticoids (GCs) cause apoptosis in lymphoid lineage cells and are therefore widely used in the therapy of lymphoid malignancies. The molecular mechanisms of the anti-leukemic GC effects are, however, poorly understood. We have previously defined a list of GC-regulated candidate genes by Affymetrix-based whole genome comparative expression profiling in children with acute lymphoblastic leukemia (ALL) during systemic GC monotherapy and in experimental systems of GC-induced apoptosis. ZBTB16, a Zink finger and BOZ-domain containing transcriptional repressor, was one of the most promising candidates derived from this screen. To investigate its possible role in GC-induced apoptosis and cell cycle arrest, we performed conditional over-expression experiments in CCRF-CEM childhood ALL cells. Transgenic ZBTB16 alone had no detectable effect on survival, however, it reduced sensitivity to GC-induced apoptosis. This protective effect was not seen when apoptosis was induced by antibodies against Fas/CD95 or 3 different chemotherapeutics. To address the molecular mechanism underlying this protective effect, we performed whole genome expression profiling in cells with conditional ZBTB16 expression. Surprisingly, ZBTB16 induction did not significantly alter the expression profile, however, it interfered with the regulation of several GC response genes. One of them, BCL2L11/Bim, has previously been shown to be responsible for cell death induction in CCRF-CEM cells. Thus, ZBTB16´s protective effect can be attributed to interference with transcriptional regulation of apoptotic genes, at least in the investigated model system.
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Project description:Jaiswal2017 - Cell cycle arrest
This model is described in the article:
ATM/Wip1 activities at
chromatin control Plk1 re-activation to determine G2 checkpoint
duration.
Jaiswal H, Benada J, Müllers E,
Akopyan K, Burdova K, Koolmeister T, Helleday T, Medema RH,
Macurek L, Lindqvist A.
EMBO J. 2017 Jul; 36(14):
2161-2176
Abstract:
After DNA damage, the cell cycle is arrested to avoid
propagation of mutations. Arrest in G2 phase is initiated by
ATM-/ATR-dependent signaling that inhibits mitosis-promoting
kinases such as Plk1. At the same time, Plk1 can counteract
ATR-dependent signaling and is required for eventual resumption
of the cell cycle. However, what determines when Plk1 activity
can resume remains unclear. Here, we use FRET-based reporters
to show that a global spread of ATM activity on chromatin and
phosphorylation of ATM targets including KAP1 control Plk1
re-activation. These phosphorylations are rapidly counteracted
by the chromatin-bound phosphatase Wip1, allowing cell cycle
restart despite persistent ATM activity present at DNA lesions.
Combining experimental data and mathematical modeling, we
propose a model for how the minimal duration of cell cycle
arrest is controlled. Our model shows how cell cycle restart
can occur before completion of DNA repair and suggests a
mechanism for checkpoint adaptation in human cells.
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BIOMD0000000641.
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2024-09-02 | BIOMD0000000641 | BioModels
Project description:The miR-16 family, which targets genes important for the G1-S transition, is a known modulator of the cell cycle, and members of this family are often deleted or down-regulated in many types of cancers. Here we report the reciprocal relationship - that of the cell cycle controlling the miR-16 family. Levels of this family increase rapidly as cells are arrested in G0. Conversely, as cells are released from G0 arrest, levels of the miR-16 family rapidly decrease. Such rapid changes are made possible by the unusual instabilities of several family members. The repression mediated by the miR-16 family is sensitive to these cell cycle changes, which suggests that the rapid up-regulation of the miR-16 family reinforces cell cycle arrest in G0. Upon cell cycle re-entry, the rapid decay of several members allows levels of the family to decrease, alleviating repression of target genes and allowing proper resumption of the cell cycle. Small RNAs were profiled by high-throughput sequencing either during synchronous release after serum starvation or during cell-cycle arrest by contact inhibition.
2011-09-15 | E-GEOD-31225 | biostudies-arrayexpress
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