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ROS-induced cytosolic release of PGAM5 accelerates cancer progression via MST3-YAP axis

ABSTRACT: ROS-induced cytosolic release of PGAM5 accelerates cancer progression via MST3-YAP axis

PROVIDER: PRJNA1043738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26908426_1.fastq.gz	Fastqsanger.gz
	SRR26908426_2.fastq.gz	Fastqsanger.gz
	SRR26908427_1.fastq.gz	Fastqsanger.gz
	SRR26908427_2.fastq.gz	Fastqsanger.gz
	SRR26908428_1.fastq.gz	Fastqsanger.gz

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ROS-induced cytosolic release of PGAM5 accelerates cancer progression via MST3-YAP axis

Project description:Aberrant mtROS release in response to mitochondrial stress are considered to be a major novel feature of neoplastic transformation. However, the molecular mechanisms by which mtROS contribute to CRC development have not been fully elucidated. In this study, we showed that upon sensing the mtROS signal, the mitochondrially localized phosphatase PGAM5 undergoes cleavage in the mitochondrial transmembrane domain, and then the Cleaved PGAM5 is released into the cytoplasm. Subsequently, Cleaved PGAM5 binds to the kinase MST3 in the cytoplasm to promote MST3 dephosphorylation, resulting in a decrease in MST3 activity. Importantly, MST3 inactivation failed to regulate YAP phosphorylation, leading to YAP translocation into the nucleus, consequently promoting CRC proliferation and metastasis. Collectively, our findings identified the PGAM5-MST3-YAP axis as an important molecular mechanism through which mtROS promotes CRC development.

2024-11-05 | GSE248431 | GEO

ROS-induced cytosolic release of mitochondrial PGAM5 accelerates colorectal cancer progression via MST3-mediated YAP activation

2024-11-05 | GSE249865 | GEO

ROS-induced cytosolic release of mitochondrial PGAM5 accelerates colorectal cancer progression via MST3-mediated YAP activation

Project description:ROS-induced cytosolic release of mitochondrial PGAM5 accelerates colorectal cancer progression via MST3-mediated YAP activation

| PRJNA1051049 | ENA

ROS-induced cytosolic release of mitochondrial PGAM5 promotes colorectal cancer progression by interacting with MST3.

Project description:Aberrant release of mitochondrial reactive oxygen species (mtROS) in response to cellular stress is well known for promoting cancer progression. However, precise molecular mechanism by which mtROS contribute to epithelial cancer progression remains only partially understood. Here, using colorectal cancer (CRC) models, we show that upon sensing excessive mtROS, phosphatase PGAM5, which normally localizes to the mitochondria, undergoes aberrant cleavage by presenilin-associated rhomboid-like protein (PARL), becoming released into the cytoplasm. Cytosolic PGAM5 then directly binds to and dephosphorylates MST3 kinase. This, in turn, prevents STK25-mediated LATS1/2 phosphorylation, leading to YAP activation and CRC progression. Importantly, depletion of MST3 reciprocally promotes accumulation of cytosolic PGAM5 by inducing mitochondrial damage. Taken together, these findings demonstrate how mtROS promotes CRC progression by activating YAP via a post-transcriptional positive feedback loop between PGAM5 and MST3, both of which can serve as potential targets for developing next-generation anti-colon cancer therapeutics.

| S-EPMC11802746 | biostudies-literature

Gene expression profiles of PGAM5-knockout brown adipose tissue

Project description:PGAM5 is a mitochondria-localized protein phosphatase. To analyze the effect on gene expression profiles by PGAM5 in iBAT, RNA-seq analysis was performed.

2019-10-12 | GSE138782 | GEO

Mesenchymal SLMAP coordinates with MST3 to govern gut elongation during development

Project description:Developing gut in mice undergoes rapid elongation during late embryogenesis, yet significantly slows down after birth. Precise regulatory mechanism of this dynamic morphogenetic process remains unknown. Utilizing scRNA-seq analysis, we show that YAP activity in Cxcl13high intestinal fibroblasts is the major molecular contributor to gut elongation. To determine how mesenchymal YAP activity is controlled, we identified canonical Sarcolemma membrane-associated protein (SLMAP) as its critical regulator during embryonic gut morphogenesis. Deleting Slmap in gut mesenchyme impairs YAP activity, leading to short gut and a significant decrease in intestinal epithelial cell proliferation. Mechanistically, Slmap activates YAP by directly regulating Mst3 kinase. Physiologically, Mst3 levels prominently increase over the developmental time, reaching their peak on postnatal day P14, when gut elongation in mice slows down. Depleting Mst3 in mesenchyme results in increased gut length at P14 accompanied by enhanced YAP activity. Importantly, short gut phenotype in SlmapcKO mice is partially compensated by concomitant deletion of mesenchymal Mst3. Taken together, our findings demonstrate that Slmap interacts with Mst3 kinase to dynamically regulate mesenchymal YAP activity that governs gut elongation across its embryonic and postnatal development.

2025-06-16 | GSE276611 | GEO

Mesenchymal SLMAP coordinates with MST3 to govern gut elongation during development [RNAseq_TL]

2025-06-16 | GSE276668 | GEO

Analysis of phospho-proteome change following MST3/4 depletion

Project description:Mammalian STE20-like protein kinases 3 and 4 (MST3/4) have recently emerged as crucial regulators of several key cellular processes such as proliferation, migration, and polarity. However, the downstream target pathways which are regulated by the kinase activity of MST3/4 remain poorly characterised. To assess downstream targets of MST3/4 kinases in an unbiased manner, we transiently co-depleted MST3 and MST4 in HeLa cells by siRNA and quantified the change in their phospho-proteome using SILAC.

2022-02-28 | PXD006167 | Pride

Mesenchymal SLMAP coordinates with MST3 to govern gut elongation during development (scRNA-Seq)

Project description:Developing gut in mice undergoes rapid elongation during late embryogenesis, yet significantly slows down after birth. Precise regulatory mechanism of this dynamic morphogenetic process remains unknown. Utilizing single-cell RNA-sequencing analysis, we show that YAP activity in Cxcl13high intestinal fibroblasts is the major molecular contributor to gut elongation. To determine how mesenchymal YAP activity is controlled, we identified canonical Sarcolemma membrane-associated protein (SLMAP) as its critical regulator during embryonic gut morphogenesis. Deleting Slmap in gut mesenchyme impairs YAP activity, leading to short gut and a significant decrease in intestinal epithelial cell proliferation. Mechanistically, SLMAP activates YAP by directly regulating MST3 kinase. Physiologically, MST3 levels prominently increase over the developmental time, reaching their peak on postnatal day P14, when gut elongation in mice slows down. Depleting Mst3 in mesenchyme results in increased gut length at P14 accompanied by enhanced YAP activity. Importantly, short gut phenotype in mesenchyme-specific Slmap mutant mice is partially compensated by concomitant deletion of mesenchymal Mst3. Taken together, our findings demonstrate that SLMAP interacts with MST3 kinase to dynamically regulate mesenchymal YAP activity that governs dynamic gut elongation across its embryonic and postnatal development.

2025-06-16 | GSE277051 | GEO

Contribution of STAT3, IRF1 and PGAM5 to androgen response in prostate cancer cells

Project description:To decipher the contribution of STAT3, IRF1 and PGAM5 to androgen-responsive gene expression, effect of siRNA-mediated silencing of STAT3, IRF1 and PGAM5 on expression of androgen-dependent genes was studied.

2017-05-01 | GSE81780 | GEO

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