Last update 01 Nov 2024

MST1

Last update 01 Nov 2024

Basic Info

Synonyms

D3F15S2, DNF15S2, Hepatocyte growth factor-like protein

+ [9]

Introduction-

Drugs associated with MST1

SBP-3264

Target

MST1 x MST2

Mechanism

MST1 inhibitors [+1]

Active Org.

Sanford Burnham Prebys Medical Discovery Institute

Originator Org.

Sanford Burnham Prebys Medical Discovery Institute

Active Indication

Acute Myeloid Leukemia

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

IHMT-MST1-58

Target

MST1

Mechanism

MST1 inhibitors

Active Org.

Hefei Institutes of Physical Science

Originator Org.

Hefei Institutes of Physical Science

Active Indication

Diabetes Mellitus

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

YL-602

Target

MST1 x MST2

Mechanism

MST1 agonists [+1]

Active Org.

Sichuan University

Originator Org.

Sichuan University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MST1

100 Translational Medicine associated with MST1

0 Patents (Medical) associated with MST1

1,196

Literatures (Medical) associated with MST1

01 Dec 2024·Gene

Anoikis-related genes linked with patient outcome in pancreatic cancer

Article

Author: Lin, Lizhi ; Yu, Jiaye ; Bauden, Monika ; Deng, Jing ; Ansari, Daniel ; Shen, Xian ; Andersson, Roland ; Xue, Xiangyang

Anoikis is programmed cell death occurring upon cell detachment from the extracellular matrix. Cancer cells need to evade anoikis to be able to metastasize to distant sites. However, the molecular features and prognostic value of anoikis-related genes (ARGs) in pancreatic cancer remain unclear. In this study, we utilized transcriptome data from the TCGA and GSE102238 databases to identify 64 ARGs significantly associated with prognosis. We used the "ConsensusClusterPlus" R package to stratify patients into high and low-risk prognostic subgroups. The KEGG and GSEA analyses revealed that the clusters with poor prognosis were enriched for the ECM receptor interaction pathway, the TP53 signaling pathway, and the galactose metabolism pathway, and that the cell cycle pathway was upregulated. A prognostic model consisting of seven ARGs (SERPINE1, EGF, E2F1, MSLN, RAB27B, ETV7, MST1) was constructed using LASSO regression and when combined with clinicopathological parameters using Cox regression, a prognostic Nomogram was created, which demonstrated high prognostic utility. Among the biomarker candidates, we report ETV7 as a novel, independent prognostic marker in pancreatic cancer. ETV7 was highly expressed in KRAS and TP53 co-occurrent mutant TCGA patients, indicating that it may be regulated by the two major driver genes of pancreatic cancer. Therefore, targeting ETV7 could be a potential focus for future therapeutic studies.

01 Nov 2024·Neurochemistry International

Apelin regulates mitochondrial dynamics by inhibiting Mst1-JNK-Drp1 signaling pathway to reduce neuronal apoptosis after spinal cord injury

Article

Author: Zhou, Shuai ; Li, Liming ; Huang, Fei ; Zhang, Luping ; Lv, Ang ; Liu, Qing ; Guo, Qixuan ; Lin, Yabin

In the secondary injury stage of spinal cord injury, mitochondrial dysfunction leads to decreased ATP production, increased ROS production, and activation of the mitochondria-mediated apoptosis signaling pathway. This ultimately intensifies neuronal death and promotes the progression of the injury. Apelin, a peptide produced by the APLN gene, has demonstrated promise in the treatment of spinal cord injury. The aim of this study was to investigate how Apelin protects neurons after spinal cord injury by influencing the mitochondrial dynamics. The results showed that Apelin has the ability to reduce mitochondrial fission, enhance the mitochondrial membrane potential, improve antioxidant capacity, facilitate the clearance of excess ROS, and ultimately decrease apoptosis in PC12 cells. Moreover, Apelin is overexpressed in neurons in the damaged part of the spinal cord, contributing to reduce mitochondrial fission, improve antioxidant capacity, increase ATP production, decrease apoptosis, promote spinal cord morphological repair, maintain the number of nissl bodies, and enhance signal transduction in the descending spinal cord pathway. Apelin exerts its protective effect by inhibiting the Mst1-JNK-Drp1 signaling pathway. In summary, our study further improved the effect of Apelin in the treatment of spinal cord injury, revealed the mechanism of Apelin in protecting damaged neurons after spinal cord injury by maintaining mitochondrial homeostasis, and provided a new therapeutic mechanism for Apelin in spinal cord injury.

30 Oct 2024·Bioscience Reports

Effect of the polyphenol flavonoids fisetin and quercetin on the adipogenic differentiation of human mesenchymal stromal cells

Article

Author: Srisook, Pimonwan ; Manochantr, Sirikul ; Charoenwongpaiboon, Thanapon ; Laowtammathron, Chuti ; Issaragrisil, Surapol ; Lorthongpanich, Chanchao ; Kheolamai, Pakpoom ; Septham, Praphasri

AbstractFisetin and quercetin, polyphenol flavonoids, have been shown to have a wide range of beneficial pharmacological effects including anti-inflammatory, antioxidative, and anti-cancer. Our previous work shows that fisetin also affects the specification of the adipogenic-osteogenic lineage of human mesenchymal stem cells (hMSCs) by modulating the Hippo-YAP signaling pathway. Although quercetin has a structure similar to that of fisetin, its effects on the functional properties of hMSCs have not yet been investigated. The objective of the present study is to determine the effects of quercetin on the various properties of hMSCs, including proliferation, migration, and differentiation capacity toward adipogenic and osteogenic lineages. The results show that while fisetin increases hMSC adipogenic differentiation, quercetin inhibited adipogenic differentiation of hMSCs. The inhibition is mediated, at least in part, by the activation of hippo signaling and up-regulation of miR-27b, which inhibits the expression of genes involved in all critical steps of lipid droplet biogenesis, resulting in a decrease in the number of lipid droplets in hMSCs. It is possible that the lack of hydroxylation of the 5 position on the A ring of quercetin could be responsible for its different effect on the adipogenic-osteogenic lineage specification of hMSCs compared with fisetin. Molecular docking and molecular dynamics simulation suggested that fisetin and quercetin possibly bind to serine / threonine protein kinases 4 (STK4/MST1), which is an upstream kinase responsible for LATS phosphorylation. Taken together, our results demonstrate more insight into the mechanism underlying the role of flavonoid fisetin and quercetin in the regulation of adipogenesis.

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MST1

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