ArticleOncoTargets and therapy2018
Overexpression of Mst1 reduces gastric cancer cell viability by repressing the AMPK-Sirt3 pathway and activating mitochondrial fission.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Retraction Note: TAZ inhibition promotes IL-2-induced apoptosis of hepatocellular carcinoma cells by activating the JNK/F-actin/mitochondrial fission pathway.Cancer cell international · 2026Article
- TRIM21 is critical in regulating hepatocellular carcinoma growth and response to therapy by altering the MST1/YAP pathway.Cancer science · 2024Article
- Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- MST1 mediates doxorubicin-induced cardiomyopathy by SIRT3 downregulation.Cellular and molecular life sciences : CMLS · 2023Article
- Association of mitochondrial homeostasis and dynamic balance with malignant biological behaviors of gastrointestinal cancer.Journal of translational medicine · 2023Review
- Targeting the Hippo Pathway in Gastric Cancer and Other Malignancies in the Digestive System: From Bench to Bedside.Biomedicines · 2022Review
- L22 ribosomal protein is involved in dynamin-related protein 1-mediated gastric carcinoma progression.Bioengineered · 2022Article
- Role of non-coding RNAs and exosomal non-coding RNAs in retinoblastoma progression.Frontiers in cell and developmental biology · 2022Review
- Inhibition of HDACs Suppresses Cell Proliferation and Cell Migration of Gastric Cancer by Regulating E2F5 Targeting BCL2.Life (Basel, Switzerland) · 2021Article
- MicroRNA-139-5p Promotes Functional Recovery and Reduces Pain Hypersensitivity in Mice with Spinal Cord Injury by Targeting Mammalian Sterile 20-like Kinase 1.Neurochemical research · 2021Article
- Mst2 Overexpression Inhibits Thyroid Carcinoma Growth and Metastasis by Disrupting Mitochondrial Fitness and Endoplasmic Reticulum Homeostasis.Journal of oncology · 2021Article
- Mammalian STE20-like Kinase 1 Knockdown Attenuates TNFα-Mediated Neurodegenerative Disease by Repressing the JNK Pathway and Mitochondrial Stress.Neurochemical research · 2019Article
- Mst1 overexpression combined with Yap knockdown augments thyroid carcinoma apoptosis via promoting MIEF1-related mitochondrial fission and activating the JNK pathway.Cancer cell international · 2019Article
Corrections and comments
- Retraction · 2024-04-03Author Unresponsive · Concerns/Issues about Image · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveMammalian sterile 20-like kinase 1 (Mst1) plays a critical role in regulating cell survival and apoptosis. However, its influence on gastric cancer cell viability is not understood. Our study aims to explore the specific role of Mst1 in gastric cancer. MATERIALS AND
methodsCellular viability was measured via TUNEL staining, MTT assays, and Western blotting. Immunofluorescence was performed to observe mitochondrial fission. Mst1 overexpression assays were conducted to observe the regulatory mechanisms of Mst1 in mitochondrial fission and cell apoptosis.
resultsThe results demonstrated that Mst1 was downregulated in AGS cells when compared with GES-1 cells. However, overexpression of Mst1 reduced cell viability and increased apoptosis in AGS cells. Molecular experiments showed that Mst1 overexpression mediated mitochondrial damage, as evidenced by decreased ATP production, increased ROS generation, more cyt-c translocation from the mitochondria into the cytoplasm and nucleus, and activated the caspase-9-related apoptotic pathway. Furthermore, we found that mitochondrial fission was required for Mst1-induced mitochondrial dysfunction; inhibition of mitochondrial fission sustained mitochondrial homeostasis in response to Mst1 overexpression. In addition, our data revealed that Mst1 controlled mitochondrial fission via repressing the AMPK-Sirt3 pathway. Activation of the AMPK-Sirt3 pathway negated the promoting effect of Mst1 overexpression on mitochondrial fission.
conclusionAltogether, our data identified Mst1 as a novel tumor-suppressive factor in promoting cell death in gastric cancer cells by triggering mitochondrial fission and blocking the AMPK-Sirt3 axis.
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Registered trials
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