Ets1 facilitates EMT/invasion through Drp1-mediated mitochondrial fragmentation in ovarian cancer

Ghosh, Deepshikha; Pakhira, Suman; Ghosh, Damayanti Das; Roychoudhury, Susanta; Roy, Sib Sankar

doi:10.1016/j.isci.2023.107537

Cited by 5 publications

(1 citation statement)

References 52 publications

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“…Sirtuin direct homolog SIRT6 can promote extracellular signal regulated kinase1/2 (ERK1/2), driving activation and phosphorylation of mitochondrial fission-associated protein DRP1, which positively regulates mitochondrial fission and reduces cell invasion by decreasing formation of stress fibers in ovarian cancer cells ( 33 ). Epithelial-mesenchymal transition (EMT) promoter Ets1 can promote EMT/invasion through DRP1-mediated mitochondrial fragmentation of ovarian cancer ( 34 ).…”

Section: Mechanisms Of Cellular Organelles In Ovarian Cancer Pathogen...mentioning

confidence: 99%

Independent organelle and organelle—organelle interactions: essential mechanisms for malignant gynecological cancer cell survival

Shen,

Chen,

et al. 2024

Front. Immunol.

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Different eukaryotic cell organelles (e.g., mitochondria, endoplasmic reticulum, lysosome) are involved in various cancer processes, by dominating specific cellular activities. Organelles cooperate, such as through contact points, in complex biological activities that help the cell regulate energy metabolism, signal transduction, and membrane dynamics, which influence survival process. Herein, we review the current studies of mechanisms by which mitochondria, endoplasmic reticulum, and lysosome are related to the three major malignant gynecological cancers, and their possible therapeutic interventions and drug targets. We also discuss the similarities and differences of independent organelle and organelle–organelle interactions, and their applications to the respective gynecological cancers; mitochondrial dynamics and energy metabolism, endoplasmic reticulum dysfunction, lysosomal regulation and autophagy, organelle interactions, and organelle regulatory mechanisms of cell death play crucial roles in cancer tumorigenesis, progression, and response to therapy. Finally, we discuss the value of organelle research, its current problems, and its future directions.

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Section: Mechanisms Of Cellular Organelles In Ovarian Cancer Pathogen...mentioning

confidence: 99%

Independent organelle and organelle—organelle interactions: essential mechanisms for malignant gynecological cancer cell survival

Shen,

Chen,

et al. 2024

Front. Immunol.

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Wnt/β-catenin-driven EMT regulation in human cancers

Xue,

Yang,

Chen

et al. 2024

Cell. Mol. Life Sci.

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Metastasis accounts for 90% of cancer-related deaths among the patients. The transformation of epithelial cells into mesenchymal cells with molecular alterations can occur during epithelial–mesenchymal transition (EMT). The EMT mechanism accelerates the cancer metastasis and drug resistance ability in human cancers. Among the different regulators of EMT, Wnt/β-catenin axis has been emerged as a versatile modulator. Wnt is in active form in physiological condition due to the function of GSK-3β that destructs β-catenin, while ligand–receptor interaction impairs GSK-3β function to increase β-catenin stability and promote its nuclear transfer. Regarding the oncogenic function of Wnt/β-catenin, its upregulation occurs in human cancers and it can accelerate EMT-mediated metastasis and drug resistance. The stimulation of Wnt by binding Wnt ligands into Frizzled receptors can enhance β-catenin accumulation in cytoplasm that stimulates EMT and related genes upon nuclear translocation. Wnt/β-catenin/EMT axis has been implicated in augmenting metastasis of both solid and hematological tumors. The Wnt/EMT-mediated cancer metastasis promotes the malignant behavior of tumor cells, causing therapy resistance. The Wnt/β-catenin/EMT axis can be modulated by upstream mediators in which non-coding RNAs are main regulators. Moreover, pharmacological intervention, mainly using phytochemicals, suppresses Wnt/EMT axis in metastasis suppression. Graphical abstract

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ETS1 drives EGF-induced glycolytic shift and metastasis of epithelial ovarian cancer cells

Chatterjee,

Ghosh,

Chowdhury

et al. 2024

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Ets1 facilitates EMT/invasion through Drp1-mediated mitochondrial fragmentation in ovarian cancer

Cited by 5 publications

References 52 publications

Independent organelle and organelle—organelle interactions: essential mechanisms for malignant gynecological cancer cell survival

Independent organelle and organelle—organelle interactions: essential mechanisms for malignant gynecological cancer cell survival

Wnt/β-catenin-driven EMT regulation in human cancers

ETS1 drives EGF-induced glycolytic shift and metastasis of epithelial ovarian cancer cells

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