The role of ion homeostasis imbalance due to citrate accumulation in fluoroacetic acid (FAA) toxicity in Neurospora crassa

Monteiro, João; Marks, Clive A.; Braga, Patrícia C.; Bernardino, Raquel L.; Alves, Marco G.; Lobo-da-Cunha, Alexandre; Videira, Arnaldo; Pereira, Filipe

doi:10.1016/j.cbpc.2023.109661

Cited by 1 publication

(1 citation statement)

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“…Research has revealed that an imbalance in ion proportions within mitochondria can lead to conformational changes in mitochondrial calcium uptake and ATP synthase dimers. This alteration prompts the opening of mPTP, causing decrease in MMP and ultimately cul minating in cell death[ 29 ]. The opening of mPTP allows unrestricted movement of ions and small molecules, resulting in mitochondrial depolarization and ATP consumption, thereby triggering cell death[ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial carrier homolog 2 increases malignant phenotype of human gastric epithelial cells and promotes proliferation, invasion, and migration of gastric cancer cells

Zhang,

Huang,

et al. 2024

World J Gastrointest Oncol

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BACKGROUND The precise role of mitochondrial carrier homolog 2 (MTCH2) in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated. AIM To determine the role of MTCH2 in gastric cancer. METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues, constructed MTCH2-overexpressing and MTCH2-knockdown cell models, and evaluated the proliferation, migration, and invasion of human gastric epithelial cells (GES-1) and human gastric cancer cells (AGS) cells. The mitochondrial membrane potential (MMP), mitochondrial permeability transformation pore (mPTP) and ATP fluorescence probe were used to detect mitochondrial function. Mitochondrial function and ATP synthase protein levels were detected via Western blotting. RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues. Overexpression of MTCH2 promoted colony formation, invasion, migration, MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis; knockdown of MTCH2 had the opposite effect, promoting overactivation of the mPTP and promoting apoptosis. CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation, invasion, and migration of gastric cancer cells by regulating mitochondrial function, providing a basis for targeted therapy for gastric cancer cells.

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Section: Discussionmentioning

confidence: 99%