Dias Bárbara Dos Santos, Antunes Symara Rodrigues, Pinheiro Danilo do Rosário, Burbano Rommel Mario Rodriguez, Borges Bárbara do Nascimento
Albert Einstein Research and Educational Institute, Hospital Israelita Albert Einstein, São Paulo, São Paulo estado, Brazil.
Metropolitan University Center of the Amazon, Belém, Pará, Brazil.
J Med Primatol. 2025 Apr;54(2):e70017. doi: 10.1111/jmp.70017.
Gastric cancer (GC) remains among the top five global health problems. Therefore, comprehending the tumor energetic behavior is critical to understanding its progression. This study aimed to investigate mitochondrial DNA (mtDNA) alterations in GC cancer cell lines in an animal model.
Four mitochondrial genes (COI, ATP8, ND1, and ND3) were analyzed in GC (AGP01, ACP02, ACP03, and PG100) and control (Walker 256 carcinosarcoma) cell lines inoculated in Sapajus apella, exposed and not exposed to N-methyl-N-nitrosourea.
Two synonymous alterations were identified in ND1. In ND3, a non-synonymous alteration (A10398G ➔ Thr114Ala) may decrease the respiratory chain Complex I efficiency, enhancing cellular reactive oxygen species and contributing to mtDNA damage. As alterations in ND1 and ND3 were observed in highly aggressive cell lines, our results suggest these genes may play crucial roles in energetic efficiency and gastric carcinogenesis.
胃癌（GC）仍然是全球五大健康问题之一。因此，了解肿瘤的能量代谢行为对于理解其进展至关重要。本研究旨在研究动物模型中胃癌细胞系的线粒体DNA（mtDNA）改变。
对接种于黑帽卷尾猴体内、暴露和未暴露于N-甲基-N-亚硝基脲的胃癌（AGP01、ACP02、ACP03和PG100）和对照（Walker 256癌肉瘤）细胞系中的四个线粒体基因（COI、ATP8、ND1和ND3）进行分析。
在ND1中鉴定出两个同义改变。在ND3中，一个非同义改变（A10398G→Thr114Ala）可能会降低呼吸链复合体I的效率，增加细胞活性氧并导致mtDNA损伤。由于在高侵袭性细胞系中观察到ND1和ND3的改变，我们的结果表明这些基因可能在能量效率和胃癌发生中起关键作用。
