Scholarlink

<p>Hyperglycemic conditions up - regulate TIMM44, an inner mitochondrial membrane protein. Its expression is related to many cancers, yet its role in gastric cancer (GC) remains unproven. To study this, we used western blot and qRT - PCR to measure protein and mRNA levels. Flow cytometry analyzed cell cycle progression. CCK − 8, colony formation, wound healing, Transwell, and EdU assays evaluated cell viability, migratory and invasion abilities. TUNEL - based method detected apoptosis, and immunohistochemical assay compared TIMM44 expression in GC and adjacent non - cancerous tissues. The results showed TIMM44 was highly expressed in GC tissues. Over - expressing TIMM44 promoted AGS and HGC27 cells’ viability, proliferation, invasion, and migration, while its depletion inhibited these. Forced TIMM44 expression increased Gαi1 and Akt phosphorylation. In conclusion, TIMM44 is crucial in the Gαi1 - PI3K - AKT - mTOR pathway, enhancing GC cells’ malignancy and potentially threatening patient survival.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mechanistic study of TIMM44 mediating gastric carcinogenesis via the Gαi1-PI3K-AKT-mTOR signaling pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月5日

查看全文
  • Ting Chen,
  • Rong Xu,
  • Xiaojing Shi,
  • Dongliang Yang,
  • Yi Du,
  • Yu Song,
  • Yan Lv,
  • Yanan Chen

摘要

Hyperglycemic conditions up - regulate TIMM44, an inner mitochondrial membrane protein. Its expression is related to many cancers, yet its role in gastric cancer (GC) remains unproven. To study this, we used western blot and qRT - PCR to measure protein and mRNA levels. Flow cytometry analyzed cell cycle progression. CCK − 8, colony formation, wound healing, Transwell, and EdU assays evaluated cell viability, migratory and invasion abilities. TUNEL - based method detected apoptosis, and immunohistochemical assay compared TIMM44 expression in GC and adjacent non - cancerous tissues. The results showed TIMM44 was highly expressed in GC tissues. Over - expressing TIMM44 promoted AGS and HGC27 cells’ viability, proliferation, invasion, and migration, while its depletion inhibited these. Forced TIMM44 expression increased Gαi1 and Akt phosphorylation. In conclusion, TIMM44 is crucial in the Gαi1 - PI3K - AKT - mTOR pathway, enhancing GC cells’ malignancy and potentially threatening patient survival.