KAT7 promoted gastric cancer progression through promoting YAP1 activation

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Lysine acetyltransferase 7 (KAT7) is upregulated in gastric cancer (GC) tissues.
• Elevated KAT7 expression correlates with poor prognosis and metastasis in GC patients.
• The precise function of KAT7 in GC pathogenesis is not fully understood.

Purpose of the Study:

• To elucidate the specific role and molecular mechanisms of KAT7 in GC progression.
• To investigate the impact of KAT7 on GC cell proliferation, migration, and invasion.
• To explore the relationship between KAT7 and the Yes-associated protein 1 (YAP1) pathway in GC.

Main Methods:

• Overexpression and inhibition of KAT7 in GC cell lines.
• Assessment of cell proliferation, migration, and invasion assays.
• Analysis of cell cycle distribution and epithelial-mesenchymal transition (EMT) markers.
• Investigation of YAP1 transcription, nuclear translocation, and functional impact via gene silencing.

Main Results:

• KAT7 overexpression significantly enhanced GC cell growth, migration, and invasion.
• KAT7 inhibition demonstrated opposite effects, suppressing GC cell progression.
• KAT7 influenced cell cycle distribution and promoted EMT in GC cells.
• KAT7 was found to promote YAP1 transcription and nuclear translocation.
• YAP1 silencing partially reversed the pro-tumorigenic effects of KAT7.

Conclusions:

• KAT7 acts as a crucial driver of GC progression by promoting cell proliferation, migration, invasion, and EMT.
• The KAT7-mediated promotion of GC progression involves the activation of the YAP1 pathway.
• These findings highlight KAT7 as a potential therapeutic target for gastric cancer.