Conclusions
This study revealed the regulatory mechanism of STK11 mutation affecting tumor proliferation by impacting CD4+ T cell activity in LUAD. It suggested that STK11 may be a possible biological target for LUAD patients, and inhibiting STK11 mutation or cutting off its regulatory pathway for immune function may be an effective strategy for STK11-mutated tumor patients.
Material and methods
qRT-PCR experiments verified the STK11 level in different cell models. Cell Counting Kit-8 (CCK-8) and colony formation experiments evaluated proliferation ability. CCK-8 detected activity of CD4+ T cells. Immunohistochemistry detected levels of related genes. Immunofluorescence assayed levels of CD4+ T cell infiltration.
Methods
qRT-PCR experiments verified the STK11 level in different cell models. Cell Counting Kit-8 (CCK-8) and colony formation experiments evaluated proliferation ability. CCK-8 detected activity of CD4+ T cells. Immunohistochemistry detected levels of related genes. Immunofluorescence assayed levels of CD4+ T cell infiltration.
Results
STK11 mutation could accelerate proliferation of LUAD cells and impact activity of CD4+ T cells. Further research found that STK11 mutation affected tumor proliferation by impacting CD4+ T cell activity in LUAD. Conclusions: This study revealed the regulatory mechanism of STK11 mutation affecting tumor proliferation by impacting CD4+ T cell activity in LUAD. It suggested that STK11 may be a possible biological target for LUAD patients, and inhibiting STK11 mutation or cutting off its regulatory pathway for immune function may be an effective strategy for STK11-mutated tumor patients.