2024 Asia Conference on Lung Cancer (ACLC) - Poster & ePosters-PP01.49

PP01.49 - Yuan Xu

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The study investigates the role of KCNK3, a potassium channel also known as TASK-1, in the context of lung adenocarcinoma (LUAD). The researchers aim to understand how KCNK3 affects cell proliferation and glucose metabolism in LUAD through various molecular pathways.<br /><br />Key findings indicate that KCNK3 is significantly downregulated in LUAD tissues compared to normal adjacent tissues. The experimental approach involved RNA sequencing, real-time PCR, western blotting, and immunohistochemistry to analyze KCNK3 expression levels. The study further employed gain and loss-of-function assays, metabolomics analysis, and immunofluorescence to explore the role of KCNK3 in cancer progression and metabolic processes specific to LUAD cells.<br /><br />The results demonstrate that overexpression of KCNK3 significantly regulates oncogenic processes and glycometabolism in LUAD. KCNK3 was found to influence differential metabolites mainly involved in the AMPK signaling pathway. The research highlights that KCNK3 inhibits the proliferation and glucose metabolism of LUAD cells via the activation of the AMPK-TXNIP pathway. This establishes a novel insight into the potential mechanism by which KCNK3 could serve as a therapeutic target or biomarker for LUAD.<br /><br />This study presents the first detailed analysis of the regulatory role of the FENDRR/miR-6815-5p axis in early-stage LUAD progression, suggesting that further in vitro and in vivo research is essential for comprehensive understanding. Overall, KCNK3 presents as a crucial molecular player whose modulation affects key metabolic and proliferative signaling pathways in lung adenocarcinoma.

Keywords

KCNK3

TASK-1

lung adenocarcinoma

LUAD

cell proliferation

glucose metabolism

AMPK signaling pathway

FENDRR/miR-6815-5p axis

biomarker

therapeutic target