KM04416 suppressed lung adenocarcinoma progression by promoting immune infiltration

TL;DR

This study shows that the drug KM04416 can slow lung cancer growth by boosting immune cell activity.

Contribution

The study identifies KM04416 as a GPD2 inhibitor that suppresses lung adenocarcinoma progression through immune infiltration.

Findings

GPD2 is overexpressed in lung adenocarcinoma tissues and linked to poor survival.

KM04416 inhibits LUAD cell progression by targeting GPD2.

Low GPD2 expression correlates with high immune cell infiltration in LUAD.

Abstract

Lung adenocarcinoma (LUAD) is a malignant tumor originating from the bronchial mucosa or glands of the lung, with the fastest increasing morbidity and mortality. Therefore, the prognosis of lung cancer remains poor. Glycerol-3-phosphate dehydrogenase 2 (GPD2) is a widely existing protein pattern sequence in biology and is closely related to tumor progression. The therapy values of GPD2 inhibitor in LUAD were unclear. Therefore, we aimed to analyze the therapy values of GPD2 inhibitor in LUAD.

The Cancer Genome Atlas (TCGA)-LUAD database was used to analyze the expression levels of GPD2 in LUAD tissues. The relationship between GPD2 expression and LUAD patient survival was analyzed by Kaplan-Meier method. Moreover, KM04416 as a target inhibitor of GPD2 was used to further investigate the therapy value of GPD2 inhibitor in LUAD cells lines (A549 cell and H1299 cell). The TISIDB website was used to investigate the associations between GPD2 expression and immune cell infiltration in LUAD.

The results showed that GPD2 is overexpressed in LUAD tissues and significantly associated with poor survival. KM04416 can suppress the progression of LUAD cells by targeting GPD2. Low expression of GPD2 is related to high infiltration of immune cells.

In summary, our present study found that targeting inhibition of GPD2 by KM04416 can suppress LUAD progression via adjusting immune cell infiltration.

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