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KM04416 通过促进免疫浸润抑制肺腺癌进展。

KM04416 suppressed lung adenocarcinoma progression by promoting immune infiltration.

机构信息

Department of Pulmonary and Critical Care Medicine, Respiratory Medicine Center of Fujian Province, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.

Department of Oncology, Dongguan People 's Hospital, Dongguan, China.

出版信息

J Cardiothorac Surg. 2024 Jul 25;19(1):465. doi: 10.1186/s13019-024-02971-w.

Abstract

OBJECTIVES

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.

MATERIALS AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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

摘要

目的

肺腺癌(LUAD)是一种起源于支气管黏膜或肺腺的恶性肿瘤,发病率和死亡率增长最快。因此,肺癌的预后仍然较差。甘油-3-磷酸脱氢酶 2(GPD2)是生物学中广泛存在的蛋白模式序列,与肿瘤进展密切相关。GPD2 抑制剂在 LUAD 中的治疗价值尚不清楚。因此,我们旨在分析 GPD2 抑制剂在 LUAD 中的治疗价值。

材料和方法

使用癌症基因组图谱(TCGA)-LUAD 数据库分析 LUAD 组织中 GPD2 的表达水平。通过 Kaplan-Meier 方法分析 GPD2 表达与 LUAD 患者生存的关系。此外,使用 KM04416 作为 GPD2 的靶标抑制剂进一步研究 GPD2 抑制剂在 LUAD 细胞系(A549 细胞和 H1299 细胞)中的治疗价值。使用 TISIDB 网站研究 GPD2 表达与 LUAD 中免疫细胞浸润的相关性。

结果

结果表明,GPD2 在 LUAD 组织中过表达,与预后不良显著相关。KM04416 可以通过靶向 GPD2 抑制 LUAD 细胞的进展。GPD2 的低表达与免疫细胞的高浸润有关。

结论

综上所述,本研究发现,通过调节免疫细胞浸润,KM04416 靶向抑制 GPD2 可以抑制 LUAD 的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6353/11270931/815fe63e00c2/13019_2024_2971_Fig1_HTML.jpg

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