Expression Profile of Metabotropic Glutamate Receptors in Lung Adenocarcinoma: GRM5 and Validation of Its Targeting Drug Cinchonine

TL;DR

This study identifies GRM5 as a potential target for treating lung adenocarcinoma and shows that cinchonine enhances its antitumor effects.

Contribution

The study validates GRM5 as a therapeutic target and identifies cinchonine as a potential GRM5 agonist for lung adenocarcinoma treatment.

Findings

GRM5 is significantly associated with LUAD prognosis and tumor immune microenvironment.

Cinchonine treatment enhances GRM5's antitumor effects by inducing apoptosis and inhibiting proliferation.

Transcriptome sequencing identified four downstream targets and signaling pathways linked to GRM5.

Abstract

The incidence and mortality rates of lung adenocarcinoma (LUAD) continue to rise, highlighting an urgent need for novel therapeutic targets. In this study, bioinformatics analysis revealed that members of the metabotropic glutamate receptor (mGluR) family are significantly correlated with the expression profile, prognosis, genetic mutations, and tumor immune microenvironment of LUAD, with GRM5 being the most significantly associated member. Overexpression of GRM5 has been shown to inhibit LUAD proliferation and induce apoptosis, while cinchonine (CN) treatment further enhances these effects, suggesting that CN may act as a GRM5 agonist to synergistically exert antitumor activity. Transcriptome sequencing further identified four key downstream targets and their associated signaling pathways. In summary, this study confirms that GRM5 can serve as a potential prognostic biomarker and therapeutic target for LUAD, while the small-molecule compound CN shows promise as an antitumor candidate drug targeting GRM5.

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