ArticleChinese medicine2026
Targeting oncogenic NTSR1 with liensinine reprograms Gq-mediated signaling to suppress lung adenocarcinoma.
Article in Chinese medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLung adenocarcinoma (LUAD) is a leading cause of cancer death. Neurotensin receptor 1 (NTSR1), a G protein-coupled receptor, is overexpressed in LUAD and linked to poor prognosis, but its therapeutic potential is underexplored.
methodsThis study combined multi-database bioinformatics to systematically evaluate the expression, prognostic relevance, genetic alterations, and immune-microenvironment association of NTSR1 across cancer types. The ONE-GO biosensor, SPR, PRESTO-Tango, and in-cell ELISA assays was used to confirm that liensinine specifically inhibits NTSR1-mediated G-protein signaling. Functional consequences of NTSR1 depletion and liensinine treatment-including effects on proliferation, apoptosis, and global transcription-were examined in vitro via CCK-8, flow cytometry, RNA-seq and Western blot. Key findings were validated by RT-qPCR in cellular models and further supported using LUAD patient cohorts from the UALCAN platform.
resultsBioinformatics analysis confirmed significant upregulation of NTSR1 in LUAD, and its high expression was closely associated with advanced tumor stage, remodeled immune microenvironment, and poor overall patient survival. ONE-GO profiling revealed preferential coupling of NTSR1 to Gα
conclusionsNTSR1 is a key oncogenic driver in LUAD. Liensinine is a novel NTSR1 antagonist that suppresses tumors by selectively inhibiting Gq signaling and reprogramming the transcriptional landscape.
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