ArticleTranslational oncology2026
11-Oxo-mogroside V attenuates lung adenocarcinoma progression by disrupting metabolic homeostasis and suppressing TGFβ2/Myc-dependent oncogenic signaling.
Article in Translational oncology, 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-related mortality worldwide, with nonsmokers comprising a notable proportion of cases. The complexity of its molecular pathogenesis poses substantial challenges for the development of effective therapeutic strategies. Traditional Chinese medicine-derived compounds have garnered attention for their multi-target engagement and favorable safety profiles.
objectiveThis study aimed to characterize the antitumor effects and elucidate the mechanistic basis of 11-oxo-mogroside V, a bioactive triterpenoid saponin from Siraitia grosvenorii, in LUAD.
methodsIn vitro assays (CCK-8, flow cytometry, wound-healing, metabolic measurements) were performed on lung adenocarcinoma cells. In vivo efficacy was evaluated using a xenograft mouse model with bioluminescent monitoring and TUNEL staining. Transcriptomic profiling, molecular docking, immunoblotting, and co-immunoprecipitation elucidated mechanistic pathways.
results11-oxo-mogroside V (800 μg/mL, 72 h) significantly reduced cell viability, induced G0/G1 arrest, and promoted apoptosis (apoptotic rate increased from 3.01% to 12.00%, P < 0.0001). Migration was suppressed (wound closure reduced from 77.66% to 43.98%, P < 0.0001). Metabolic disruption was evidenced by decreased intracellular ATP, glucose uptake, and LDH activity. In vivo, 11-oxo-mogroside V (100 mg/kg, daily) markedly inhibited tumor growth (photon flux reduced from 2.65 × 10¹⁰ to 1.50 × 10¹⁰, P < 0.0001) and increased apoptosis (TUNEL-positive cells from 0.40% to 5.97%, P < 0.0001). Mechanistically, RNA-seq analysis and molecular docking suggested TGFB2, HDAC1, and c-Myc as potential molecular targets, with docking simulations indicating favorable binding affinities. Western blot confirmed downregulation of TGFB2, Smad2/3, TGIF, HDAC1, c-Myc, and Bcl2, alongside upregulation of Bax, with co-IP demonstrating HDAC1-TGIF1 interaction.
conclusion11-oxo-mogroside V exerts potent anti-LUAD activity by disrupting metabolic homeostasis and suppressing TGFβ2/HDAC1/c-Myc signaling, positioning it as a promising lead compound for therapeutic development.
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