C₁₈H₁₇NO₆ inhibits proliferation and induces apoptosis in human osteosarcoma U2OS cells via the PI3K/AKT signaling pathway.
4 affiliations
- 1Department of Otolaryngology, Affiliated Hospital of Yunnan University, Kunming, China.
- 2Department of Otolaryngology-Head and Neck Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, China.
- 3Department of Otolaryngology, Yan'an Hospital of Kunming City, Kunming, China.
- 4Department of Otolaryngology, 920th Hospital, Joint Logistics Support Force of the Chinese People's Liberation Army, Kunming, China.
Abstract
C18H17NO6 is a dibenzofuran derivative of (+)-usnic acid extracted from Usnea lichens. The present study aimed to investigate the effects and potential mechanisms of C18H17NO6 on human osteosarcoma U2OS cells. U2OS cells were treated with different concentrations of C18H17NO6. Cell proliferation was detected using the cell counting kit-8 (CCK-8) assay. Cell apoptosis was determined by TdT-mediated dUTP nick-end labeling (TUNEL) staining and flow cytometry [FCM; Annexin-V and propidium iodide (PI)], and cell cycle distribution was analyzed by FCM. Protein and messenger RNA (mRNA) expression levels were measured by western blot and quantitative real-time polymerase chain reaction (qRT-PCR). In vivo experiments were performed using a U2OS xenograft mouse model. Additionally, a PI3K agonist (740Y-P) and a PI3K inhibitor (LY294002) were used to verify the involvement of the PI3K/AKT pathway. C18H17NO6 inhibited U2OS cell proliferation in a dose- and time-dependent manner, induced apoptosis, and caused S-phase cell cycle arrest. It downregulated Ki67, proliferating cell nuclear antigen (PCNA), Bcl-2, p-AKT, and p-PI3K, while upregulating Bax, cleaved caspase-3, and cleaved caspase-9. In a U2OS xenograft mouse model, C18H17NO6 significantly suppresses tumor growth, preserves body weight, and reduces serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, without significantly affecting creatinine (CREA) or urea nitrogen (UREA); it also inhibits p-PI3K and p-AKT in tumor tissues. The PI3K agonist 740Y-P reversed the C18H17NO6-induced downregulation of PI3K/AKT phosphorylation, whereas the PI3K inhibitor LY294002 mimicked the effects of C18H17NO6. C18H17NO6 exerts significant antitumor effects in vitro and in vivo by inhibiting the PI3K/AKT signaling pathway.
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BibTeX
@article{qu2026c₁₈h₁₇no₆,
title = {{C₁₈H₁₇NO₆ inhibits proliferation and induces apoptosis in human osteosarcoma U2OS cells via the PI3K/AKT signaling pathway.}},
author = {Qianqian Qu and Enzi Feng and Shiwen Zhang and Zhongshun He and Jing Pan and Jin Wang and Yanli Yang},
journal = {Translational cancer research},
year = {2026},
month = sep,
doi = {10.21037/tcr-2026-1764},
url = {https://europepmc.org/article/MED/42997691},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - C₁₈H₁₇NO₆ inhibits proliferation and induces apoptosis in human osteosarcoma U2OS cells via the PI3K/AKT signaling pathway.
AU - Qianqian Qu
AU - Enzi Feng
AU - Shiwen Zhang
AU - Zhongshun He
AU - Jing Pan
AU - Jin Wang
AU - Yanli Yang
PY - 2026
DA - 2026/09/28
JO - Translational cancer research
DO - 10.21037/tcr-2026-1764
UR - https://europepmc.org/article/MED/42997691
AB - C18H17NO6 is a dibenzofuran derivative of (+)-usnic acid extracted from Usnea lichens. The present study aimed to investigate the effects and potential mechanisms of C18H17NO6 on human osteosarcoma U2OS cells. U2OS cells were treated with different concentrations of C18H17NO6. Cell proliferation was detected using the cell counting kit-8 (CCK-8) assay. Cell apoptosis was determined by TdT-mediated dUTP nick-end labeling (TUNEL) staining and flow cytometry [FCM; Annexin-V and propidium iodide (PI)], and cell cycle distribution was analyzed by FCM. Protein and messenger RNA (mRNA) expression levels were measured by western blot and quantitative real-time polymerase chain reaction (qRT-PCR). In vivo experiments were performed using a U2OS xenograft mouse model. Additionally, a PI3K agonist (740Y-P) and a PI3K inhibitor (LY294002) were used to verify the involvement of the PI3K/AKT pathway. C18H17NO6 inhibited U2OS cell proliferation in a dose- and time-dependent manner, induced apoptosis, and caused S-phase cell cycle arrest. It downregulated Ki67, proliferating cell nuclear antigen (PCNA), Bcl-2, p-AKT, and p-PI3K, while upregulating Bax, cleaved caspase-3, and cleaved caspase-9. In a U2OS xenograft mouse model, C18H17NO6 significantly suppresses tumor growth, preserves body weight, and reduces serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, without significantly affecting creatinine (CREA) or urea nitrogen (UREA); it also inhibits p-PI3K and p-AKT in tumor tissues. The PI3K agonist 740Y-P reversed the C18H17NO6-induced downregulation of PI3K/AKT phosphorylation, whereas the PI3K inhibitor LY294002 mimicked the effects of C18H17NO6. C18H17NO6 exerts significant antitumor effects in vitro and in vivo by inhibiting the PI3K/AKT signaling pathway.
SN - 2218-676X
SN - 2219-6803
ER -