Study on the mechanism of gracillin inhibiting the proliferation of lung cancer NCI-H1299 cells based on MAPK signaling pathway
Bang Xiao, Minhong Zhang, Hai Liu, Aiping Cui, Yihe Tian, Fosheng Tang, Shichen Liao, Mingchun Li, Hao Huang, Weijie Peng, Jianqiong Yang
TL;DR
This study shows that gracillin, a natural compound, can inhibit lung cancer cell growth by triggering autophagy through the MAPK signaling pathway.
Contribution
The study reveals a novel mechanism by which gracillin induces autophagic cell death in lung cancer via MAPK pathway modulation.
Findings
Gracillin significantly inhibits NCI-H1299 cell proliferation and induces autophagic cell death.
Gracillin activates the MAPK pathway by increasing p-ERK and decreasing p-JNK levels.
Gracillin upregulates WIPI1, an autophagy-related protein, potentially downstream of the ERK pathway.
Abstract
In this study, we investigated the potential of gracillin, a steroidal saponin compound, as an anticancer agent against non-small cell lung cancer (NSCLC) and explored its impact on autophagy mechanisms. Gracillin significantly inhibited NCI-H1299 cell proliferation and induced autophagic cell death. Mechanistically, gracillin activated the MAPK signaling pathway, evidenced by increased p-ERK and decreased p-JNK levels, suggesting their roles in mediating autophagy induction. Additionally, gracillin upregulated WIPI1 expression, a key autophagy-related protein potentially downstream of the ERK pathway. Evaluation in a xenograft mouse model demonstrated robust anticancer efficacy of gracillin with no significant adverse effects observed. These findings highlight gracillin as a promising candidate for NSCLC therapy, leveraging its ability to induce autophagy through MAPK pathway…
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Taxonomy
TopicsCytokine Signaling Pathways and Interactions · Medicinal Plant Pharmacodynamics Research · Cancer Research and Treatments