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Effect of luteolin on glioblastoma's immune microenvironment and tumor growth suppression
Shengliang Zong1, Xinqiao Li1, Guoqing Zhang1
1Department of Neurosurgery, The First Hospital of China Medical University, No. 155 North Nanjing Street, Heping District, Shenyang, Liaoning Province 110001, China.
Background:
Glioblastoma is the most malignant and prevalent primary human brain tumor, and the immunological microenvironment controlled by glioma stem cells is one of the essential elements contributing to its malignancy. The use of medications to ameliorate the tumor microenvironment may give a new approach for glioma treatment.
Methods:
Glioma stem cells were separated from clinical patient-derived glioma samples for molecular research. Other studies, including CCK8, EdU, Transwell, and others, supported luteolin's ability to treat glioma progenitor cells. Network pharmacology and molecular docking models were used to study the drug target, and qRT-PCR, WB, and IF were used to evaluate the molecular mechanism. Intracranial xenografts were examined using HE and IHC, while macrophage polarization was examined using FC.
Results:
We originally discovered that luteolin inhibits glioma stem cells. IL6 released by glioma stem cells is blocked during medication action and inhibits glioma stem cell proliferation and invasion via the IL6/STAT3 signaling pathway. Additionally, luteolin inhibits the secretion of TGFβ1, affects the polarization function of macrophages in the microenvironment, inhibits the polarization of M2 macrophages in TAM, and further inhibits various functions of glioma stem cells by affecting the IL6/STAT3 signaling pathway, luteolin crosstalk TGFβ1/SMAD3 signaling pathway, and so on.
Conclusions:
Through the suppression of the immunological microenvironment and inhibition of the IL6/STAT3 signaling pathway, our study determined the inhibitory effect of luteolin on glioma stem cells. This medication's dual inhibitory action, which has a significant negative impact on the glioma stem cells' malignant process, makes it both a viable anti-glioma medication and a candidate for targeted glioma microenvironment therapy.
Insights
Luteolin effectively inhibits glioma stem cells by targeting the IL6/STAT3 pathway and modulating the tumor microenvironment. This dual action suppresses tumor growth and invasion, offering a promising therapeutic strategy for glioblastoma.
Area of Science:
- Neuro-oncology
- Immunology
- Pharmacology
Background:
- Glioblastoma is a highly malignant brain tumor where the tumor microenvironment, influenced by glioma stem cells, significantly contributes to its progression.
- Targeting the tumor microenvironment presents a novel therapeutic avenue for glioblastoma treatment.
Purpose of the Study:
- To investigate the inhibitory effects of luteolin on glioma stem cells and elucidate its underlying molecular mechanisms.
- To explore luteolin's impact on the tumor immunological microenvironment and its potential as an anti-glioma therapeutic.
Main Methods:
- Glioma stem cells were isolated from patient samples.
- Cellular assays (CCK8, EdU, Transwell) evaluated luteolin's efficacy.
- Network pharmacology and molecular docking identified drug targets.
- Molecular mechanisms were assessed using qRT-PCR, Western blot, and immunofluorescence.
- In vivo studies involved intracranial xenografts (HE, IHC) and macrophage polarization analysis (FC).
Main Results:
- Luteolin demonstrated significant inhibition of glioma stem cell proliferation and invasion.
- Luteolin blocked IL6 secretion, impacting the IL6/STAT3 signaling pathway.
- Luteolin inhibited TGFβ1 secretion, affecting macrophage polarization (M2 TAMs) and influencing the tumor microenvironment.
Conclusions:
- Luteolin exhibits potent anti-glioma stem cell activity by suppressing the tumor's immunological microenvironment and inhibiting the IL6/STAT3 signaling pathway.
- Luteolin's dual inhibitory action on glioma stem cells and the tumor microenvironment positions it as a potential anti-glioma drug and a candidate for targeted microenvironment therapy.
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