STS ⅡA inhibited angiogenesis of lung adenocarcinoma by activating FOXO3 to inhibit CXCL1/STAT3/VEGF pathway
Copyright © 2024. Published by Elsevier Ltd..
BACKGROUND: Lung adenocarcinoma (LUAD) is the most popular type of lung cancer. Sulfotanshinone IIA sodium (STS IIA) has been proven to have an anticancer effect. However, its role in LUAD and its underlying mechanism remain unclear.
OBJECTIVE: To investigate the role and mechanism of STS IIA in LUAD angiogenesis.
METHODS: The mRNA levels of genes, including forkhead box O3 (FOXO3) and chemokine C-X-C motif ligand 1 (CXCL1), were detected by qRT-PCR. The levels of proteins, including FOXO3, CXCL1, and vascular endothelial growth factor (VEGF), were measured by Western blot. The proliferation and angiogenesis of human umbilical vein endothelial cells (HUVECs) were detected by the EdU assay and the tubule formation assay, respectively. The binding relationship between FOXO3 and CXCL1 was detected by dual-luciferase reporter assay.
RESULTS: Our results illustrated that different concentrations of STS IIA inhibited the proliferation and angiogenesis of HUVECs. FOXO3 regulated the proliferation and angiogenesis of HUVECs inhibited by STS ⅡA via targeting CXCL1. Subsequently, we proved that exogenous CXCL1 alleviated the inhibition of proliferation and angiogenesis of HUVECs regulated by STS IIA via activating the STAT3/VEGF pathway. Finally, we found that STS IIA inhibited the angiogenesis of lung adenocarcinoma though FOXO3 to inhibit the CXCL1/STAT3/VEGF pathway.
CONCLUSION: Our study finally elucidated the underlying molecular mechanism by which STS ⅡA inhibits LUAD angiogenesis.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:240 |
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| Enthalten in: |
Toxicon : official journal of the International Society on Toxinology - 240(2024) vom: 01. März, Seite 107627 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wang, Bu [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 06.03.2024 Date Revised 06.03.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.toxicon.2024.107627 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 100 | 1 | |a Wang, Bu |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a STS ⅡA inhibited angiogenesis of lung adenocarcinoma by activating FOXO3 to inhibit CXCL1/STAT3/VEGF pathway |
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| 500 | |a Date Revised 06.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2024. Published by Elsevier Ltd. | ||
| 520 | |a BACKGROUND: Lung adenocarcinoma (LUAD) is the most popular type of lung cancer. Sulfotanshinone IIA sodium (STS IIA) has been proven to have an anticancer effect. However, its role in LUAD and its underlying mechanism remain unclear | ||
| 520 | |a OBJECTIVE: To investigate the role and mechanism of STS IIA in LUAD angiogenesis | ||
| 520 | |a METHODS: The mRNA levels of genes, including forkhead box O3 (FOXO3) and chemokine C-X-C motif ligand 1 (CXCL1), were detected by qRT-PCR. The levels of proteins, including FOXO3, CXCL1, and vascular endothelial growth factor (VEGF), were measured by Western blot. The proliferation and angiogenesis of human umbilical vein endothelial cells (HUVECs) were detected by the EdU assay and the tubule formation assay, respectively. The binding relationship between FOXO3 and CXCL1 was detected by dual-luciferase reporter assay | ||
| 520 | |a RESULTS: Our results illustrated that different concentrations of STS IIA inhibited the proliferation and angiogenesis of HUVECs. FOXO3 regulated the proliferation and angiogenesis of HUVECs inhibited by STS ⅡA via targeting CXCL1. Subsequently, we proved that exogenous CXCL1 alleviated the inhibition of proliferation and angiogenesis of HUVECs regulated by STS IIA via activating the STAT3/VEGF pathway. Finally, we found that STS IIA inhibited the angiogenesis of lung adenocarcinoma though FOXO3 to inhibit the CXCL1/STAT3/VEGF pathway | ||
| 520 | |a CONCLUSION: Our study finally elucidated the underlying molecular mechanism by which STS ⅡA inhibits LUAD angiogenesis | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Angiogenesis | |
| 650 | 4 | |a Lung adenocarcinoma | |
| 650 | 4 | |a Sulfotanshinone IIA sodium | |
| 650 | 7 | |a Vascular Endothelial Growth Factor A |2 NLM | |
| 650 | 7 | |a CXCL1 protein, human |2 NLM | |
| 650 | 7 | |a Chemokine CXCL1 |2 NLM | |
| 650 | 7 | |a FOXO3 protein, human |2 NLM | |
| 650 | 7 | |a Forkhead Box Protein O3 |2 NLM | |
| 650 | 7 | |a STAT3 protein, human |2 NLM | |
| 650 | 7 | |a STAT3 Transcription Factor |2 NLM | |
| 700 | 1 | |a Zou, Fang |e verfasserin |4 aut | |
| 700 | 1 | |a Xin, Gu |e verfasserin |4 aut | |
| 700 | 1 | |a Xiang, Bao-Li |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Jian-Qing |e verfasserin |4 aut | |
| 700 | 1 | |a Yuan, Sheng-Fang |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Xiu-Long |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Zhi-Hua |e verfasserin |4 aut | |
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