EH-42 : A Novel Small Molecule Induces Apoptosis and Inhibits Migration and Invasion of Human Hepatoma Cells through Suppressing STAT3 Signaling Pathway
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
BACKGROUND: Since signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in hepatocellular carcinoma (HCC) and plays a key role in this tumor progression. Inhibition of the STAT3 signaling pathway has been considered as an effective therapeutic strategy for suppressing HCC development.
OBJECTIVE: In this study, we investigated the anti-cancer effects of EH-42 on HCC cells and tried to explain the underlying mechanism.
METHODS: MTT assay, colon formation assay and AnnexinV-FITC/PI double-staining assay were performed to assess the effects of EH-42 on cell growth and survival. Wound healing assay and transwell invasion assay were performed to assess the effects of EH-42 on cell migration and invasion. Western blotting assay was performed to analyze the effects of EH-42 on relative proteins.
RESULTS: According to the MTT assay, colon formation assay and AnnexinV-FITC/PI doublestaining assay, EH-42 could suppress the growth and induce apoptosis of HCC cells in a dosedependent manner. Further western blotting assay showed that the inhibitory effects of EH-42 on cell growth and survival were caused by activating caspase 3/9, suppressing the phospho-STAT3 (Tyr 705) and downregulating anti-apoptotic proteins like Bcl-2/Bcl-xL. Moreover, migration and invasion abilities of HCC cells were also inhibited by EH-42 in the wound healing assay and transwell invasion assay. The potential mechanism was that EH-42 could inhibit HCC metastasis via reversing epithelial-mesenchymal transition and downregulating the secretion of MMPs.
CONCLUSION: Taken together, these findings suggested that EH-42 could be a potential therapeutic agent for HCC treatment.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2019 |
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| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:19 |
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| Enthalten in: |
Current cancer drug targets - 19(2019), 7 vom: 01., Seite 583-593 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Gong, Qi-Zhe [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 03.09.2020 Date Revised 03.09.2020 published: Print Citation Status MEDLINE |
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| doi: |
10.2174/1568009619666181226094814 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM292148895 |
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| 100 | 1 | |a Gong, Qi-Zhe |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a EH-42 |b A Novel Small Molecule Induces Apoptosis and Inhibits Migration and Invasion of Human Hepatoma Cells through Suppressing STAT3 Signaling Pathway |
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| 500 | |a Date Revised 03.09.2020 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
| 520 | |a BACKGROUND: Since signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in hepatocellular carcinoma (HCC) and plays a key role in this tumor progression. Inhibition of the STAT3 signaling pathway has been considered as an effective therapeutic strategy for suppressing HCC development | ||
| 520 | |a OBJECTIVE: In this study, we investigated the anti-cancer effects of EH-42 on HCC cells and tried to explain the underlying mechanism | ||
| 520 | |a METHODS: MTT assay, colon formation assay and AnnexinV-FITC/PI double-staining assay were performed to assess the effects of EH-42 on cell growth and survival. Wound healing assay and transwell invasion assay were performed to assess the effects of EH-42 on cell migration and invasion. Western blotting assay was performed to analyze the effects of EH-42 on relative proteins | ||
| 520 | |a RESULTS: According to the MTT assay, colon formation assay and AnnexinV-FITC/PI doublestaining assay, EH-42 could suppress the growth and induce apoptosis of HCC cells in a dosedependent manner. Further western blotting assay showed that the inhibitory effects of EH-42 on cell growth and survival were caused by activating caspase 3/9, suppressing the phospho-STAT3 (Tyr 705) and downregulating anti-apoptotic proteins like Bcl-2/Bcl-xL. Moreover, migration and invasion abilities of HCC cells were also inhibited by EH-42 in the wound healing assay and transwell invasion assay. The potential mechanism was that EH-42 could inhibit HCC metastasis via reversing epithelial-mesenchymal transition and downregulating the secretion of MMPs | ||
| 520 | |a CONCLUSION: Taken together, these findings suggested that EH-42 could be a potential therapeutic agent for HCC treatment | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a STAT3 | |
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| 650 | 4 | |a hepatocellular carcinoma | |
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| 700 | 1 | |a Gong, Gui-Yi |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Jian |e verfasserin |4 aut | |
| 700 | 1 | |a Wen, Xiao-Dong |e verfasserin |4 aut | |
| 700 | 1 | |a Feng, Feng |e verfasserin |4 aut | |
| 700 | 1 | |a Qu, Wei |e verfasserin |4 aut | |
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