Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway
AbstractTaccalonolide A has been reported to have anti-tumour efficiency. However, the underlying mechanism for taccalonolides A therapy of hepatocellular carcinoma (HCC) is still obscure. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Apoptosis was determined by flow cytometry....
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2020-01-01
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Series: | Artificial Cells, Nanomedicine, and Biotechnology |
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Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2020.1773484 |
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author | Hui Tian Zhenkun He |
author_facet | Hui Tian Zhenkun He |
author_sort | Hui Tian |
collection | DOAJ |
description | AbstractTaccalonolide A has been reported to have anti-tumour efficiency. However, the underlying mechanism for taccalonolides A therapy of hepatocellular carcinoma (HCC) is still obscure. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Apoptosis was determined by flow cytometry. Protein expression of B cell lymphoma (Bcl-2), Bcl-2 associated X (Bax), sonic hedgehog (Shh), Smoothened (Smo) and Gli family zinc finger 1 (Gli1) was analyzed by western blot. The expression of Shh, Smo and Gli1 mRNA was determined using quantitative real-time polymerase chain reaction (qRT-PCR). Results showed that taccalonolide A inhibited cell proliferation, induced apoptosis and cell cycle arrest at the G0/G1 phase, and improved the cytotoxicity of sorafenib in HCC cells. The expressions of Shh, Smo, Gli1 mRNA and protein were decreased after taccalonolide A treatment. More importantly, activation of the Shh pathway attenuated taccalonolide A-induced inhibition on cell viability and promotion on apoptosis and cell cycle arrest in HCC. Also, activation of the Shh pathway neutralized the effect of taccalonolide A on sorafenib cytotoxicity in HCC. We clarified that taccalonolide A suppressed cell viability facilitated apoptosis, and improved the cytotoxicity of sorafenib in HCC by inhibition of the activation of the Shh pathway, providing alternative treatments for HCC. |
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id | doaj.art-4137575516e641d19ecaaa3aa937579d |
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issn | 2169-1401 2169-141X |
language | English |
last_indexed | 2024-03-13T01:40:33Z |
publishDate | 2020-01-01 |
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series | Artificial Cells, Nanomedicine, and Biotechnology |
spelling | doaj.art-4137575516e641d19ecaaa3aa937579d2023-07-03T14:04:56ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2020-01-0148193994710.1080/21691401.2020.1773484Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathwayHui Tian0Zhenkun He1Department of Infectious Disease, Huaihe Hospital of Henan University, Kaifeng, Henan, ChinaDepartment of Infectious Disease, Huaihe Hospital of Henan University, Kaifeng, Henan, ChinaAbstractTaccalonolide A has been reported to have anti-tumour efficiency. However, the underlying mechanism for taccalonolides A therapy of hepatocellular carcinoma (HCC) is still obscure. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Apoptosis was determined by flow cytometry. Protein expression of B cell lymphoma (Bcl-2), Bcl-2 associated X (Bax), sonic hedgehog (Shh), Smoothened (Smo) and Gli family zinc finger 1 (Gli1) was analyzed by western blot. The expression of Shh, Smo and Gli1 mRNA was determined using quantitative real-time polymerase chain reaction (qRT-PCR). Results showed that taccalonolide A inhibited cell proliferation, induced apoptosis and cell cycle arrest at the G0/G1 phase, and improved the cytotoxicity of sorafenib in HCC cells. The expressions of Shh, Smo, Gli1 mRNA and protein were decreased after taccalonolide A treatment. More importantly, activation of the Shh pathway attenuated taccalonolide A-induced inhibition on cell viability and promotion on apoptosis and cell cycle arrest in HCC. Also, activation of the Shh pathway neutralized the effect of taccalonolide A on sorafenib cytotoxicity in HCC. We clarified that taccalonolide A suppressed cell viability facilitated apoptosis, and improved the cytotoxicity of sorafenib in HCC by inhibition of the activation of the Shh pathway, providing alternative treatments for HCC.https://www.tandfonline.com/doi/10.1080/21691401.2020.1773484Taccalonolide AsorafenibShh pathwayhepatocellular carcinoma |
spellingShingle | Hui Tian Zhenkun He Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway Artificial Cells, Nanomedicine, and Biotechnology Taccalonolide A sorafenib Shh pathway hepatocellular carcinoma |
title | Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway |
title_full | Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway |
title_fullStr | Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway |
title_full_unstemmed | Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway |
title_short | Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway |
title_sort | anti hepatoma effect of taccalonolide a through suppression of sonic hedgehog pathway |
topic | Taccalonolide A sorafenib Shh pathway hepatocellular carcinoma |
url | https://www.tandfonline.com/doi/10.1080/21691401.2020.1773484 |
work_keys_str_mv | AT huitian antihepatomaeffectoftaccalonolideathroughsuppressionofsonichedgehogpathway AT zhenkunhe antihepatomaeffectoftaccalonolideathroughsuppressionofsonichedgehogpathway |