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Article: Osthole inhibits the migration and invasion of highly metastatic breast cancer cells by suppressing ITGα3/ITGβ5 signaling

TitleOsthole inhibits the migration and invasion of highly metastatic breast cancer cells by suppressing ITGα3/ITGβ5 signaling
Authors
Keywordsbreast cancer
FAK/Src/Rac1 pathway
ITGα3
ITGβ5
metastasis
osthole
Wenshen Zhuanggu Formula
Issue Date2022
Citation
Acta Pharmacologica Sinica, 2022, v. 43, n. 6, p. 1544-1555 How to Cite?
AbstractMetastasis is the leading cause of death in breast cancer patients. Osthole, as an active compound detected in the traditional Chinese medicine Wenshen Zhuanggu Formula, has shown a promising anti-metastatic activity in human breast cancer cells, but the underlying mechanisms remain ambiguous. In this study we elucidated the anti-metastatic mechanisms of osthole in highly metastatic breast cancer cells and a zebrafish xenograft model. We showed that the expression of integrin α3 (ITGα3) and integrin β5 (ITGβ5) was upregulated in highly metastatic MDA-MB-231, MDA-MB-231BO breast cancer cell lines but was downregulated in poorly metastatic MCF-7 breast cancer cell line, which might be the key targets of osthole’s anti-metastatic action. Furthermore, we showed that knockdown of ITGα3 and ITGβ5 attenuated breast cancer cell migration and invasion possibly via suppression of FAK/Src/Rac1 pathway, whereas overexpression of ITGα3 and ITGβ5 caused the opposite effects. Consistently, osthole significantly inhibited breast cancer metastasis by downregulating ITGα3/ITGβ5 signaling in vitro and in vivo. These results provide new evidence that osthole may be developed as a candidate therapeutic drug for metastatic breast cancer.
Persistent Identifierhttp://hdl.handle.net/10722/335870
ISSN
2023 Impact Factor: 6.9
2023 SCImago Journal Rankings: 1.882
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, Yue qiang-
dc.contributor.authorSong, Hai yan-
dc.contributor.authorZhou, Zhong yan-
dc.contributor.authorMa, Jiao-
dc.contributor.authorLuo, Zhan yang-
dc.contributor.authorZhou, Ying-
dc.contributor.authorWang, Jian yi-
dc.contributor.authorLiu, Sheng-
dc.contributor.authorHan, Xiang hui-
dc.date.accessioned2023-12-28T08:49:22Z-
dc.date.available2023-12-28T08:49:22Z-
dc.date.issued2022-
dc.identifier.citationActa Pharmacologica Sinica, 2022, v. 43, n. 6, p. 1544-1555-
dc.identifier.issn1671-4083-
dc.identifier.urihttp://hdl.handle.net/10722/335870-
dc.description.abstractMetastasis is the leading cause of death in breast cancer patients. Osthole, as an active compound detected in the traditional Chinese medicine Wenshen Zhuanggu Formula, has shown a promising anti-metastatic activity in human breast cancer cells, but the underlying mechanisms remain ambiguous. In this study we elucidated the anti-metastatic mechanisms of osthole in highly metastatic breast cancer cells and a zebrafish xenograft model. We showed that the expression of integrin α3 (ITGα3) and integrin β5 (ITGβ5) was upregulated in highly metastatic MDA-MB-231, MDA-MB-231BO breast cancer cell lines but was downregulated in poorly metastatic MCF-7 breast cancer cell line, which might be the key targets of osthole’s anti-metastatic action. Furthermore, we showed that knockdown of ITGα3 and ITGβ5 attenuated breast cancer cell migration and invasion possibly via suppression of FAK/Src/Rac1 pathway, whereas overexpression of ITGα3 and ITGβ5 caused the opposite effects. Consistently, osthole significantly inhibited breast cancer metastasis by downregulating ITGα3/ITGβ5 signaling in vitro and in vivo. These results provide new evidence that osthole may be developed as a candidate therapeutic drug for metastatic breast cancer.-
dc.languageeng-
dc.relation.ispartofActa Pharmacologica Sinica-
dc.subjectbreast cancer-
dc.subjectFAK/Src/Rac1 pathway-
dc.subjectITGα3-
dc.subjectITGβ5-
dc.subjectmetastasis-
dc.subjectosthole-
dc.subjectWenshen Zhuanggu Formula-
dc.titleOsthole inhibits the migration and invasion of highly metastatic breast cancer cells by suppressing ITGα3/ITGβ5 signaling-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/s41401-021-00757-7-
dc.identifier.pmid34426644-
dc.identifier.scopuseid_2-s2.0-85113779341-
dc.identifier.volume43-
dc.identifier.issue6-
dc.identifier.spage1544-
dc.identifier.epage1555-
dc.identifier.eissn1745-7254-
dc.identifier.isiWOS:000687548800001-

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