Abstract:
Background:Acute lymphoblastic leukemia (ALL) is an aggressive hematopoietic malignancy that is most commonly observed in children. Alantolactone (ALT) has been reported to exhibit anti-tumor activity in different types of cancer. The aim of the present study was to investigate the anti-tumor activity and molecular mechanism of ALT in ALL. Methods:ALL cell lines were treated with 1, 5 and 10 μM ALT, and cell viability was assessed using an MTT assay and RNA sequencing. Flow cytometry, JC-1 staining and immunofluorescence staining assays were used to measure cell apoptosis and autophagy. Additionally, western blot analysis was used to detect expression of apoptosis and autophagy related proteins. Finally, the effects of ALT on tumor growth were assessed in a BV173 xenograft nude mouse model. Results:ALT inhibited the proliferation of ALL cells in a dose-dependent manner. Additionally, it was demonstrated that ALT inhibited cell proliferation, colony formation, autophagy, induced apoptosis and reduced tumor growth in vivo through upregulating the expression of adaptor related protein complex 2 subunit mu 1 (AP2M1). Moreover, the autophagy activator rapamycin, attenuated the pro-apoptotic effects of ALT on BV173 and NALM6 cell lines. Overexpression of AP2M1 decreased the expression of Beclin1 and the LC3-II/LC3-1 ratio, and increased p62 expression. Knockdown of Beclin1 increased the levels of bax, cleaved caspase 3 and cytochrome C, and decreased bcl-2 expression. Conclusions:The present study demonstrated that ALT exerts anti-tumor activity through inducing apoptosis and inhibiting autophagy by upregulating AP2M1 in ALL, highlighting a potential therapeutic strategy for treatment of ALL.
journal_name
Cancer Cell Intjournal_title
Cancer cell internationalauthors
Shi C,Lan W,Wang Z,Yang D,Wei J,Liu Z,Teng Y,Gu M,Yuan T,Cao F,Zhou J,Li Ydoi
10.1186/s12935-020-01537-9subject
Has Abstractpub_date
2020-09-09 00:00:00pages
442issn
1475-2867pii
1537journal_volume
20pub_type
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pub_type: 杂志文章
doi:10.1186/s12935-020-01736-4
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pub_type: 杂志文章,评审
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更新日期:2015-05-23 00:00:00
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journal_title:Cancer cell international
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pub_type: 杂志文章
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journal_title:Cancer cell international
pub_type: 杂志文章
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