Butein inhibits cell proliferation and induces cell cycle arrest in acute lymphoblastic leukemia via FOXO3a/p27kip1 pathway

Tang, Yan; Huang, Li; Lin, Wen Hao; Wang, Li Na; Tian, Yun; Shi, Dingbo; Wang, Jingshu; Qin, Ge; Li, Anchuan; Liang, Yan; Zhou, Huan; Ke, Zhi Yong; Huang, Wenlin; Deng, Wuguo; Li, Xue

doi:10.18632/oncotarget.7624

Cited by 24 publications

(17 citation statements)

References 39 publications

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“…Apoptosis induction is an important biological effect after butein treatment and different molecular mechanisms including PI3K/Akt/mTOR pathway inhibition 22 , suppression of STAT3 activation 47 , reactive oxygen species generation 48 , inhibition of cyclooxygenase-2 expression 49 were reported to be engaged in the apoptosis induction by butein. Consistent with the concentrations used in other studies 23 , 24 , 50 , in our study, at the concentration rang of 10-60μM, butein dose-dependently inhibited HCC cell proliferation, colony formation and induced G2/M cell cycle arrest and apoptosis. Differently, for the first time, we clarified that Aurora B was a potential target of butein in HCC.…”

Section: Discussionsupporting

confidence: 92%

Butein suppresses hepatocellular carcinoma growth via modulating Aurora B kinase activity

Zhou¹,

Li²,

Yu³

et al. 2018

Int. J. Biol. Sci.

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Aurora B is aberrantly expressed in various tumors and shown to be a promising target for cancer therapy. Butein, a chalcone isolated from Rhus cerniciflua, has demonstrated antitumor activities in different cancers. In this study, we aimed to validate whether Aurora B kinase was the direct target of butein to exhibit its potency in hepatocellular carcinoma (HCC). Comparing with the normal cell line and tissue, Aurora B was overexpressed in all tested HCC cells and the majority of tumor tissue. Knocking down of Aurora B with shRNA substantially inhibited HCC cell proliferation, colony formation and delayed tumor growth in nude mice. Except computer docking, a series of kinase assays revealed butein directly interacted with Aurora B and inhibited its kinase activity. Along with the decrease of Aurora B and histone H3 phosphorylation, HCC cells were induced G2/M cell cycle arrest and subjected to cell apoptosis. Butein-mediated antitumor activities were substantially impaired in Aurora B knockdown cells, suggesting Aurora B was an important target of butein in HCC. Oral administration of butein substantially restrained HCC xenograft growth and the expressions of Ki67 and phosphor-histone H3 were significantly decreased in butein-treated tissue. To the best of our knowledge, our studies revealed that Aurora B was the direct target of butein in HCC.

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Section: Discussionsupporting

confidence: 92%

Butein suppresses hepatocellular carcinoma growth via modulating Aurora B kinase activity

Zhou¹,

Li²,

Yu³

et al. 2018

Int. J. Biol. Sci.

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“…Foxo3a plays a vital role in gene regulation in tumorigenesis. Resent research report that as transcription factor, Foxo3a inhibited proliferation and induced cell cycle arrest by controlling cyclin-dependent kinase inhibitor p27kip1 [39], contributing to cancer cell apoptosis by regulation of proapoptotic member [40]. Previous reports have showed Foxo3a were overexpressed in less aggressive types of GC [41,42].…”

Section: Discussionmentioning

confidence: 99%

Foxo3a-dependent miR-633 regulates chemotherapeutic sensitivity in gastric cancer by targeting Fas-associated death domain

Pang

Zhou

et al. 2019

RNA Biology

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2019) Foxo3a-dependent miR-633 regulates chemotherapeutic sensitivity in gastric cancer by targeting Fas-associated death domain, RNA Biology, 16:2, 233-248, ABSTRACTThe development of chemotherapeutic drugs resistance such as doxorubicin (DOX) and cisplatin (DDP) is the major barrier in gastric cancer therapy. Emerging evidences reveal that microRNAs (miRNAs) contribute to chemosensitivity. In this study, we investigated the role of miR-633, an oncogenic miRNA, in gastric cancer chemoresistance. In gastric cancer tissue and cell lines, miR-633 expression was highly increased and correlated with down regulation of Fas-associated protein with death domain (FADD). Inhibition of miR-633 significantly increased FADD protein level and enhanced DOX/DDP induced apoptosis in vitro. MiR-633 antagomir administration remarkably decreased tumor growth in combination with DOX in vivo, suggesting that miR-633 targets FADD to block gastric cancer cell death. We found that the promoter region of miR-633 contained putative binding sites for forkhead box O 3 (Foxo3a), which can directly repress miR-633 transcription. In addition, we observed that DOX-induced nuclear accumulation of Foxo3a leaded to the suppression of miR-633 transcription. Together, our study revealed that miR-633/FADD axis played a significant role in the chemoresistance and Foxo3a regulated this pathway in gastric cancer. Thus, miR-633 antagomir resensitized gastric cancer cells to chemotherapy drug and had potentially therapeutic implication. ARTICLE HISTORY

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“…Similarly, the preceding reports have also suggested the same activities against different cancer cells such as breast, blood, liver, cervical etc. (Yang et al, 2012;Liao et al, 2018;Tang et al, 2016;Yang et al, 2018). For instance, Yang et al, (2018) reported that butein reduced the viability of cervical cancer cells through a proapoptotic effect by blocking inhibitor of apoptosis (IAP) proteins and activating extrinsic as well as intrinsic proapoptotic cascades.…”

Section: Discussionmentioning

confidence: 99%

An Investigation on the Therapeutic Potential of Butein, A Tretrahydroxychalcone Against Human Oral Squamous Cell Carcinoma

Bordoloi

Monisha

Roy

et al. 2019

Asian Pac J Cancer Prev

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Background: Oral squamous cell carcinoma (OSCC) is one of the most predominant cancers in India. With advances in the field of oncology, a number of therapies have emerged; however, they are minimally effective. Consequently, there is a need to develop safe and effective regimens for the treatment of OSCC. Butein, a tetrahydroxychalcone has been found to exhibit potent antioxidant, anti-inflammatory, and also anti-tumor effects against several cancer types. However, its effect on OSCC is not studied yet. Methods: The effect of butein on the viability, apoptosis, migration and invasion of OSCC cells was evaluated using MTT, colony formation, PI/FACS, live and dead, scratch wound healing, and matrigel invasion assays. Further Western blot analysis was done to evaluate the expression of different proteins involved in the regulation of cancer hallmarks. Results: This is the first report exemplifying the anti-cancer effect of butein against OSCC. Our results showed that butein exhibited potent anti-proliferative, cytotoxic, anti-migratory, and anti-invasive effects in OSCC cells. It suppressed the expression of NF-κB and NF-κB-regulated gene products such as COX-2, survivin and MMP-9 which are involved in the regulation of different processes like proliferation, survival, invasion, and metastasis of OSCC cells. Conclusion Collectively, these results suggest that butein has immense potential in the management of OSCC. Nonetheless, in vivo validation is critical before moving to clinical trials.

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Butein inhibits cell proliferation and induces cell cycle arrest in acute lymphoblastic leukemia via FOXO3a/p27kip1 pathway

Cited by 24 publications

References 39 publications

Butein suppresses hepatocellular carcinoma growth via modulating Aurora B kinase activity

Butein suppresses hepatocellular carcinoma growth via modulating Aurora B kinase activity

Foxo3a-dependent miR-633 regulates chemotherapeutic sensitivity in gastric cancer by targeting Fas-associated death domain

An Investigation on the Therapeutic Potential of Butein, A Tretrahydroxychalcone Against Human Oral Squamous Cell Carcinoma

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