Apigenin inhibits the proliferation of adenoid cystic carcinoma via suppression of glucose transporter-1

Jin, Fang; Bao, Yang‐Yang; Zhou, Shui‐Hong; Fan, Jun

doi:10.3892/mmr.2015.4233

Cited by 36 publications

(27 citation statements)

References 24 publications

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“…It was previously demonstrated that APG caused arrest of the cell cycle in G 0 /G 1 -phase by reducing the level of cyclin D1 in LNCaP and PC-3 prostate cancer cell lines (1). However, in other studies, APG caused cell-cycle arrest at the G 2 -phase by decreasing cyclin B in human colon carcinoma and pancreatic cancer cells (10), or regulated other cell-cycle phases by affecting cyclin A and cell division cycle 25A and cell division cycle 25C in different cell types (8,(69)(70)(71). The results of the cell-cycle assay of the present study suggested that APG arrested Rad54 -/cells in G 2 /M-phase.…”

Section: Discussioncontrasting

confidence: 55%

Critical roles of Rad54 in tolerance to apigenin‑induced Top1‑mediated DNA damage

Zhao

et al. 2021

Exp Ther Med

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Apigenin (APG), a flavone sub-class of flavonoids, possesses a diverse range of biological activities, including anti-cancer and anti-inflammatory effects. Previous studies identified the genotoxicity of APG in certain cancer cells, which may be associated with its anticancer effect. However, the DNA damage repair mechanism induced by APG has remained elusive. In order to clarify the molecular mechanisms, the present study determined the toxicity of APG to the wild-type (WT) DT40 chicken B-lymphocyte cell line, as well as to DT40 cells with deletions in various DNA repair genes, and their sensitivities were compared. It was demonstrated that cells deficient of Rad54, a critical homologous recombination gene, were particularly sensitive to APG. Cell-cycle analysis demonstrated that APG caused an increase in the G 2 /M-phase population of Rad54-/cells that was greater than that in WT cells. Furthermore, it was demonstrated by immunofluorescence assay that Rad54-/cells exhibited significantly increased numbers of γ-phosphorylated H2AX variant histone foci and chromosomal aberrations compared to the WT cells in response to APG. Of note, the in vitro complex of enzyme assay indicated that APG induced increased topoisomerase I (Top1) covalent protein DNA complex in Rad54-/cells compared to WT cells. Finally, these results were verified using the TK6 human lymphoblastoid cell line and it was demonstrated that, as for DT40 cells, Rad54 deficiency sensitized TK6 cells to APG. The present study demonstrated that Rad54 was involved in the repair of APG-induced DNA damage, which was associated with Top1 inhibition.

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Section: Discussioncontrasting

confidence: 55%

Critical roles of Rad54 in tolerance to apigenin‑induced Top1‑mediated DNA damage

Zhao

et al. 2021

Exp Ther Med

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“…Mori et al detected higher expression of GLUT-1 mRNA in ACC than in normal salivary glands by RT-PCR [60]. In our previous study, GLUT-1 mRNA and protein showed high expression in ACC-2 cell lines [63]. Demasi et al found higher expression of GLUT-1 in high-grade MEC than in low-grade MEC of the salivary gland as detected by IHC.…”

Section: Introductionmentioning

confidence: 85%

Roles of GLUT-1 and HK-II expression in the biological behavior of head and neck cancer

et al. 2019

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“…In addition, in renal cell carcinoma cells, apigenin caused DNA damage in ACHN cells in a time- and dose-dependent manner and induced G2/M phase cell cycle arrest through ataxia telangiectasia mutated (ATM) signal modulation [ 30 ]. In adenoid cystic carcinoma (ACC), apigenin induced G2/M-phase arrest and inhibited ACC-2 cell growth and proliferation in a dose- and time-dependent manner by decreasing the expression of Glucose transporter-1 (GLUT-1) [ 31 ]. And in human papillary thyroid carcinoma BCPAP cells, apigenin treatment caused G2/M cell cycle arrest via down-regulation of Cdc25c expression and stimulated the accumulation of reactive oxygen species (ROS) production, leading to induction of DNA damage [ 32 ].…”

Section: Apigenin In Cancer Therapymentioning

confidence: 99%

Apigenin in cancer therapy: anti-cancer effects and mechanisms of action

et al. 2017

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Apigenin is a common dietary flavonoid that is abundantly present in many fruits, vegetables and Chinese medicinal herbs and serves multiple physiological functions, such as strong anti-inflammatory, antioxidant, antibacterial and antiviral activities and blood pressure reduction. Therefore, apigenin has been used as a traditional medicine for centuries. Recently, apigenin has been widely investigated for its anti-cancer activities and low toxicity. Apigenin was reported to suppress various human cancers in vitro and in vivo by multiple biological effects, such as triggering cell apoptosis and autophagy, inducing cell cycle arrest, suppressing cell migration and invasion, and stimulating an immune response. In this review, we focus on the most recent advances in the anti-cancer effects of apigenin and their underlying mechanisms, and we summarize the signaling pathways modulated by apigenin, including the PI3K/AKT, MAPK/ERK, JAK/STAT, NF-κB and Wnt/β-catenin pathways. We also discuss combinatorial strategies to enhance the anti-cancer effect of apigenin on various cancers and its use as an adjuvant chemotherapeutic agent to overcome cancer drug resistance or to alleviate other adverse effects of chemotherapy. The functions of apigenin against cancer stem cells are also summarized and discussed. These data demonstrate that apigenin is a promising reagent for cancer therapy. Apigenin appears to have the potential to be developed either as a dietary supplement or as an adjuvant chemotherapeutic agent for cancer therapy.

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Apigenin inhibits the proliferation of adenoid cystic carcinoma via suppression of glucose transporter-1

Cited by 36 publications

References 24 publications

Critical roles of Rad54 in tolerance to apigenin‑induced Top1‑mediated DNA damage

Critical roles of Rad54 in tolerance to apigenin‑induced Top1‑mediated DNA damage

Roles of GLUT-1 and HK-II expression in the biological behavior of head and neck cancer

Apigenin in cancer therapy: anti-cancer effects and mechanisms of action

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