A trienone analog of curcumin, 1,7-bis(3-hydroxyphenyl)-1,4,6-heptatrien-3-one, possesses ROS- and caspase-mediated apoptosis in human oral squamous cell carcinoma cells in vitro

Utaipan, Tanyarath; Boonyanuphong, P.; Chuprajob, Thipphawan; Suksamrarn, Apichart; Chunglok, Warangkana

doi:10.1186/s13765-020-0491-8

Cited by 17 publications

(9 citation statements)

References 36 publications

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“…The leading causes of OSCC treatment failure include metastatic spread, recurrence and poor drug efficacy ( 10 ). Furthermore, previous studies have reported that OSCC treatment failure is associated with drug resistance, which is mainly attributed to chemotherapeutic drug transportation, metabolic reprogramming, redox status and DNA repair ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

“…Increments in reactive oxygen species (ROS) may induce OSCC cell death, and a decreasing trend in ROS is observed in patients with advanced stage OSCC, suggesting that ROS may be an important potential antitumor target in OSCC therapeutic strategies. In recent years, a number of medicinal herbs and their active ingredients have been reported to induce ROS-mediated apoptosis in OSCC cells, including curcumin ( 10 ), β-lapachone ( 14 ) and erufosine ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

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Lycorine hydrochloride induces reactive oxygen species‑mediated apoptosis via the mitochondrial apoptotic pathway and the JNK signaling pathway in the oral squamous cell carcinoma HSC‑3 cell line

Liao

et al. 2021

Oncol Lett

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Poor drug efficacy is a prominent cause of oral squamous cell carcinoma (OSCC) treatment failure. Although increased efforts in developing OSCC therapeutic strategies have been achieved in recent decades, the 5-year survival rate of patients with OSCC remains poor and effective drugs to treat OSCC are lacking. The aim of the present study was to investigate the apoptotic effect caused by lycorine hydrochloride (LH) and to identify its mechanism in the OSCC HSC-3 cell line. The findings demonstrated that LH effectively induced HSC-3 cell apoptosis and cell cycle arrest at the G 0 /G 1 phase, resulting in the inhibition of cell proliferation. Furthermore, it was found that LH increased reactive oxygen species (ROS) production, triggered mitochondrial membrane potential (MMP) disorder, enhanced the protein expression levels of Bax, Bim, cleaved caspase-9, caspase-3 and poly(ADP-ribose) polymerase 1 and decreased Mcl-1 expression. The protein expression levels of important members of the JNK signaling pathway, including phosphorylated (p)-JNK, p-mitogen-activated protein kinase kinase 4 and p-c-Jun, were significantly increased in LH-treated cells, accompanied by an increase in ROS. However, N-acetyl cysteine (NAC), a potent antioxidant, reversed the upregulated mRNA expression of c-Jun, as well as the enhanced ROS production, the disorder of MMP and the apoptosis of HSC-3 cells induced by LH. These results suggested that LH may induce HSC-3 cell apoptosis via the ROS-mediated mitochondrial apoptotic pathway and the JNK signaling pathway, which indicated that LH may be a potential drug candidate for anti-OSCC therapy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lycorine hydrochloride induces reactive oxygen species‑mediated apoptosis via the mitochondrial apoptotic pathway and the JNK signaling pathway in the oral squamous cell carcinoma HSC‑3 cell line

Liao

et al. 2021

Oncol Lett

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“…2 ). The majority of chemotherapy drugs induce apoptosis ( 31 , 32 ). The results revealed that the co-treatment with C5E and gemcitabine was markedly more effective compared with the individual treatments alone at inducing S phase cell cycle arrest and early apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Synergistic effect of the herbal mixture C5E on gemcitabine treatment in PANC‑1 cells

et al. 2021

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The present study aimed to determine the anticancer effect of the herbal mixture extract C5E in the pancreatic cancer cell line, PANC-1, in the absence or presence of gemcitabine treatment, a chemotherapeutic drug used for the treatment of pancreatic cancer. The anticancer effects of C5E, gemcitabine and C5E plus gemcitabine in PANC-1 cells following 72 h of treatment were investigated. The effect of each treatment on cell cycle arrest, apoptosis and the proportion of side population (SP) cells was determined using flow cytometric analysis following propidium iodide (PI), Annexin V-FITC/PI double staining and Hoechst 33342 staining, respectively. SP cells share similar characteristics to cancer stem-like cells, and a reduction in the SP is considered to be indicative of an anticancer effect. The percentage of SP cells and the cell viability of general PANC-1 cells were significantly decreased in response to all treatments. The percentage of SP cells was reduced from 8.2% (control) to 3.9, 7.2 and 5.1% following the treatment with C5E, gemcitabine and the co-treatment, respectively. All three treatments were discovered to inhibit cell viability by arresting the cell cycle at the S phase and promoted cell death by inducing early apoptosis, with the levels of apoptosis being increased from 1.9% (control) to 7.3, 2.5 and 12.0% following the treatment with C5E, gemcitabine and the co-treatment, respectively. The mRNA expression levels of sonic hedgehog, which is implicated in the development of certain types of cancer, were downregulated to a greater extent following the co-treatment with C5E and gemcitabine compared with the treatment with either C5E or gemcitabine alone. As the co-treatment with gemcitabine and C5E was more effective than each individual treatment, the present study suggested that the combined treatment may exhibit synergistic effects in PANC-1 cells.

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“…Therefore, the trienone analogs in this study should improve their stability and activity. Recently, the trienone analogs including T-BDMC have been reported as candidates for developing potent anticancer agents against human oral squamous cell carcinoma with less toxicity against Vero cells, a normal cell line, than their respective curcuminoid analogs 10 , 37 . However, there is no report about the pharmacokinetic activity and bioavailability of the trienone analogs.…”

Section: Discussionmentioning

confidence: 99%

Trienone analogs of curcuminoids induce fetal hemoglobin synthesis via demethylation at Gγ-globin gene promoter

Nuamsee

Chuprajob

Pabuprapap

et al. 2021

Sci Rep

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The reactivation of γ-globin chain synthesis to combine with excess free α-globin chains and form fetal hemoglobin (HbF) is an important alternative treatment for β-thalassemia. We had reported HbF induction property of natural curcuminoids, curcumin (Cur), demethoxycurcumin (DMC) and bis-demethoxycurcumin (BDMC), in erythroid progenitors. Herein, the HbF induction property of trienone analogs of the three curcuminoids in erythroleukemic K562 cell lines and primary human erythroid progenitor cells from β-thalassemia/HbE patients was examined. All three trienone analogs could induce HbF synthesis. The most potent HbF inducer in K562 cells was trienone analog of BDMC (T-BDMC) with 2.4 ± 0.2 fold increase. In addition, DNA methylation at CpG − 53, − 50 and + 6 of Gγ-globin gene promoter in K562 cells treated with the compounds including T-BDMC (9.3 ± 1.7%, 7.3 ± 1.7% and 5.3 ± 0.5%, respectively) was significantly lower than those obtained from the control cells (30.7 ± 3.8%, 25.0 ± 2.9% and 7.7 ± 0.9%, respectively P < 0.05). The trienone compounds also significantly induced HbF synthesis in β-thalassemia/HbE erythroid progenitor cells with significantly reduction in DNA methylation at CpG + 6 of Gγ-globin gene promoter. These results suggested that the curcuminoids and their three trienone analogs induced HbF synthesis by decreased DNA methylation at Gγ-globin promoter region, without effect on Aγ-globin promoter region.

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A trienone analog of curcumin, 1,7-bis(3-hydroxyphenyl)-1,4,6-heptatrien-3-one, possesses ROS- and caspase-mediated apoptosis in human oral squamous cell carcinoma cells in vitro

Cited by 17 publications

References 36 publications

Lycorine hydrochloride induces reactive oxygen species‑mediated apoptosis via the mitochondrial apoptotic pathway and the JNK signaling pathway in the oral squamous cell carcinoma HSC‑3 cell line

Lycorine hydrochloride induces reactive oxygen species‑mediated apoptosis via the mitochondrial apoptotic pathway and the JNK signaling pathway in the oral squamous cell carcinoma HSC‑3 cell line

Synergistic effect of the herbal mixture C5E on gemcitabine treatment in PANC‑1 cells

Trienone analogs of curcuminoids induce fetal hemoglobin synthesis via demethylation at Gγ-globin gene promoter

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