Anticancer Efficacy and Mechanism of Amentoflavone for Sensitizing Oral Squamous Cell Carcinoma to Cisplatin

Chen, Cheng Hsien; Huang, Yi Tsau; Lee, Yuan-Hao; Tan, Zhao Lin; Tsai, Chia‐Jung; Chuang, Yaochen; Tu, Hsi Feng; Liu, Ta Chih; Hsu, Fei Ting

doi:10.21873/anticanres.14695

Cited by 20 publications

(15 citation statements)

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“…Increasing evidences demonstrate that AMF controls cell proliferation, apoptosis, invasion, metastasis, autophagy, transcription and drug-resistance in various types of cancers, such as lung cancer ( Banerjee et al, 2002a ; Banerjee et al, 2002b ; Jung et al, 2017 ; Hu et al, 2018 ; Park and Kim, 2019 ; Shen et al, 2019 ; Kim et al, 2020 ; Chen et al, 2021 ), cervical cancer ( Lee et al, 2011 ), ovarian cancer ( Liu et al, 2017a ; Zhang et al, 2020 ), bladder cancer ( Chiang et al, 2019 ), osteosarcoma ( Pan et al, 2017 ; Lee et al, 2019 ), melanoma ( Guruvayoorappan and Kuttan, 2007 ; 2008b ; a ; Siveen and Kuttan, 2011 ), breast cancer ( Lee et al, 2009 ; Pei et al, 2012 ; Lee et al, 2013 ; Chen et al, 2015 ; Aliyev et al, 2021 ), liver cancer ( Zheng et al, 2016 ; Chen et al, 2017a ; Lee et al, 2018a ; Lee et al, 2018b ; Tsai et al, 2018 ), brain cancer ( Yen et al, 2018 ; Zhaohui et al, 2018 ; Hsu et al, 2019 ; Chen et al, 2020c ), and oral squamous cell carcinoma ( Chen et al, 2020b ) via regulating kinds of signaling pathways ( Figure 2 ). These studies provide a lot of evidences that AMF is a potential effective multi-targeting drug for the prevention and treatment of a variety of cancers.…”

Section: The Multifunctional Biological Activities Of Amentoflavonementioning

confidence: 99%

“…AMF has been shown to exhibit multiple biological activities including anti-inflammatory ( Tordera et al, 1994 ; Kim et al, 1998 ; Oh et al, 2013 ; An et al, 2016 ; Cai et al, 2019 ), antibacterial ( Hwang et al, 2013 ), antifungal ( Jung et al, 2006 ; Jung et al, 2007 ; Hwang et al, 2012 ), antivirus ( Lin et al, 1997 ; Wilsky et al, 2012 ; Coulerie et al, 2013 ), anti-oxidative ( Bonacorsi et al, 2012 ; Li et al, 2020 ), anti-angiogenesis ( Guruvayoorappan and Kuttan, 2008c ; Tarallo et al, 2011 ; Zhang et al, 2014 ), neuroprotection ( Cao et al, 2017 ; Chen et al, 2018 ; Rong et al, 2019 ; Zhao et al, 2019 ; Cao et al, 2021 ), osteogenesis ( Zha et al, 2016 ), anti-arthritis ( Bais et al, 2017 ; Vasconcelos et al, 2019 ), radioprotection ( Park et al, 2011 ; Xu et al, 2014 ; Qu et al, 2019 ), antidiabetic ( Qin et al, 2018 ; Su et al, 2019 ) and antidepressant ( Ishola et al, 2012 ). It is reported that AMF exerts anti-cancer activity through a variety of mechanisms ( Guruvayoorappan and Kuttan, 2007 ; Lee et al, 2011 ; Pei et al, 2012 ; Zheng et al, 2016 ; Liu et al, 2017a ; Pan et al, 2017 ; Chiang et al, 2019 ; Hsu et al, 2019 ; Park and Kim, 2019 ; Chen et al, 2020b ). In this review, the biological activities of AMF will be discussed comprehensively.…”

Section: Introductionmentioning

confidence: 99%

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Insights Into Amentoflavone: A Natural Multifunctional Biflavonoid

Xiong

Tang²,

Lai³

et al. 2021

Front. Pharmacol.

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Amentoflavone is an active phenolic compound isolated from Selaginella tamariscina over 40 years. Amentoflavone has been extensively recorded as a molecule which displays multifunctional biological activities. Especially, amentoflavone involves in anti-cancer activity by mediating various signaling pathways such as extracellular signal-regulated kinase (ERK), nuclear factor kappa-B (NF-κB) and phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), and emerges anti-SARS-CoV-2 effect via binding towards the main protease (Mpro/3CLpro), spike protein receptor binding domain (RBD) and RNA-dependent RNA polymerase (RdRp) of SARS-CoV-2. Therefore, amentoflavone is considered to be a promising therapeutic agent for clinical research. Considering the multifunction of amentoflavone, the current review comprehensively discuss the chemistry, the progress in its diverse biological activities, including anti-inflammatory, anti-oxidation, anti-microorganism, metabolism regulation, neuroprotection, radioprotection, musculoskeletal protection and antidepressant, specially the fascinating role against various types of cancers. In addition, the bioavailability and drug delivery of amentoflavone, the molecular mechanisms underlying the activities of amentoflavone, the molecular docking simulation of amentoflavone through in silico approach and anti-SARS-CoV-2 effect of amentoflavone are discussed.

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Section: The Multifunctional Biological Activities Of Amentoflavonementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Insights Into Amentoflavone: A Natural Multifunctional Biflavonoid

Xiong

Tang²,

Lai³

et al. 2021

Front. Pharmacol.

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show abstract

“…Finally, slides were fixed with DAPI mounting buffer and allowed it dry in dark. The fluorescence signal from NF-κB in cells were observed and photographed by Zeiss Axio Scope A1 fluorescence microscope ( 18 ).…”

Section: Methodsmentioning

confidence: 99%

Suppression of EGFR/PKC-δ/NF-κB Signaling Associated With Imipramine-Inhibited Progression of Non-Small Cell Lung Cancer

et al. 2021

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BackgroundAnti-depressants have been reported to own anti-tumor potential types of cancers; however, the role of imipramine in non-small cell lung cancer (NSCLC) has not been elucidated. Epidermal growth factor receptor (EGFR) was known to be one of the key regulators that control NSCLC progression. Whether EGFR would be the target of imipramine for suppressing tumor signaling transduction and results in anti-tumor potential is remaining unclear.MethodsWe used CL-1-5-F4 cells and animal models to identify the underlying mechanism and therapeutic efficacy of imipramine. Cytotoxicity, apoptosis, invasion/migration, DNA damage, nuclear translocation of NF-κB, activation of NF-κB, phosphorylation of EGFR/PKC-δ/NF-κB was assayed by MTT, flow cytometry, transwell, wound healing assay, comet assay, immunofluorescence staining, NF-κB reporter gene assay and Western blotting, respectively. Tumor growth was validated by CL-1-5-F4/NF-κB-luc2 bearing animal model.ResultsImipramine effectively induces apoptosis of NSCLC cells via both intrinsic and extrinsic apoptosis signaling. DNA damage was increased, while, invasion and migration potential of NSCLC cells was suppressed by imipramine. The phosphorylation of EGFR/PKC-δ/NF-κB and their downstream proteins were all decreased by imipramine. Similar tumor growth inhibition was found in imipramine with standard therapy erlotinib (EGFR inhibitor). Non-obvious body weight loss and liver pathology change were found in imipramine treatment mice.ConclusionImipramine-triggered anti-NSCLC effects in both in vitro and in vivo model are at least partially attributed to its suppression of EGFR/PKC-δ/NF-κB pathway.

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“…A549 cells were treated with regorafenib 10 μM, cisplatin 15 μM and combination for 48 h. Cells were then fixed, permeabilized by 4% paraformaldehyde, blocked by 1% BSA, stained by AIF and followed with Alexa Fluor 488 secondary antibody conjugation. Detail procedure was described in previous study (21). AIF nuclear translocation was finally imaged by Zeiss Axio Scope.A1 fluorescence microscope (Germany).…”

Section: Methodsmentioning

confidence: 99%

Induction of Apoptosis and Inhibition of EGFR/NF-κB Signaling Are Associated With Regorafenib-sensitized Non-small Cell Lung Cancer to Cisplatin

Chiou

Hsu

et al. 2021

In Vivo

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Background/Aim: The combination of regorafenib with cisplatin/pemetrexed has indicated controllable safety and encouraging antitumor activity in non-small cell lung cancer (NSCLC) patients. However, the anti-NSCLC effects and action mechanisms of regorafenib combined with cisplatin is ambiguous. The major goal of the study was to study the inhibitory effects and action mechanisms of regorafenib combined with cisplatin in NSCLC cells. Materials and Methods: Cell viability, flow cytometry, immunofluorescence staining, western blotting, migration, and invasion assays were employed to verify the anti-NSCLC effects and mechanisms of regorafenib in combination with cisplatin. Results: Cisplatin-induced epidermal growth factor receptor (EGFR)/nuclear factor ĸB (NF-ĸB) signaling was effectively inhibited by regorafenib treatment. Regorafenib, erlotinib (EGFR inhibitor) and QNZ (NF-ĸB inhibitor) may all enhance the cytotoxicity effect of cisplatin. The invasion ability was effectively decreased by combination treatment. Caspase-dependent and -independent apoptosis was activated by cisplatin combined with regorafenib. Conclusion: Apoptosis induction and EGFR/NF-ĸB inactivation correlate with regorafenib-enhanced anti-NSCLC efficacy of cisplatin.This study provides evidence of the therapeutic efficacy of regorafenib in combination with cisplatin on NSCLC.Cisplatin, a platinum-based anticancer drug, is standard treatment for advanced non-small cell lung cancer (NSCLC). DNA damage-induced apoptosis correlates with the anticancer mechanism of cisplatin (1, 2). Cell and animal models have revealed that enhancement of apoptosis induction and suppression of oncogenic signaling such as Wnt, AKT, epidermal growth factor receptor (EGFR), and nuclear factor-kappaB (NF-ĸB) by potential complementary approaches have been reported to sensitize NSCLC cells to cisplatin (3-6). For instance, sodium valproate, a histone deacetylase inhibitor, and microRNA miR-381 have been found to enhance anti-NSCLC efficacy of cisplatin through inducing apoptosis and inhibiting NF-ĸB signaling, respectively (7, 8).Several tyrosine kinase inhibitors (TKIs) targeting EGFR and anaplastic lymphoma kinase (ALK) have been shown to improve survival of NSCLC patients receiving platinum-based doublet chemotherapy (9, 10). Regorafenib, an oral multitarget TKI, is used for the treatment of solid tumors such as hepatocellular carcinoma (HCC), renal cell carcinoma, differentiated thyroid cancer, and metastatic colorectal cancer (11,12). Induction of apoptosis and down-regulation of AKT/NF-ĸB signaling were associated with regorafenibinhibited progression of NSCLC cells (13). In addition, the combination of regorafenib with cisplatin/pemetrexed has shown manageable tolerability and encouraging antitumor 2569 This article is freely accessible online.

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Anticancer Efficacy and Mechanism of Amentoflavone for Sensitizing Oral Squamous Cell Carcinoma to Cisplatin

Cited by 20 publications

References 28 publications

Insights Into Amentoflavone: A Natural Multifunctional Biflavonoid

Insights Into Amentoflavone: A Natural Multifunctional Biflavonoid

Suppression of EGFR/PKC-δ/NF-κB Signaling Associated With Imipramine-Inhibited Progression of Non-Small Cell Lung Cancer

Induction of Apoptosis and Inhibition of EGFR/NF-κB Signaling Are Associated With Regorafenib-sensitized Non-small Cell Lung Cancer to Cisplatin

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