6,8-Dihydroxy-7-methoxy-1-methyl-azafluorenone Induces Caspase-8- and -9-mediated Apoptosis in Human Cancer Cells

Banjerdpongchai, Ratana; Khaw-on, Patompong; Ristee, Chantrarat; Pompimon, Wilart

doi:10.7314/apjcp.2013.14.4.2637

Cited by 14 publications

(3 citation statements)

References 16 publications

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“…Therefore, the activity of caspase-3 is considered as an appropriate measure of cytotoxic responsiveness. Previous studies reported that many drugs induced apoptosis mainly through mitochondria/ caspase pathway in Human Gastric Cancer (Sun et al, 2013), Breast Cancer (Zhou et al, 2013), human leukemic and hepatocellular carcinoma (Banjerdpongchai et al, 2013). In this study, we found the combination group and irradiation group could significantly increase caspase-3 activity.…”

Section: Jia Liu Et Alsupporting

confidence: 60%

Fenofibrate Increases Radiosensitivity in Head and Neck Squamous Cell Carcinoma via Inducing G2/M Arrest and Apoptosis

Liu¹,

Ge²,

Zhu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Radiation therapy is an important treatment for head and neck squamous cell carcinoma (HNSCC). However, how to promote radiation sensitivity in HNSCC remains a challenge. This study aimed to investigate the radiosensitizing effects of fenofibrate on HNSCC and explore the underlying mechanisms. HNSCC cell lines CNE-2 and KB were subjected to ionizing radiation (IR), in the presence or absence of fenofibrate treatment. Cell growth and survival, apoptosis and cell cycle were evaluated. In addition, CNE-2 cells were xenografted into nude mice and subjected to IR and/ or fenofibrate treatment. The expression of cyclinB and CDK1 was detected by Western blotting. Our results showed that fenofibrate efficiently radiosensitized HNSCC cells and xenografts in mice, and induced apoptosis and G2/M arrest via reducing the activity of the CDK1/cyclinB1 kinase complex. These data suggest that fenofibrate could be a promising radiosensitizer for HNSCC radiotherapy.

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Section: Jia Liu Et Alsupporting

confidence: 60%

Fenofibrate Increases Radiosensitivity in Head and Neck Squamous Cell Carcinoma via Inducing G2/M Arrest and Apoptosis

Liu¹,

Ge²,

Zhu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…The chromogenic substrate of each type of caspase, viz., caspase-3, Asp-Glu-Val-Asp- p -NA (DEVD- p -NA); caspase-8, Ile-Glu-Thr-Asp- p -NA (IETD- p -NA); and caspase-9, Leu-Glu-His-Asp- p -NA (LEHD- p -NA), was added to the reaction buffer of the cell lysate. The cell lysate was incubated with each substrate for 60 minutes, and then caspase-3, caspase-8, and caspase-9 activities were measured using a microplate reader at 405 nm (BioTek, Winooski, VT, USA) [32].…”

Section: Methodsmentioning

confidence: 99%

Dihydrochalcone Derivative Induces Breast Cancer Cell Apoptosis via Intrinsic, Extrinsic, and ER Stress Pathways but Abolishes EGFR/MAPK Pathway

Rachakhom

Khaw-on

Pompimon

et al. 2019

BioMed Research International

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Dihydrochalcone derivatives are active compounds that have been purified from the Thai medicinal plant Cyathostemma argenteum. The objectives of this study were to investigate the effects of two dihydrochalcone derivatives on human breast cancer MDA-MB-231 and MCF-7 cell proliferation and to study the relevant mechanisms involved. The two dihydrochalcone derivatives are 4′,6′-dihydroxy-2′,4-dimethoxy-5′-(2″-hydroxybenzyl)dihydrochalcone (compound 1) and calomelanone (2′,6′-dihydroxy-4,4′-dimethoxydihydrochalcone, compound 2), both of which induced cytotoxicity toward both cell lines in a dose-dependent manner by using MTT assay. Treatment with both derivatives induced apoptosis as determined by annexin V-FITC/propidium iodide employing flow cytometry. The reduction of mitochondrial transmembrane potential (staining with 3,3′-dihexyloxacarbocyanine iodide, DiOC6, employing a flow cytometer) was established in the compound 1-treated cells. Compound 1 induced caspase-3, caspase-8, and caspase-9 activities in both cell lines, as has been determined by specific colorimetric substrates and a spectrophotometric microplate reader which indicated the involvement of both the extrinsic and intrinsic pathways. Calcium ion levels in mitochondrial and cytosolic compartments increased in compound 1-treated cells as detected by Rhod-2AM and Fluo-3AM intensity, respectively, indicating the involvement of the endoplasmic reticulum (ER) stress pathway. Compound 1 induced cell cycle arrest via enhanced atm and atr expressions and by upregulating proapoptotic proteins, namely, Bim, Bad, and tBid. Moreover, compound 1 significantly inhibited the EGFR/MAPK signaling pathway. In conclusion, compound 1 induced MDA-MB-231 and MCF-7 cell apoptosis via intrinsic, extrinsic, and ER stress pathways, whereas it ameliorated the EGFR/MAPK pathway in the MCF-7 cell line. Consequently, it is believed that compound 1 could be effectively developed for cancer treatments.

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“…For example, they have been reported to have antifungal, antimicrobial, and antimalarial activities [54–56]. They were also shown to have cytotoxic properties to induce cancer cells into apoptosis [57–59]. Moreover, an arylindenopyrimidine was shown to be a potent dual A2A/A1 receptor antagonist that might have the potential for the treatment of neurodegenerative disorder such as Parkinson's disease [60].…”

Section: Discussionmentioning

confidence: 99%

Identification of a new class of WNT1 inhibitor: Cancer cells migration, G-quadruplex stabilization and target validation

Chang

Chen

et al. 2015

Oncotarget

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Developing the Wnt pathway inhibitors has been considered as a therapeutic approach for cancers and other Wnt-related diseases. Previously we found that the G-rich sequence of WNT1 promoter is capable of forming G-quadruplex structure and stabilizing agents for Wnt1-mediated signaling pathway. Using a established cell-based drug screen system that enabled the evaluation of WNT1 expression activity in a G-quadruplex structure dependent manner, we evaluated a series of 6-substituted 9-chloro-11H-indeno[1,2-c]quinolin-11-one derivatives that potentially inhibit the Wnt1-mediated signaling pathway. The most potent compound SJ26 showed repression of WNT1 activity in a G-quadruplex structure-dependent manner. Moreover, compound SJ26 inhibited the WNT1-mediated downstream signaling pathway and suppressed migration activity of cancer cells. Thus, we have identified a tetracyclic azafluorenone, SJ26, that is capable of binding to G-quadruplex DNA structure, repressing WNT1 expression, and inhibiting cell migration.

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6,8-Dihydroxy-7-methoxy-1-methyl-azafluorenone Induces Caspase-8- and -9-mediated Apoptosis in Human Cancer Cells

Cited by 14 publications

References 16 publications

Fenofibrate Increases Radiosensitivity in Head and Neck Squamous Cell Carcinoma via Inducing G2/M Arrest and Apoptosis

Fenofibrate Increases Radiosensitivity in Head and Neck Squamous Cell Carcinoma via Inducing G2/M Arrest and Apoptosis

Dihydrochalcone Derivative Induces Breast Cancer Cell Apoptosis via Intrinsic, Extrinsic, and ER Stress Pathways but Abolishes EGFR/MAPK Pathway

Identification of a new class of WNT1 inhibitor: Cancer cells migration, G-quadruplex stabilization and target validation

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