Curcumin analog HO‐3867 triggers apoptotic pathways through activating JNK1/2 signalling in human oral squamous cell carcinoma cells

Chen, Chi‐Wei; Hsieh, Ming‐Ju; Ju, Po-Chung; Hsieh, Yi‐Hsien; Su, Chung‐Kuang; Chen, Yen‐Lin; Yang, Shun‐Fa

doi:10.1111/jcmm.17248

Cited by 19 publications

(20 citation statements)

References 76 publications

(128 reference statements)

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“…HO-3867 has previously been known to cause apoptosis to cancer cells through the targeting of several key growth-regulatory proteins such as the Janus kinase (JAK) as well as STAT3 pathway to cause apoptosis among oral, ovarian, endometrial, and pancreatic cancers [35][36][37][38]. The compound has also been researched in terms of its ability to repress migration and invasion activity [39].…”

Section: Discussionmentioning

confidence: 99%

HO-3867 Induces Apoptosis via the JNK Signaling Pathway in Human Osteosarcoma Cells

Lu¹,

Chou

Yang

et al. 2022

Pharmaceutics

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Metastatic osteosarcoma often results in poor prognosis despite the application of surgical en bloc excision along with chemotherapy. HO-3867 is a curcumin analog that induces cell apoptosis in several cancers, but the apoptotic effect and its mechanisms on osteosarcoma cells are still unknown. After observing the decrease in cellular viability of three human osteosarcoma U2OS, HOS, and MG-63 cell lines, and the induction of cellular apoptosis and arrest in sub-G1 phase in U2OS and HOS cells by HO-3867, the human apoptosis array showed that heme oxygenase (HO)-1 and cleaved caspase-3 expressions had significant increases after HO-3867 treatment in U2OS cells and vice versa for cellular inhibitors of apoptosis (cIAP)1 and X-chromosome-linked IAP (XIAP). Western blot analysis verified the results and showed that HO-3867 activated the initiators of both extrinsic caspase 8 and intrinsic caspase 9, and significantly increased cleaved PARP expression in U2OS and HOS cells. Moreover, with the addition of HO-3867, ERK1/2, and JNK1/2 phosphorylation were increased in U2OS and HOS cells. Using the inhibitor of JNK (JNK in 8), HO-3867’s increases in cleaved caspases 3, 8, and 9 could be expectedly suppressed, indicating that JNK signaling is responsible for both apoptotic pathways, including extrinsic and intrinsic, in U2OS and HOS cells caused by HO-3867. Through JNK signaling, HO-3867 has proven to be effective in causing both extrinsic and intrinsic apoptotic pathways of human osteosarcoma cells.

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Section: Discussionmentioning

confidence: 99%

HO-3867 Induces Apoptosis via the JNK Signaling Pathway in Human Osteosarcoma Cells

Lu¹,

Chou

Yang

et al. 2022

Pharmaceutics

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“…The whole-cell lysates for the array with 350 µg of protein were examined according to the guidelines of the kit’s manufacturers. Dot blots were visualized by exposure to an X-ray film and photographed and detected with a Bio-Rad, Hercules, CA, USA Molecular Imager Gel Doc XR system [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

CLEFMA Induces the Apoptosis of Oral Squamous Carcinoma Cells through the Regulation of the P38/HO-1 Signalling Pathway

Chen

Lin

Yang

et al. 2022

Cancers

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The purpose of this research was to evaluate the impact and the underlying molecular mechanism of CLEFMA-induced cell death in human OSCC. The anti-tumour properties of CLEFMA in oral cancer were explored using colony formation, flow cytometry, human apoptosis array, Western blot, and immunohistochemistry assays. The in vivo anti-tumour effect of CLEFMA administered by oral gavage was evaluated using SCC-9-derived xenograft-bearing nude mouse models. CLEFMA significantly suppressed colony formation and elicited cellular apoptosis in oral cancer cells. CLEFMA treatment remarkably increased phosphorylated p38 and HO-1 along with cleavage of poly ADP-ribose polymerase and activation of caspase-8, -9, and -3 in HSC-3 and SCC-9 cells. Administration of HO-1 small interfering RNA significantly protected the cells from CLEFMA-induced caspase-3, -8, and -9 activation. Attenuation of p38 activity by the pharmacologic inhibitor SB203580 dramatically reduced CLEFMA-induced caspase-3, -8, and -9 activation and HO-1 expression in OSCC. The subcutaneous murine xenograft models showed that CLEFMA in vivo suppressed tumour growth in implanted SCC-9 cells. All of these findings indicated that CLEFMA induced apoptosis through the p38-dependent rise in HO-1 signal transduction cascades in OSCC.

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“…Curcumin is multiple bioactive, including anti‐inflammatory, antioxidant antimicrobial and anti‐cancer; however, low potency and poor absorption profile hinder the clinical use of curcumin 7–11 . Diphenyl difluoroketone (EF‐24), a synthetic curcumin analog, has superior water solubility and systemic bioavailability than curcumin 12 .…”

Section: Introductionmentioning

confidence: 99%

EF‐24 inhibits TPA‐induced cellular migration and MMP‐9 expression through the p38 signaling pathway in cervical cancer cells

Lee

Lin

et al. 2022

Environmental Toxicology

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Diphenyl difluoroketone (EF-24), a synthetic curcumin analog, has enhanced bioavailability over curcumin. EF-24 acts more powerful bioactivity for anti-inflammatory and anti-cancer activity. However, the effects and mechanism of EF-24 on cervical cancer has not been fully investigated. Herein, this study evaluated the effects of EF-24 on TPA-induced cellular migration of cervical cancer. The results showed that EF-24 substantially reduced the cellular migration and cellular invasion of the HeLa and SiHa cells. Moreover, gelatin zymography, western blotting analyses and real-time PCR revealed that EF-24 suppressed Matrix metalloproteinase-9 (MMP-9) activity, protein expression and mRNA levels. Mechanistically, EF-24 inhibited the phosphorylation of the p38 signaling pathway. In conclusion, EF-24 inhibited TPA-induced cellular migration and cellular invasion of cervical cancer cell lines through modulating MMP-9 expression via downregulating signaling p38 pathway and EF-24 may have potential to serve as a chemopreventive agent of cervical cancer.

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Curcumin analog HO‐3867 triggers apoptotic pathways through activating JNK1/2 signalling in human oral squamous cell carcinoma cells

Cited by 19 publications

References 76 publications

HO-3867 Induces Apoptosis via the JNK Signaling Pathway in Human Osteosarcoma Cells

HO-3867 Induces Apoptosis via the JNK Signaling Pathway in Human Osteosarcoma Cells

CLEFMA Induces the Apoptosis of Oral Squamous Carcinoma Cells through the Regulation of the P38/HO-1 Signalling Pathway

EF‐24 inhibits TPA‐induced cellular migration and MMP‐9 expression through the p38 signaling pathway in cervical cancer cells

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