Candidone Inhibits Migration and Invasion, and Induces Apoptosis in HepG2 Cells

Boonyarat, Chantana; Sangchavee, Kanlaya; Plekratoke, Kusawadee; Yenjai, Chavi; Reubroycharoen, Prasert; Kaewamatawong, Rawiwun; Waiwut, Pornthip

doi:10.1248/bpb.b20-00718

Cited by 5 publications

(3 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inhibition of DRONC, the fly ortholog of CASP-9, affected border cell migration in Drosophila ovary . Other studies that described an association between CASP-9 level/activity and altered cell migration have been published, but in these studies, apoptosis was induced by drug treatment or gene overexpression, thus making the conclusion about direct link between CASP-9 and cell migration impossible. − …”

Section: Discussionmentioning

confidence: 99%

Caspase-9 Is a Positive Regulator of Osteoblastic Cell Migration Identified by diaPASEF Proteomics

Říhová,

Lapčík,

Veselá

et al. 2024

J. Proteome Res.

View full text Add to dashboard Cite

Caspase-9 is traditionally considered the initiator caspase of the intrinsic apoptotic pathway. In the past decade, however, other functions beyond initiation/execution of cell death have been described including cell type-dependent regulation of proliferation, differentiation/maturation, mitochondrial, and endosomal/lysosomal homeostasis. As previous studies revealed nonapoptotic functions of caspases in osteogenesis and bone homeostasis, this study was performed to identify proteins and pathways deregulated by knockout of caspase-9 in mouse MC3T3-E1 osteoblasts. Data-independent acquisition−parallel accumulation serial fragmentation (diaPASEF) proteomics was used to compare protein profiles of control and caspase-9 knockout cells. A total of 7669 protein groups were quantified, and 283 upregulated/141 downregulated protein groups were associated with the caspase-9 knockout phenotype. The deregulated proteins were mainly enriched for those associated with cell migration and motility and DNA replication/repair. Altered migration was confirmed in MC3T3-E1 cells with the genetic and pharmacological inhibition of caspase-9. ABHD2, an established regulator of cell migration, was identified as a possible substrate of caspase-9. We conclude that caspase-9 acts as a modulator of osteoblastic MC3T3-E1 cell migration and, therefore, may be involved in bone remodeling and fracture repair.

show abstract

Section: Discussionmentioning

confidence: 99%

Caspase-9 Is a Positive Regulator of Osteoblastic Cell Migration Identified by diaPASEF Proteomics

Říhová,

Lapčík,

Veselá

et al. 2024

J. Proteome Res.

View full text Add to dashboard Cite

show abstract

“…Its better activity might come from its higher lipophilicity, resulting in more diffusion into the cells. [31][32][33] This study indicated that 7-methoxyheptaphylline sensitized TRAIL-induced cell death of HT29 cell by upregulating DR5 expression through JNK regulation.…”

Section: Discussionmentioning

confidence: 99%

7-Methoxyheptaphylline Enhances TRAIL-Induced Apoptosis of Colorectal Adenocarcinoma Cell <i>via</i> JNK-Mediated DR5 Expression

Boonyarat

Yenjai

2023

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

A cytokine known as TNF-related apoptosis-inducing ligand (TRAIL) has the ability to precisely cause the death of cancer cells, while normal cells are left undisturbed. Recent studies show that certain cancer cells are sensitive to the apoptotic effect of TRAIL. In this study, HT29 colorectal adenocarcinoma cells exposed to TRAIL were treated with heptaphylline and 7methoxyheptaphylline from Clausena harmandiana in an effort to comprehend the mechanisms involved behind this activity. The MTT test was utilized to determine cell survival, and phase contrast microscopy was used to examine cell morphology. Through using real-time RT-PCR, Western blotting, and RT-PCR, the molecular mechanisms were investigated. According to the findings, whilst hepataphylline caused cytotoxicity in normal colon FHC cells, in comparison to healthy colon FHC cells, 7-methoxyheptaphylline inhibited cancer cells in a concentrationdependent manner. Heptaphylline alone or in conjunction with TRAIL showed no discernible effect on TRAL-induced HT29 cell death, but 7-methoxyheptaphylline boosted caspase-3 cleavage. The study showed that the JNK pathway was responsible for the 7methoxyheptaphylline's enhancement of the DR5 (death receptor 5) mRNA, TRAIL receptor, and protein. The results demonstrated that the 7-methoxyheptaphylline of Clausena harmandiana increased the expression of DR5 via the JNK pathway, intensifying TRAILinduced HT29 cell death.

show abstract

“…In response to cell stress signals, activation of MAPKs, including ERK1/2, JNK and p-38, is essential for cell growth, proliferation, and differentiation, leading to a decrease in apoptotic cell death. 9,[36][37][38][39][40] However, hyperactivation of the MAPK pathway has been associated with the development of MDR in cancer cells. 9,39,41,42) Our results showed that rhinacanthin-C was able to inhibit the sustained activation of the MAPK signaling pathway, as evidenced by the reduction in phosphorylated forms of ERK1/2, JNK and p-38 in MCF-7/DOX cells after 24-h of exposure, followed by a significant increase in the number of apoptotic cells.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis Inducing Activity of Rhinacanthin-C in Doxorubicin-Resistant Breast Cancer MCF-7 Cells

Chaisit

Jianmongkol

2021

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Rhinacanthin-C is a natural bioactive naphthoquinone ester with potential chemotherapeutic value in cancer treatment. In this study, we investigated its apoptotic induction ability and the involved mechanisms through the mitogen-activated protein kinases (MAPK) and protein kinase B/glycogen synthase kinase-3β/ nuclear factor erythroid 2-related factor 2 (Akt/GSK-3β/Nrf2) signaling pathways in doxorubicin-resistant breast cancer MCF-7 (MCF-7/DOX) cells. Our 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that rhinacanthin-C (3-28 µM) significantly decreased the viability of MCF-7/DOX cells and potentiated hydrogen peroxide cytotoxicity. This naphthoquinone was able to increase intracellular reactive oxygen species (ROS), as measured by the 2′,7′-dichlorofluorescein diacetate (DCFH-DA) assay. This compound increased the number of apoptotic cells by elevating the ratio of apoptotic checkpoint proteins Bax/Bcl-2 and by decreasing the expression of poly(ADP-ribose) polymerase (PARP) protein. Furthermore, Western blotting analyses showed that treatment with rhinacanthin-C (3-28 µM) for 24 h significantly decreased the expression levels of the phosphorylated forms of MAPK proteins (i.e., extracellular signal regulated protein kinase 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38), Akt, GSK-3β and Nrf2 proteins in MCF-7/DOX cells. Inhibition of the Akt/GSK-3β/Nrf2 pathway led to a significant reduction in heme oxygenase-1 (HO-1) and reduced nicotinamide adenine dinucleotide phosphate (NADP)(H): quinone oxidoreductase 1 (NQO1) proteins. These findings suggested that rhinacanthin-C was able to induce apoptosis in MCF-7/DOX cells through increased ROS production and suppression of the cell survival systems mediated by the MAPKs and Akt/GSK-3β/Nrf2 signaling pathways.

show abstract

Candidone Inhibits Migration and Invasion, and Induces Apoptosis in HepG2 Cells

Cited by 5 publications

References 22 publications

Caspase-9 Is a Positive Regulator of Osteoblastic Cell Migration Identified by diaPASEF Proteomics

Caspase-9 Is a Positive Regulator of Osteoblastic Cell Migration Identified by diaPASEF Proteomics

7-Methoxyheptaphylline Enhances TRAIL-Induced Apoptosis of Colorectal Adenocarcinoma Cell <i>via</i> JNK-Mediated DR5 Expression

Apoptosis Inducing Activity of Rhinacanthin-C in Doxorubicin-Resistant Breast Cancer MCF-7 Cells

Contact Info

Product

Resources

About