Casticin inhibits human prostate cancer DU 145 cell migration and invasion
            <i>via</i>
            Ras/Akt/NF‐κB signaling pathways

Lin, Chia Chang; Chen, Kuen‐Bao; Tsai, Chang Hai; Tsai, Fuu Jen; Huang, Chih‐Yang; Tang, Chih Hsin; Yang, Jai Sing; Hsu, Yu-Chin; Peng, Shu‐Fen; Chung, Jing Gung

doi:10.1111/jfbc.12902

Cited by 95 publications

(70 citation statements)

References 60 publications

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“…Casticin significantly reduced the cell migration rate by 77.41% after 48 h of 5 µM compared to the control of DU145 cells [99] and inhibited cell migration by 93% after 24 h of 200 nM in human melanoma A375.S2 cancer cells [123]. In addition, MMP-2/-9 activities were inhibited in a concentration-and time-dependent manner in DU145 cells [124]. Moreover, casticin significantly inhibited the motility ability of MDA-MB-231 and 4T1 cells [51].…”

Section: Effect Of Casticin On Metastasismentioning

confidence: 89%

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An Overview of the Potential Antineoplastic Effects of Casticin

et al. 2020

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Cancer persists as one of the leading causes of deaths worldwide, contributing to approximately 9.6 million deaths per annum in recent years. Despite the numerous advancements in cancer treatment, there is still abundant scope to mitigate recurrence, adverse side effects and toxicities caused by existing pharmaceutical drugs. To achieve this, many phytochemicals from plants and natural products have been tested against cancer cell lines in vivo and in vitro. Likewise, casticin, a flavonoid extracted from the Vitex species, has been isolated from the leaves and seeds of V. trifolia and V. agnus-castus. Casticin possesses a wide range of therapeutic properties, including analgesic, anti-inflammatory, antiangiogenic, antiasthmatic and antineoplastic activities. Several studies have been conducted on the anticancer effects of casticin against cancers, including breast, bladder, oral, lung, leukemia and hepatocellular carcinomas. The compound inhibits invasion, migration and proliferation and induces apoptosis (casticin-induced, ROS-mediated and mitochondrial-dependent) and cell cycle arrest (G0/G1, G2/M, etc.) through different signaling pathways, namely the PI3K/Akt, NF-κB, STAT3 and FOXO3a/FoxM1 pathways. This review summarizes the chemo-preventive ability of casticin as an antineoplastic agent against several malignancies.

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Section: Effect Of Casticin On Metastasismentioning

confidence: 89%

“…The role of the compound in regulating EMT is depicted in Figure 4. DU145 cells [124]. Moreover, casticin significantly inhibited the motility ability of MDA-MB-231 and 4T1 cells [51].…”

Section: Effect Of Casticin On Metastasismentioning

confidence: 95%

An Overview of the Potential Antineoplastic Effects of Casticin

et al. 2020

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“…Our previous results show that food ingredients and phytochemicals exhibit various diverse biological activities [37][38][39][40][41]. Particularly various phytoextracts and their active principles have shown to provide effective cardioprotection against various challenges [42][43][44][45][46][47][48][49][50].…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine reverses high-glucose induced hypoxic effects by negatively regulating HIF-1α induced BNIP3 expression to ameliorate H9c2 cardiomyoblast apoptosis

et al. 2020

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Background: Diabetic patients are highly vulnerable to hypoxic injury, which is associated with hypoxia induced BNIP3 expression that subsequently activate apoptosis. Our previous research show that Tetramethylpyrazine (TMP), a food flavoring agent, represses the hypoxia induced BNIP3 expression attenuate myocardial apoptosis. In this study, we evaluate the effect of TMP to provide protection against hypoxia aggravated high-glucose associated cellular apoptosis. Methods: The cytoprotective effect of TMP against high glucose induced cellular damages was determined on embryo derived H9c2 cardiomyoblast cells that were subjected to 5% hypoxia for 24 h and subjected to different duration of 33 mM high glucose challenge. Further, the involvement of HIF-1α and BNIP3 in cellular damage and the mechanism of protection of TMP were determined by overexpression and silencing HIF-1α and BNIP3 protein expression. Results: The results show that hypoxic effects on cell viability aggravates with high glucose challenge and this augmentative effect is mediated through BNIP3 in H9c2 cardiomyoblast cells. However, TMP administration effectively reversed the augmented HIF-1α levels and BNIP3 elevation. TMP improved the survival of H9c2 cells and effectively suppressed apoptosis in H9c2 cells. Further comparison on the effects of TMP on H9c2 cells challenged with high glucose and those challenged with hypoxia show that TMP precisely regulated the hypoxic intensified apoptotic effects in high-glucose condition. Conclusion: The results clearly show that flavoring agent-TMP attenuates cytotoxicity amplified by hypoxia challenge in high glucose condition by destabilizing HIF-1α.

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“…In this study, murine anti-CSNK2A1 (GTX107897) monoclonal antibodies were used to detect CSNK2A1 via western blotting procedures described previously [13] . Briefly, frozen liver tissue samples were homogenized with 3 volumes of 10 mM ice-cold phosphate buffer (pH 7.0) containing 1 mM EDTA, 0.25 M sucrose, 1 mM sodium azide, and 0.1 mM phenylmethylsulfonyl fluoride.…”

Section: Western Blot Analysismentioning

confidence: 99%

Effects of Casein Kinase 2 Alpha 1 Gene Expression on Mice Liver Susceptible to Type 2 Diabetes Mellitus and Obesity

et al. 2020

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Diabetes mellitus (DM) is a chronic disease found worldwide. Notably, BKS.Cg-Dock7 m +/+ Lepr db /JNarl mice are useful animal models for studying type 2 diabetes mellitus (T2DM). In this study, we investigated casein kinase 2 alpha 1 (CSNK2A1) gene and protein expression in the liver tissues of mice at different ages (4, 16, and 32 weeks) using real-time quantitative polymerase chain reactions, western blotting, immunohistochemistry, and enzyme-linked immunosorbent assay. Our data paved the way for exploring BKS.Cg-Dock7 m +/+ Lepr db /JNarl in the mouse model by demonstrating a significant increase in gene and protein expression in T2DM (+Lepr db /+Lepr db) mouse liver when compared to control (+Dock7 m /+Dock7 m) mouse liver. We also observed that CSNK2A1 protein level in the serum of T2DM patient group was higher than that of the control group, although the data was not statistically significant. Based on our findings, we can now understand the role of CSNK2A1 gene upregulation when encountering T2DM pathologies.

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Casticin inhibits human prostate cancer DU 145 cell migration and invasion via Ras/Akt/NF‐κB signaling pathways

Cited by 95 publications

References 60 publications

An Overview of the Potential Antineoplastic Effects of Casticin

An Overview of the Potential Antineoplastic Effects of Casticin

Tetramethylpyrazine reverses high-glucose induced hypoxic effects by negatively regulating HIF-1α induced BNIP3 expression to ameliorate H9c2 cardiomyoblast apoptosis

Effects of Casein Kinase 2 Alpha 1 Gene Expression on Mice Liver Susceptible to Type 2 Diabetes Mellitus and Obesity

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