Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid inhibits growth of human lung cancer A549 cells by arresting cell cycle and triggering apoptosis

Li, Li; Chen, George G.; Lu, Ying; Liu, Yi; Wu, Ke; Gong, Xun; Gou, Zhan Ping; Li, Ming Yue; Liang, Nian Ci

doi:10.1007/s11670-012-0109-8

Cited by 19 publications

(17 citation statements)

References 37 publications

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“…In vitro , 5F has been shown to kill various human cancer cells including lung cancer cells, laryngeal cancer cells, thyroid carcinoma cells, gastric cancer cells and colorectal cancer cells via apoptotic pathways (3–7). Since 5F can induce apoptosis in cells of various types of cancer, it may also be a potential apoptosis-inducing drug in NPC therapy.…”

Section: Introductionmentioning

confidence: 99%

Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

Liu

et al. 2013

Oncology Reports

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Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F), a compound isolated from Pteris semipinnata L. (PsL), inhibits cell proliferation and induces cell apoptosis in several cancer lines. We found that 5F induced apoptosis and G2 phase cell cycle arrest in the CNE-2Z nasopharyngeal carcinoma (NPC) cells, accompanied by a decrease of NF-κB expression. 5F suppressed the viability of CNE-2Z cells in a time- and dose-dependent manner. 5F induced G2/M phase cell cycle arrest, but did not induce p21. Further analysis revealed that CNE-2Z cells harbored two p53 mutations. 5F treatment resulted in mitochondrial apoptosis, associated with increased Bax/Bcl-2 ratio, upregulation of cytochrome c in the cytosol, decreased NF-κB-p65 and increased IκB. Of note, 5F significantly sensitized CNE-2Z cells to cisplatin. 5F did not increase ROS, but reduced ROS production alone or in combination with cisplatin. Our data suggest that 5F is a potential anti-NPC drug for the development of single agent therapy and therapy in combination with cisplatin.

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Section: Introductionmentioning

confidence: 99%

Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

Liu

et al. 2013

Oncology Reports

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“…Originally found in Pteris semipinnata, 11α-OH KA was shown to inhibit cell proliferation and induce apoptosis in several cell lines [17,18]. When human lung cancer A549 cells are treated with 20-80 μg/mL (approximately 60-240 μ M ) of 11α-OH KA, the induction of the apoptotic factor p21 and activation of caspase-3 are observed [17].…”

Section: Discussionmentioning

confidence: 99%

“…When human lung cancer A549 cells are treated with 20-80 μg/mL (approximately 60-240 μ M ) of 11α-OH KA, the induction of the apoptotic factor p21 and activation of caspase-3 are observed [17]. In addition, 11α-OH KA induces mitochondrial mediated apoptosis in human nasopharyngeal carcinoma CNE-2Z cells, which is accompanied by a decrease of Bcl-2 and NF-κB protein levels [18]. However, no other physiologically relevant activity of 11α-OH KA, including suppression of melanogenesis, had been reported prior to the present report, which is the first study on the effect of 11α-OH KA on melanogenesis in mouse and human.…”

Section: Discussionmentioning

confidence: 99%

The Importance of 11α-OH, 15-oxo, and 16-en Moieties of 11α-Hydroxy-15-oxo-kaur-16-en-19-oic Acid in Its Inhibitory Activity on Melanogenesis

Kuroi

Sugimura²,

Kumagai³

et al. 2017

Skin Pharmacol Physiol

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Cosmetic industries have an interest in exploring and developing materials that have the potential to regulate melanin synthesis in human skin. Although melanin protects the skin from ultraviolet irradiation, excess melanin can be undesirable, particularly on the face where spots or freckles are associated with an appearance of aging. In this study, we found that ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic acid (11α-OH KA) in Pteris dispar Kunze strongly inhibited melanin synthesis by suppressing tyrosinase gene expression. The melanogenic transcription factor microphthalmia-associated transcription factor (MITF) is required for this suppression. However, 11α-OH KA did not modulate the expression level or activity of MITF. Structure-activity relationship analyses suggested that the 11α-OH, 15-oxo, and 16-en moieties of 11α-OH KA are essential for the suppression of melanin synthesis. On the other hand, the 19-COOH moiety is important for preventing cellular toxicity associated with 11α-OH KA and its related compounds. These results suggest that 11α-OH KA is an attractive target for potential use in the production of cosmetic items.

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“…This self-destructive cellular process is critical for organ development, tissue remodeling, immune regulation and several disease conditions (19). Numerous antitumor agents exert their therapeutic effects by inducing apoptosis (20)(21)(22)(23)(24). Mitochondria have an essential role in the regulation of cell apoptosis, and there are certain proteins that are closely associated with cell apoptosis in the intermembrane (25).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of apoptosis induction in human hepatocellular carcinoma cells following treatment with a gecko peptides mixture

Jin

Duan

et al. 2016

Biomedical Reports

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Abstract. The aim of the present study was to investigate the apoptotic effect and molecular mechanisms of gecko peptides mixture (GPM) on the human liver carcinoma HepG2 cell line in vitro. The methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay was performed to identify the dose-(0.10, 0.15, 0.20, 0.25 and 0.30 mg/ml) and time-dependent (24, 48 and 72 h) inhibitory effect of GPM on HepG2 cells and their proliferation. Hoechst 33258 staining was carried out to detect the nuclear change coupled with apoptosis induced by GPM. Western blotting was used to evaluate apoptosis-related protein expression changes induced by GPM, including caspase, cytochrome c (Cyt c) and apoptosis-inducing factor (AIF). MTT results showed that GPM significantly inhibited the proliferation of HepG2 cells in a dose-and time-dependent manner. Hoechst 33258 staining demonstrated that GPM induced typical apoptotic morphological changes, while western blotting analysis revealed that GPM increased caspase-3, caspase-9, Cyt c and AIF protein expression levels in HepG2 cells treated with 0.06 or 0.08 mg/ml for 24 h. In conclusion, GPM could induce apoptosis by activating the intrinsic mitochondrial apoptotic pathways.

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Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid inhibits growth of human lung cancer A549 cells by arresting cell cycle and triggering apoptosis

Abstract: 5F could inhibit the proliferation of A549 cells by arresting the cells in G2 phase and by inducing mitochondrial-mediated apoptosis.

Cited by 19 publications

References 37 publications

Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

The Importance of 11α-OH, 15-oxo, and 16-en Moieties of 11α-Hydroxy-15-oxo-kaur-16-en-19-oic Acid in Its Inhibitory Activity on Melanogenesis

Mechanism of apoptosis induction in human hepatocellular carcinoma cells following treatment with a gecko peptides mixture

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