Induction of laryngeal cancer cell death by Ent‐11‐hydroxy‐15‐oxo‐kaur‐16‐en‐19‐oic acid

Vlantis, Alexander C.; Lo, CM; Chen, George G.; Liang, Nian Ci; Lui, Vivian Wai Yan; Wu, Kefeng; Deng, Yi; Gong, Xuejun; Lu, Yingnian; Tong, Michael C. F.; Hasselt, C. Andrew van

doi:10.1002/hed.21357

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…Ent-11-hydroxy-15-oxo-kaur-16-en-19-oic acid (5F) is  an active compound in Pteris semipinnata L (PsL) [4][5][6] . Earlier studies from our laboratory demonstrated 5F could inhibit the in vitro growth of a number of tumors (e.g., colorectal cancer, gastric cancer, anaplastic thyroid carcinoma, liver cancer and laryngeal cancer) via a mitochondrial-mediated apoptotic mechanism [7][8][9][10][11] . We have also compared 5F with 7-hydroxystaurosporine (UCN01), which is currently being evaluated in clinical trials as an antitumor drug in the United State and Japan [12,13] .…”

Section: Introductionmentioning

confidence: 99%

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

Chen

et al. 2012

Chin. J. Cancer Res.

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Section: Introductionmentioning

confidence: 99%

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

Chen

et al. 2012

Chin. J. Cancer Res.

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“…The activation of EGFR is a frequent event in HNSCC, and has provided the molecular basis for current efforts aimed at evaluating the clinical activity of EGFR inhibitors in HNSCC [21], [22]. However, to date, the role of EGFR-dependent NFκB in the functional orchestration of HNSCC progression and metastasis is poorly realized [22], [23]. Since NFκB is able to regulate more than 150 genes, and is able to functionally orchestrate many steps in carcinogenesis, tumor progression and metastasis, it is important to delineate the efficacy of potential EGFR-TK inhibitors that target the NFκB-dependent HNSCC cell survival advantage.…”

Section: Introductionmentioning

confidence: 99%

Irreversible EGFR Inhibitor EKB-569 Targets Low-LET γ-Radiation-Triggered Rel Orchestration and Potentiates Cell Death in Squamous Cell Carcinoma

et al. 2011

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EKB-569 (Pelitinib), an irreversible EGFR tyrosine kinase inhibitor has shown potential therapeutic efficiency in solid tumors. However, cell-killing potential in combination with radiotherapy and its underlying molecular orchestration remain to be explored. The objective of this study was to determine the effect of EKB-569 on ionizing radiation (IR)-associated NFκB-dependent cell death. SCC-4 and SCC-9 cells exposed to IR (2Gy) with and without EKB-569 treatment were analyzed for transactivation of 88 NFκB pathway molecules, NFκB DNA-binding activity, translation of the NFκB downstream mediators, Birc1, 2 and 5, cell viability, metabolic activity and apoptosis. Selective targeting of IR-induced NFκB by EKB-569 and its influence on cell-fate were assessed by overexpressing (p50/p65) and silencing (ΔIκBα) NFκB. QPCR profiling after IR exposure revealed a significant induction of 74 NFκB signal transduction molecules. Of those, 72 were suppressed with EKB-569. EMSA revealed a dose dependent inhibition of NFκB by EKB-569. More importantly, EKB-569 inhibited IR-induced NFκB in a dose-dependent manner, and this inhibition was sustained up to at least 72 h. Immunoblotting revealed a significant suppression of IR-induced Birc1, 2 and 5 by EKB-569. We observed a dose-dependent inhibition of cell viability, metabolic activity and apoptosis with EKB-569. EKB-569 significantly enhanced IR-induced cell death and apoptosis. Blocking NFκB improved IR-induced cell death. Conversely, NFκB overexpression negates EKB-569 -induced cell-killing. Together, these pre-clinical data suggest that EKB-569 is a radiosensitizer of squamous cell carcinoma and may mechanistically involve selective targeting of IR-induced NFκB-dependent survival signaling. Further pre-clinical in-vivo studies are warranted.

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“…Additionally, 5F possesses seven chiral atoms, the configuration of which, as obtained by anomalous dispersion, is R-C4, S-C5, R-C8, S-C9, R-C12 and R-C15 (6). Previous studies have reported that 5F induces apoptosis in and inhibits the proliferation of lung, liver, anaplastic thyroid, stomach, colon and throat cancer cells (7)(8)(9)(10)(11) However, whether 5F exerts anti-tumor effects during the progression of breast cancer remains unclear. The present study examined the functions of 5F in the growth and apoptosis of three breast cancer cell lines, including MDA-MB-231, MCF-7 and SK-BR-3.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of breast cancer cell growth by the Pteris?semipinnata extract ent‑11α‑hydroxy‑15‑oxo‑kaur‑16‑en‑19‑oic‑acid

Meng

Long

et al. 2017

Oncol Lett

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Abstract. Previous studies have demonstrated strong anti-tumor effects of ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F), an extract from Pteris semipinnata, in liver, lung, stomach and anaplastic thyroid cancer cells. However, whether 5F inhibits the growth of breast cancer cells remains unclear. The present study assessed the effect of 5F on breast cancer cells. The breast cancer cell lines MCF-7, MDA-MB-231 and SK-BR-3 were each treated with 0, 5, 10, 20 and 40 µg/ml 5F. Morphological changes in the breast cancer cells were assessed using fluorescence microscopy. The proliferation and apoptosis of the breast cancer cells were also examined using Cell Counting Kit-8 and flow cytometry. The levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X apoptosis regulator (Bax), Bcl-2 antagonist/killer (Bak) 1 and caspase-3 in the breast cancer cells were assessed. The results of the present study demonstrated that 5F inhibited the proliferation of MCF-7, MDA-MB-231 and SK-BR-3 breast cancer cells in a concentration-and time-dependent manner. Treatment with 5F also induced the apoptosis of breast cancer cells. MDA-MB-231, MCF-7, and SK-BR-3 cells exhibited apoptotic rates of 40.13, 60.44, and 70.49%, respectively, following incubation with 5F for 24 h. Furthermore, 5F significantly decreased the expression of Bcl-2 and increased the expression of Bax, Bak, and caspase-3 in a concentration-dependent manner. The results of the present study revealed that the P. semipinnata extract 5F inhibited the growth of human breast cancer cells in a timeand concentration-dependent manner, and that 5F induced apoptosis of human breast cancer cells.

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Induction of laryngeal cancer cell death by Ent‐11‐hydroxy‐15‐oxo‐kaur‐16‐en‐19‐oic acid

Abstract: 5F induces apoptosis of laryngeal cancer cells by inhibiting NF-κB activation/induction, suppressing pro-proliferative and anti-apoptotic molecules, and promoting pro-apoptotic Bax.

Cited by 10 publications

References 29 publications

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

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

Irreversible EGFR Inhibitor EKB-569 Targets Low-LET γ-Radiation-Triggered Rel Orchestration and Potentiates Cell Death in Squamous Cell Carcinoma

Inhibition of breast cancer cell growth by the Pteris?semipinnata extract ent‑11α‑hydroxy‑15‑oxo‑kaur‑16‑en‑19‑oic‑acid

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