mTOR inhibition of cardamonin on antiproliferation of A549 cells is involved in a FKBP12 independent fashion

Tang, Ying; Fang, Qi; Shi, Daohua; Niu, Peiguang; Chen, Yaoyao; Deng, Jie

doi:10.1016/j.lfs.2014.01.066

Cited by 36 publications

(44 citation statements)

References 33 publications

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“…2 Cardamonin inhibits the neurospere formation and expression of CD133 + GSCs. a The CD133 + GSCs were treated with cardamonin at different concentrations (20,30, and 40 μM) for 7 days, and the neurosphere formation was observed using a microscope (magnification, ×20). b The viability of CD133 + GSCs was evaluated by MTT assay after 72-h incubation of cardamonin (20, 30, and 40 μM).…”

Section: Cardamonin Potentiates the Proapoptotic Effects Of Temozolommentioning

confidence: 99%

“…The bars represented the means ± SD of three separate experiments. c The expression levels of CD133 in CD133 + GSCs treated with different concentrations (20,30, and 40 μM) of cardamonin by Western blot assay. β-actin was used as loading control of TMZ.…”

Section: Cardamonin Potentiates the Proapoptotic Effects Of Temozolommentioning

confidence: 99%

“…Recent studies revealed that cardamonin not only possesses anti-inflammation activity, but also suppresses the proliferation of human tumor cells, including myeloma and colorectal carcinoma [16][17][18][19]. However, the mechanism underlying the inhibition effects of cardamonin on the cancer cells is not well documented, although inhibition of mTOR, Tgase-2, and NF-kB may be associated with its bioactivity [20][21][22]. In the present study, we investigated the effects of cardamonin on the self-renewal and cell apoptosis in GSCs and its association with STAT3 pathway.…”

Section: Introductionmentioning

confidence: 99%

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Cardamonin induces apoptosis by suppressing STAT3 signaling pathway in glioblastoma stem cells

Liu

Zhao

et al. 2015

Tumor Biol.

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Glioblastoma stem cells (GSCs) are the initiating cells in glioblastoma multiforme (GBM) and contribute to the resistance of GBM to chemotherapy and radiation. In the present study, we investigated the effects of cardamonin (3,4,2,4-tetrahydroxychalcone) on the self-renewal and apoptosis of GSCs, and if its action is associated with signal transducer and activator of transcription 3 (STAT3) pathway. CD133(+) GSCs, a kind of GSCs line, was established from human glioblastoma tissues. Cardamonin inhibited the proliferation and induced apoptosis in CD133+ GSCs. The proapoptotic effects of temozolomide (TMZ) were further enhanced by cardamonin in CD133+ GSCs and U87 cells in vitro. For in vivo study, injection of 5 × 10(5) cells of CD133+ GSCs subcutaneously (s.c.) into nude mice, 100 % of large tumors were developed within 8 weeks in all mice; in contrast, only one out of five mice developed a small tumor when 5 × 10(5) cells of CD133(-) GMBs cells were injected. Cardamonin also inhibited STAT3 activation by luciferase assay and suppressed the expression of the downstream genes of STAT3, such as Bcl-XL, Bcl-2, Mcl-1, survivin, and VEGF. Furthermore, cardamonin locked nuclear translocation and dimerization of STAT3 in CD133(+) GSCs. Docking analysis confirmed that cardamonin molecule was successfully docked into the active sites of STAT3 with a highly favorable binding energy of -10.78 kcal/mol. The study provides evidence that cardamonin is a novel inhibitor of STAT3 and has the potential to be developed as a new anticancer agent targeting GSCs. This study also reveals that targeting STAT3 signal pathway is an important strategy for the treatment of human GBM.

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Section: Cardamonin Potentiates the Proapoptotic Effects Of Temozolommentioning

confidence: 99%

Section: Cardamonin Potentiates the Proapoptotic Effects Of Temozolommentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cardamonin induces apoptosis by suppressing STAT3 signaling pathway in glioblastoma stem cells

Liu

Zhao

et al. 2015

Tumor Biol.

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“…However, the underlying mechanism has not been previously studied. Our previous studies demonstrated that cardamonin inhibits the proliferation, angiogenesis and metastasis of non-small cell lung carcinoma cells, epithelial ovarian cancer cells and Lewis lung carcinoma cells by inhibition of mTOR activation (25)(26)(27)). In the current study, the therapeutic potency of cardamonin combined with cisplatin in ovarian cancer was evaluated and the underlying mechanism was investigated.…”

Section: Introductionmentioning

confidence: 99%

Cardamonin enhances the anti-proliferative effect of cisplatin on ovarian cancer

et al. 2018

Self Cite

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Abstract. The mammalian target of rapamycin (mTOR) is well-known as a promising therapeutic target in various cancer cells. mTOR activation decreases the sensitivity of ovarian cancer to cisplatin. Cardamonin inhibits the proliferation of various cancer cells by mTOR suppression. The present study examined whether cardamonin combined with cisplatin is efficacious for the anti-proliferation of ovarian cancer cells. The anti-proliferative effect was determined by MTT and cell cycle assays. Activation of the mTOR signal pathway and the expression of anti-apoptotic proteins were evaluated by western blot analysis. Cardamonin significantly enhanced the effects of cisplatin on cell proliferation and cell cycle progression. The expression of B cell lymphoma-2, X-linked inhibitor of apoptosis protein and Survivin was significantly decreased following combination treatment. Furthermore, the activation of mTOR and its downstream 70 kDa ribosomal protein S6 kinase was inhibited by cardamonin. These results demonstrated that the combinatorial effects of cardamonin and cisplatin on anti-proliferation were enhanced by suppressing the expression of anti-apoptotic proteins and activation of mTOR in ovarian cancer cells.

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“…Cardamonin possesses the anti‐inflammation activity and anticancer activities via inhibiting the proliferation of tumor cells and reduces tumor growth in mice . It was reported that cardamonin exerted the antitumor effects on cancer cells through modulation of various signaling transductions including mTOR, STAT3, Wnt/β‐catenin, and NF‐κB signaling pathways . Cardamonin also suppressed the level of transglutaminase‐2 resulting in blocking cell migration and invasion, and it also showed metastasis inhibitory effect on highly metastatic Lewis lung carcinoma cells .…”

Section: Introductionmentioning

confidence: 99%

Cardamonin induces immune responses and enhances survival rate in WEHI‐3 cell–generated mouse leukemia in vivo

Liao

Shih

et al. 2019

Environmental Toxicology

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Cardamonin, a monomeric alkaloid, is isolated from Alpinia conchigera Griff and other natural plants. Recently, it has been focused on its anticancer activities, and no information showing its immune effects on leukemia mice was reported. In this study, we investigated the immune effects of cardamonin on WEHI‐3 cell–generated leukemia mice. Forty BALB/c mice were randomly divided into four groups: Group I mice were normal animals and groups II‐IV were leukemia. Group II mice, as a positive control, were administered with normal diet, and group III and IV mice were treated with 1 and 5 mg/kg of cardamonin, respectively, by intraperitoneal injection every 2 days for 14 days. The population of white blood cells, macrophage phagocytosis, and the proliferations of T and B cells were analyzed by flow cytometry. Another forty mice were also separated randomly into four groups for the determination of survival rate. Results showed that cardamonin did not affect body weight. Cardamonin decreased CD3, CD11b, and Mac‐3 cell populations but increased CD19 number. Cardamonin enhanced phagocytic abilities of macrophages from the peripheral blood mononuclear cells of leukemia mice. Furthermore, cardamonin at 1 mg/kg treatment improved the survival rate of leukemia mice in vivo. Therefore, cardamonin could be applied for a leukemia therapeutic reagent at a defined dose.

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mTOR inhibition of cardamonin on antiproliferation of A549 cells is involved in a FKBP12 independent fashion

Cited by 36 publications

References 33 publications

Cardamonin induces apoptosis by suppressing STAT3 signaling pathway in glioblastoma stem cells

Cardamonin induces apoptosis by suppressing STAT3 signaling pathway in glioblastoma stem cells

Cardamonin enhances the anti-proliferative effect of cisplatin on ovarian cancer

Cardamonin induces immune responses and enhances survival rate in WEHI‐3 cell–generated mouse leukemia in vivo

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