Cardamonin inhibits the proliferation and metastasis of non-small-cell lung cancer cells by suppressing the PI3K/Akt/mTOR pathway

Zhou, Xiaoshu; Zhou, Rui; Li, Qianwen; Jie, Xiaohua; Hong, Jiaxin; Zong, Yan; Dong, Xiaorong; Zhang, Sheng; Li, Zhenyu; Wu, Gang

doi:10.1097/cad.0000000000000709

Cited by 49 publications

(44 citation statements)

References 31 publications

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“…Previously, Cavin3 had been found to be overexpressed in lung cancer, but the role of Cavin3 in lung cancer progression was not particularly clear. Besides, Cavin3 is a part of the mTOR pathway, thus clarifying the effect of Cavin3 on lung cancer occurrence and development which might make it possible for the mTORC1 pathway to be a novel regulatory target in lung cancer [15][16][17].…”

Section: Discussionmentioning

confidence: 99%

[Retracted] The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism

Sun

2020

BioMed Research International

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Objective. The purpose of this study was to describe the role of Cavin3 in the progression of lung cancer and its underlying mechanism. Methods. Totally, 200 cases of lung cancer tissues and corresponding paracancer tissues were collected. Cavin3 expression in samples was determined by qRT-PCR, and the correlation with lung cancer stages as well as prognosis was statistically analyzed combined with matched clinical information. To investigate the mechanism of Cavin3 in lung cancer progression, firstly, Cavin3 was detected in lung cancer cell lines A549, PC9, and H520. Then, cells with stable Cavin3 overexpression and Cavin3 knockout were established to determine the effect of Cavin3 overexpression on the mammalian target of rapamycin (mTOR) signaling pathway. Subsequently, cells were harvested for cell proliferation, migration, and invasion assays in vitro, as well as nude mouse transplantation tumor experiment in vivo. Results. Cavin3 was seen to be highly expressed in cancer tissues. Statistical analysis with matched clinical data showed that Cavin3 as a prognostic indicator of lung cancer had important clinical value. In addition, it could be found that high expression of Cavin3 was able to promote cell proliferation, migration, and invasion and also potentiate tumor formation in vivo. Conclusion. Cavin3 was highly expressed in lung cancer, and it was capable to promote cell proliferation, invasion, and migration.

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Section: Discussionmentioning

confidence: 99%

[Retracted] The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism

Sun

2020

BioMed Research International

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“…Moreover, it was shown that HNE loaded ß-cyclodextrin nanocarrier potentiate its antitumor effect in A375 melanoma monolayer cultures and in human reconstructed skin carrying melanoma cells [93]. CD was also shown to inhibit proliferation of non-small-cell lung cancer cells (NSCLC) [34] and SKOV3 ovarian carcinoma cells [35] with the greatest impact at 72 h at concentrations greater than 20 μM CD. However, those concentrations could not be used in our proliferation studies as they killed melanocytes and dermal fibroblasts as well.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its potential antioxidant, anti-inflammatory, and anti-infectious activity summarized, for example, by Gonçalves et al [33], CD has been described to have antineoplastic activity. CD inhibits proliferation and metastasis of the non-small-cell lung cancer cell lines A549 and H460 [34] and induces autophagic cell death in SKOV3 ovarian carcinoma cells [35]. Furthermore, migration and invasive capacity is downregulated in CD-treated triple negative breast cancer cell line BT-549 [36] and the androgen-independent DU145 prostate cancer cell line [37].…”

Section: Introductionmentioning

confidence: 99%

In vitro selective cytotoxicity of the dietary chalcone cardamonin (CD) on melanoma compared to healthy cells is mediated by apoptosis

et al. 2019

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Malignant melanoma is an aggressive type of cancer and the deadliest form of skin cancer. Even though enormous efforts have been undertaken, in particular the treatment options against the metastasizing form are challenging and the prognosis is generally poor. A novel therapeutical approach is the application of secondary plant constituents occurring in food and food products. Herein, the effect of the dietary chalcone cardamonin, inter alia found in Alpinia species, was tested using human malignant melanoma cells. These data were compared to cardamonin treated normal melanocytes and dermal fibroblasts representing healthy cells. To investigate the impact of cardamonin on tumor and normal cells, it was added to monolayer cell cultures and cytotoxicity, proliferation, tumor invasion, and apoptosis were studied with appropriate cell biological and biochemical methods. Cardamonin treatment resulted in an apoptosis-mediated increase in cytotoxicity towards tumor cells, a decrease in their proliferation rate, and a lowered invasive capacity, whereas the viability of melanocytes and fibroblasts was hardly affected at such concentrations. A selective cytotoxic effect of cardamonin on melanoma cells compared to normal (healthy) cells was shown in vitro. This study along with others highlights that dietary chalcones may be a valuable tool in anticancer therapies which has to be proven in the future in vivo.

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“…Both these paths lead to APOC3, which we found up-regulated in serum after one year of antifibrotic treatment. Both these pathways are known to be involved in the epithelial mesenchymal transition in cancer as well as fibrosis 38,39 . Salha et al described these mechanisms as essential for mesenchymal cell transmigration through support of tumor growth, increase in power and contribution to tumor-angiogenesis 40 .…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Pulmonary Fibrosis Serum proteomic analysis before and after nintedanib therapy

Landi

Bergantini²,

Cameli³

et al. 2020

Sci Rep

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Idiopathic pulmonary fibrosis (IPF) is a fatal progressive disease with a median survival of 2-5 years. Nintedanib is a small tyrosine kinase inhibitor that reduces IPF progression, significantly slowing the annual decline in Forced Vital Capacity (FVC). Very little data is available on the molecular mechanisms of this treatment in IPF, despite a growing interest in the definition of IPF pathogenesis and target therapy. A functional proteomic approach was applied to the analysis of serum samples from IPF patients in order to highlight differential proteins potentially indicative of drug-induced molecular pathways modifications and response to therapy. Twelve serum samples were collected from six IPF patients in care at Siena Regional Referral Center for Interstitial Lung Diseases (ILDs) and treated with nintedanib for one year. Serum samples were analyzed at baseline (T0 before starting therapy) and after one year of treatment (T1) and underwent differential proteomic and bioinformatic analysis. Proteomic analysis revealed 13 protein species that were significantly increased after one year of treatment. When the targets of nintedanib (VEGFR, FGFR and PDGFR) were added, enrichment analysis extracted molecular pathways and process networks involved in cell differentiation (haptoglobin and albumin), coagulation (antithrombin III), epithelial mesenchymal transition, cell proliferation and transmigration. PI3K and MAPK induced up-regulation of apolipoprotein C3. Proteomic study found 13 protein species up-regulated in IPF patients after one year of nintedanib treatment. Haptoglobin, a central hub of our analysis was validated by 2D-WB and ELISA as theranostic marker in a more numerous populations of patients.

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Cardamonin inhibits the proliferation and metastasis of non-small-cell lung cancer cells by suppressing the PI3K/Akt/mTOR pathway

Cited by 49 publications

References 31 publications

[Retracted] The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism

[Retracted] The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism

In vitro selective cytotoxicity of the dietary chalcone cardamonin (CD) on melanoma compared to healthy cells is mediated by apoptosis

Idiopathic Pulmonary Fibrosis Serum proteomic analysis before and after nintedanib therapy

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