Volatile oil from alpinia officinarum promotes lung cancer regression in vitro and in vivo

2018 ◽  
Vol 9 (9) ◽  
pp. 4998-5006 ◽  
Author(s):  
Ning Li ◽  
Qingyu Zhang ◽  
Zhenbin Jia ◽  
Xiaohong Yang ◽  
Haitao Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Underlying Mechanism ◽  
Volatile Oil ◽  
Alpinia Officinarum ◽  
Low Cytotoxicity ◽  
Cancer Intervention ◽  
Cancer Activity ◽  
Cancer Regression

The anti-lung cancer activity of volatile oil from Alpinia officinarum (VOAO) and the underlying mechanism has been studied. VOAO could be an effective, low cytotoxicity candidate for lung cancer intervention.

scholarly journals The red wine component ellagic acid induces autophagy and exhibits anti-lung cancer activity in vitro and in vivo

2018 ◽  
Vol 23 (1) ◽  
pp. 143-154 ◽  
Author(s):  
Jing Duan ◽  
Ji-Cheng Zhan ◽  
Gui-Zhen Wang ◽  
Xin-Chun Zhao ◽  
Wei-Dong Huang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Ellagic Acid ◽  
Red Wine ◽  
Cancer Activity

scholarly journals MicroRNA-425-5p Inhibits Lung Cancer Cell Growth in Vitro and in Vivo by Downregulating TFIIB-Related Factor 2

2020 ◽  
Vol 19 ◽  
pp. 153303381990111
Author(s):  
Xi Yu ◽  
Hong Zheng ◽  
Rongfei Sun ◽  
Xuejiao Qian ◽  
Ping Jiang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Underlying Mechanism ◽  
Related Factor ◽  
Cancer Type ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

Lung cancer is the most common cancer type with increasingly high incidence. MicroRNAs provide the potential biomarkers for lung cancer treatment. Thus, we aimed to investigate the function of microRNA-425-5p in lung cancer development and the underlying mechanisms. MicroRNA-425-5p overexpression inhibited A549 lung cancer cell proliferation in vitro and in vivo. On the other hand, microRNA-425-5p inhibition increased A549 proliferation. Mechanistically, the underlying mechanism by which microRNA-425-5p inhibits lung cancer cell growth was mediated through its ability in targeting and downregulating the TFIIB-related factor 2. Our results for the first time identified microRNA-425-5p as a tumor suppressor in lung cancer. Thus, microRNA-425-5p may serve as a potential therapeutic target for lung cancer.

scholarly journals Potent anti-cancer activity of Alnus nitida against lung cancer cells; in vitro and in vivo studies

2019 ◽  
Vol 110 ◽  
pp. 254-264 ◽  
Author(s):  
Moniba Sajid ◽  
Chao Yan ◽  
Dawei Li ◽  
Siva Bharath Merugu ◽  
Hema Negi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
In Vivo Studies ◽  
Anti Cancer ◽  
Cancer Activity

scholarly journals Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195

2017 ◽  
Vol 42 (6) ◽  
pp. 2453-2466 ◽  
Author(s):  
Dapeng Wu ◽  
Yong Li ◽  
Huixiang Zhang ◽  
Xigang Hu
Keyword(s):  
Lung Cancer ◽  
Colony Formation ◽  
Underlying Mechanism ◽  
Tumor Xenograft ◽  
Luciferase Reporter ◽  
Nsclc Patients ◽  
The Relationship ◽  
Variant Translocation

Background/Aims: Plasmacytoma variant translocation 1 (PVT1) exerts an oncogenic role in many tumors, including lung cancer. However, the roles of PVT1 in regulating radiosensitivity of NSCLC and its underlying mechanism are still unclear. Methods: Expression levels of PVT1 and miR-195 in NSCLC tissues and cells were examined by qRT-PCR. Effects of PVT1 and miR-195 on cell proliferation, apoptosis and colony formation abilities were assessed by MTT assay, flow cytometry and colony formation assay. Luciferase reporter assay was performed to confirm the relationship between PVT1 and miR-195. Tumor xenograft experiments were conducted to observe the effect of PVT1 on radiosensitivity of NSCLC in vivo. Results: PVT1 was negatively correlated with miR-195 expression in NSCLC tissues and associated with poor prognosis of NSCLC patients. Expression of PVT1 and miR-195 varied inversely after irradiation in NSCLC cells. PVT1 knockdown or miR-195 overexpression enhanced radiosensitivity of NSCLC in vitro by inhibiting proliferation and inducing apoptosis. PVT1 directly interacted with miR-195 and regulated its expression. Moreover, PVT1 knockdown improved radiosensitivity of NSCLC cells in vitro and in vivo by sponging miR-195. Conclusion: Knockdown of PVT1 enhances radiosensitivity of NSCLC by sponging miR-195, providing a novel therapeutic target to improve radiotherapy efficiency in NSCLC.

scholarly journals Effect of Oversulfation on the Composition, Structure, and In Vitro Anti-Lung Cancer Activity of Fucoidans Extracted from Sargassum aquifolium

Marine Drugs ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 215
Author(s):  
Hui-Hua Hsiao ◽  
Tien-Chiu Wu ◽  
Yung-Hsiang Tsai ◽  
Chia-Hung Kuo ◽  
Ren-Han Huang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Biological Activities ◽  
Annexin V ◽  
Structural Features ◽  
Signaling Cascades ◽  
Cytochrome C Release ◽  
Wide Range ◽  
Cancer Activity

Intensive efforts have been undertaken in the fields of prevention, diagnosis, and therapy of lung cancer. Fucoidans exhibit a wide range of biological activities, which are dependent on the degree of sulfation, sulfation pattern, glycosidic branches, and molecular weight of fucoidan. The determination of oversulfation of fucoidan and its effect on anti-lung cancer activity and related signaling cascades is challenging. In this investigation, we used a previously developed fucoidan (SCA), which served as a native fucoidan, to generate two oversulfated fucoidan derivatives (SCA-S1 and SCA-S2). SCA, SCA-S1, and SCA-S2 showed differences in compositions and had the characteristic structural features of fucoidan by Fourier transform infrared (FTIR) and nuclear magnetic resonance (NMR) analyses. The anticancer properties of SCA, SCA-S1, and SCA-S2 against human lung carcinoma A-549 cells were analyzed in terms of cytotoxicity, cell cycle, Bcl-2 expression, mitochondrial membrane potential (MMP), expression of caspase-3, cytochrome c release, Annexin V/propidium iodide (PI) staining, DNA fragmentation, and the underlying signaling cascades. Our findings indicate that the oversulfation of fucoidan promotes apoptosis of lung cancer cells and the mechanism may involve the Akt/mTOR/S6 pathway. Further in vivo research is needed to establish the precise mechanism whereby oversulfated fucoidan mitigates the progression of lung cancer.

scholarly journals Inhibition of Non-Small Cell Lung Cancer Proliferation and Survival by Rosemary Extract Is Associated with Activation of ERK and AMPK

Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 52
Author(s):  
Eric J. O’Neill ◽  
Jessy Moore ◽  
Joon Song ◽  
Evangelia Litsa Tsiani
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Underlying Mechanism ◽  
Small Cell ◽  
Rosemary Extract ◽  
Small Cell Lung ◽  
H1299 Cell

Non-small cell lung cancer (NSCLC) represents an aggressive form of lung cancer which often develops resistance to chemo- and radiotherapy emphasizing a need to identify novel treatment agents to combat it. Many plants contain compounds with anti-inflammatory, antimicrobial, antidiabetic, and anticancer properties and some plant-derived chemicals are used in the treatment of cancer. A limited number of in vitro and in vivo animal studies provide evidence of anticancer effects of rosemary (Rosmarinus officinalis) extract (RE); however, no studies have explored its role in H1299 NSCLC cells, and its underlying mechanism(s) of action are not understood. The current study examined the effects of RE on H1299 cell proliferation, survival, and migration using specific assays. Additionally, immunoblotting was used to investigate the effects of RE treatment on signalling molecules implicated in cell growth and survival. Treatment with RE dose-dependently inhibited H1299 proliferation with an IC50 value of 19 µg/mL. Similarly, RE dose-dependently reduced cell survival, and this reduction correlated with increased levels of cleaved poly (ADP-ribose) polymerase (PARP), a marker of apoptosis. RE was also able to inhibit cell migration as assessed with a wound healing assay. These cellular effects of RE were associated with an increase in phosphorylated levels of extracellular signal-regulated kinase (ERK), AMP-activated protein kinase (AMPK), and its downstream targets ACC, the mTORC1 protein raptor, and decreased p70S6K phosphorylation. More studies are required to fully examine the effects of RE against NSCLC.

scholarly journals E3 Ubiquitin Ligase HRD1 Promotes Lung Tumorigenesis by Promoting Sirtuin 2 Ubiquitination and Degradation

2020 ◽  
Vol 40 (7) ◽  
Author(s):  
Liu Liu ◽  
Le Yu ◽  
Cheng Zeng ◽  
Hua Long ◽  
Guangjie Duan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Ubiquitin Ligase ◽  
Cell Cycle Progression ◽  
E3 Ubiquitin Ligase ◽  
Underlying Mechanism ◽  
Tumor Formation ◽  
Human Lung Cancer ◽  
Lung Tumorigenesis

ABSTRACT The NAD-dependent histone deacetylase sirtuin 2 (SIRT2) plays critical roles in mitosis and cell cycle progression and recently was shown to suppress tumor growth and to be downregulated in several types of cancers. However, the underlying mechanism of SIRT2 downregulation remains unknown. In this study, using bioinformatics, gene expression profiling, protein overexpression approaches, and cell migration assays, we showed that E3 ubiquitin ligase 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase degradation 1 (HRD1) interacts with SIRT2 and promotes its ubiquitination and degradation. Furthermore, we found that HRD1 deficiency induces SIRT2 upregulation and inhibits the growth and tumor formation of lung cancer cells both in vitro and in vivo. Of note, we observed that SIRT2 expression is downregulated in human lung cancer and also negatively correlates with HRD1 expression in these cancers. Additionally, we found that patients with lung adenocarcinoma having lower HRD1 or higher SIRT2 expression levels tend to survive longer. On the basis of these results, we propose a mechanism of lung tumorigenesis that involves HRD1-mediated downregulation of SIRT2 and suggest that interventions targeting HRD1 activity could be a potential therapeutic strategy to treat patients with lung cancer.

scholarly journals In Vitro and In Vivo Studies of Anti-Lung Cancer Activity of Artemesia judaica L. Crude Extract Combined with LC-MS/MS Metabolic Profiling, Docking Simulation and HPLC-DAD Quantification

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 17
Author(s):  
Marwa S. Goda ◽  
Mohamed S. Nafie ◽  
Basma M. Awad ◽  
Maged S. Abdel-Kader ◽  
Amany K. Ibrahim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Liquid Chromatography ◽  
Cytotoxic Activity ◽  
Active Sites ◽  
Array Detector ◽  
Cytotoxic Activities ◽  
Promising Source ◽  
Cancer Activity

Artemisia judaica L. (Family: Asteraceae) exhibited antioxidant, anti-inflammatory, and antiapoptotic effects. The in vitro cytotoxic activity of A. judaica ethanolic extract was screened against a panel of cancer cell lines. The results revealed its cytotoxic activity against a lung cancer (A549) cell line with a promising IC50 of 14.2 μg/mL compared to doxorubicin as a standard. This was confirmed through the downregulation of antiapoptotic genes, the upregulation of proapoptotic genes, and the cell cycle arrest at the G2/M phase. Further in vivo study showed that a solid tumor mass was significantly reduced, with a tumor inhibition ratio of 54% relative to doxorubicin therapy in a Xenograft model. From a chemical point of view, various classes of natural products have been identified by liquid chromatography combined with tandem mass spectrometry (LC-MS/MS). The docking study of the detected metabolites approved their cytotoxic activity through their virtual binding affinity towards the cyclin-dependent kinase 2 (CDK-2) and epidermal growth factor receptor (EGFR) active sites. Finally, A. judaica is a fruitful source of polyphenols that are well-known for their antioxidant and cytotoxic activities. As such, the previously reported polyphenols with anti-lung cancer activity were quantified by high-performance liquid chromatography coupled with a diode array detector (HPLC-DAD). Rutin, quercetin, kaempferol, and apigenin were detected at concentrations of 6 mg/gm, 0.4 mg/gm, 0.36 mg/gm, and 3.9 mg/gm of plant dry extract, respectively. It is worth noting that kaempferol and rutin are reported for the first time. Herein, A. judaica L. may serve as an adjuvant therapy or a promising source of leading structures in drug discovery for lung cancer treatment.

scholarly journals USP9X-mediated KDM4C deubiquitination promotes lung cancer radioresistance by epigenetically inducing TGF-β2 transcription

2021 ◽  
Author(s):  
Xiaohua Jie ◽  
William Pat Fong ◽  
Rui Zhou ◽  
Ye Zhao ◽  
Yingchao Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Affinity Purification ◽  
Smad Signaling ◽  
Lung Cancer Patients ◽  
Lysine Specific Demethylase ◽  
Underlying Mechanisms ◽  
H3k9me3 Level ◽  
Critical Binding

AbstractRadioresistance is regarded as the main barrier to effective radiotherapy in lung cancer. However, the underlying mechanisms of radioresistance remain elusive. Here, we show that lysine-specific demethylase 4C (KDM4C) is overexpressed and correlated with poor prognosis in lung cancer patients. We provide evidence that genetical or pharmacological inhibition of KDM4C impairs tumorigenesis and radioresistance in lung cancer in vitro and in vivo. Moreover, we uncover that KDM4C upregulates TGF-β2 expression by directly reducing H3K9me3 level at the TGF-β2 promoter and then activates Smad/ATM/Chk2 signaling to confer radioresistance in lung cancer. Using tandem affinity purification technology, we further identify deubiquitinase USP9X as a critical binding partner that deubiquitinates and stabilizes KDM4C. More importantly, depletion of USP9X impairs TGF-β2/Smad signaling and radioresistance by destabilizing KDM4C in lung cancer cells. Thus, our findings demonstrate that USP9X-mediated KDM4C deubiquitination activates TGF-β2/Smad signaling to promote radioresistance, suggesting that targeting KDM4C may be a promising radiosensitization strategy in the treatment of lung cancer.

scholarly journals GCH1 induces immunosuppression through metabolic reprogramming and IDO1 upregulation in triple-negative breast cancer

2021 ◽  
Vol 9 (7) ◽  
pp. e002383
Author(s):  
Jin-Li Wei ◽  
Si-Yu Wu ◽  
Yun-Song Yang ◽  
Yi Xiao ◽  
Xi Jin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Molecular Taxonomy ◽  
Underlying Mechanism ◽  
Metabolic Reprogramming ◽  
Sequencing Data ◽  
Aryl Hydrocarbon

PurposeRegulatory T cells (Tregs) heavily infiltrate triple-negative breast cancer (TNBC), and their accumulation is affected by the metabolic reprogramming in cancer cells. In the present study, we sought to identify cancer cell-intrinsic metabolic modulators correlating with Tregs infiltration in TNBC.Experimental designUsing the RNA-sequencing data from our institute (n=360) and the Molecular Taxonomy of Breast Cancer International Consortium TNBC cohort (n=320), we calculated the abundance of Tregs in each sample and evaluated the correlation between gene expression levels and Tregs infiltration. Then, in vivo and in vitro experiments were performed to verify the correlation and explore the underlying mechanism.ResultsWe revealed that GTP cyclohydrolase 1 (GCH1) expression was positively correlated with Tregs infiltration and high GCH1 expression was associated with reduced overall survival in TNBC. In vivo and in vitro experiments showed that GCH1 increased Tregs infiltration, decreased apoptosis, and elevated the programmed cell death-1 (PD-1)-positive fraction. Metabolomics analysis indicated that GCH1 overexpression reprogrammed tryptophan metabolism, resulting in L-5-hydroxytryptophan (5-HTP) accumulation in the cytoplasm accompanied by kynurenine accumulation and tryptophan reduction in the supernatant. Subsequently, aryl hydrocarbon receptor, activated by 5-HTP, bound to the promoter of indoleamine 2,3-dioxygenase 1 (IDO1) and thus enhanced the transcription of IDO1. Furthermore, the inhibition of GCH1 by 2,4-diamino-6-hydroxypyrimidine (DAHP) decreased IDO1 expression, attenuated tumor growth, and enhanced the tumor response to PD-1 blockade immunotherapy.ConclusionsTumor-cell-intrinsic GCH1 induced immunosuppression through metabolic reprogramming and IDO1 upregulation in TNBC. Inhibition of GCH1 by DAHP serves as a potential immunometabolic strategy in TNBC.

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