Phenolic compound ellagic acid inhibits mitochondrial respiration and tumor growth in lung cancer

2020 ◽  
Vol 11 (7) ◽  
pp. 6332-6339 ◽  
Author(s):  
Jing Duan ◽  
Yuxiang Li ◽  
Huihan Gao ◽  
Donghui Yang ◽  
Xuan He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Tumor Growth ◽  
Phenolic Compound ◽  
Mitochondrial Respiration ◽  
Ellagic Acid ◽  
Fruits And Vegetables ◽  
Inhibit Tumor Growth ◽  
Polyphenol Compound ◽  
Natural Polyphenol

Ellagic acid (EA), a natural polyphenol compound that exists in a variety of fruits and vegetables, has been reported to inhibit tumor growth by reducing cell growth, inducing apoptosis, and damaging mitochondria.

scholarly journals Cinobufagin Suppresses Melanoma Cell Growth by Inhibiting LEF1

2020 ◽  
Vol 21 (18) ◽  
pp. 6706
Author(s):  
Geon-Hee Kim ◽  
Xue-Quan Fang ◽  
Woo-Jin Lim ◽  
Jooho Park ◽  
Tae-Bong Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Melanoma Cell ◽  
Transcriptional Activity ◽  
Melanoma Cells ◽  
Lung Cancer Cells ◽  
Luciferase Assay ◽  
Dependent Manner

Constitutive activation of the β-catenin dependent canonical Wnt signaling pathway, which enhances tumor growth and progression in multiple types of cancer, is commonly observed in melanoma. LEF1 activates β-catenin/TCF4 transcriptional activity, promoting tumor growth and progression. Although several reports have shown that LEF1 is highly expressed in melanoma, the functional role of LEF1 in melanoma growth is not fully understood. While A375, A2058, and G361 melanoma cells exhibit abnormally high LEF1 expression, lung cancer cells express lower LEF1 levels. A luciferase assay-based high throughput screening (HTS) with a natural compound library showed that cinobufagin suppressed β-catenin/TCF4 transcriptional activity by inhibiting LEF1 expression. Cinobufagin decreases LEF1 expression in a dose-dependent manner and Wnt/β-catenin target genes such as Axin-2, cyclin D1, and c-Myc in melanoma cell lines. Cinobufagin sensitively attenuates cell viability and induces apoptosis in LEF1 expressing melanoma cells compared to LEF1-low expressing lung cancer cells. In addition, ectopic LEF1 expression is sufficient to attenuate cinobufagin-induced apoptosis and cell growth retardation in melanoma cells. Thus, we suggest that cinobufagin is a potential anti-melanoma drug that suppresses tumor-promoting Wnt/β-catenin signaling via LEF1 inhibition.

scholarly journals Targeted delivery of let-7a microRNA encapsulated ephrin-A1 conjugated liposomal nanoparticles inhibit tumor growth in lung cancer

2013 ◽  
pp. 4481 ◽  
Author(s):  
Najmunnisa Nasreen ◽  
Hung-yen Lee ◽  
Kamal Mohammed ◽  
Frederic Kaye ◽  
Parvesh Sharma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Targeted Delivery ◽  
Inhibit Tumor Growth ◽  
Liposomal Nanoparticles

YTH domain family 2 promotes lung cancer cell growth by facilitating 6-phosphogluconate dehydrogenase mRNA translation

2019 ◽  
Vol 41 (5) ◽  
pp. 541-550 ◽  
Author(s):  
Hao Sheng ◽  
Zhen Li ◽  
Shixin Su ◽  
Wenjing Sun ◽  
Xiaoya Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Mrna Translation ◽  
Lung Cancer Cell ◽  
Domain Family ◽  
Cancer Cell Growth ◽  
Phosphogluconate Dehydrogenase ◽  
Yth Domain

Abstract N6-methyladenosine (m6A) is one of widespread post-transcriptional mRNA modifications in eukaryotes and the m6A modification plays critical roles in various human cancers. However, the role of m6A-binding proteins in cancer metabolism remains elusive. Here, we report that YTH domain family 2 (YTHDF2) is upregulated in lung cancer tissues, promotes lung cancer cell growth and enhances the pentose phosphate pathway (PPP) flux, which is crucial for tumor growth. Mechanistically, YTHDF2 directly binds to the m6A modification site of 6-phosphogluconate dehydrogenase (6PGD) three prime untranslated region (3′-UTR) to promote 6PGD mRNA translation in lung cancer cells. Collectively, our data indicate that YTHDF2 acts as a tumor promoter to enhance tumor growth via facilitating 6PGD mRNA translation.

scholarly journals The Influence Dose of Nicotine Exposure on H520 Smoking-related Non-Small-Cell Lung Carcinoma Cell Growth and Toxicity

2020 ◽  
Author(s):  
Jia-Ping Wu ◽  
Ching-Yi Peng
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Tumor Growth ◽  
Western Blotting ◽  
Mtt Assay ◽  
Dna Cleavage ◽  
Cancer Biology ◽  
Lung Epithelial Cells ◽  
Nicotine Exposure ◽  
Cell Lung Carcinoma

Nicotine exposure may affect NSCLC is associated with lung cancer in humans. Whether nicotine exhibits carcinogenesis promoted activities in tumor growth still unknown. Nicotine is known to have dichotomous effects on cancer biology, acting like a pro- or anti-carcinogenesis agent. There are different functions between adenocarcinoma and squamous NSCLC cancer cells. Excess generation of nicotine may inhibit mitochondrial metabolism, protein modification, and DNA cleavage. Materials and Methods: We used the H520 NSCLC line obtained from human lung epithelial cells to detected nicotine growth and toxicity using MTT assay and western blotting. The concentration of nicotine stimulated cell growth to correspond to low concentration, while high concentration was cytotoxic. Results: According to MTT assay results, at 1.0 μM nicotine has significantly enhanced the H520 cell viability (%). Nicotine induced lung cancer carcinogenesis through mechanisms of α7nAchR, EGFR, HDAC2/4/5, Cyclin D/Cyclin E, Bcl-2, p-Akt, and inflammatory proteins of NF-KappaB and COX2 increases at 1.0 μM. Apoptosis proteins were decreases at 1.0 μM nicotine by p21, p27, c-jun, and p38α using western blotting. Nicotine stimulates tumor growth is mediated through α7nicotinic-acetylcholine receptors (α7nAChR), possibly involving inflammation. On the other hand, at high nicotine concentrations (> 1.0 μM) with consistent cytotoxic effects and appeared to be due to direct cell kill. Nicotine can prevent apoptosis induced by NSCLC. Conclusion: Therefore, the effects on chemotherapeutics by NSCLC malignant cell lines, nicotine in concentrations as low as 1.0 μM decreased. These mechanisms are responsible for the genotoxic effects caused by nicotine. This leads to downstream effects on decreased apoptosis, increased cell proliferation and transformation. The malignant NSCLC cells respond to the treatment with nicotine in lung cancer, the nicotine-mediated induction of growth may provide one of its links to α7nAchR or EGFR.

scholarly journals Coated cationic lipid-nanoparticles entrapping miR-660 inhibit tumor growth in patient-derived xenografts lung cancer models

2019 ◽  
Vol 308 ◽  
pp. 44-56 ◽  
Author(s):  
Massimo Moro ◽  
Daniela Di Paolo ◽  
Massimo Milione ◽  
Giovanni Centonze ◽  
Viviana Bornaghi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cationic Lipid ◽  
Lipid Nanoparticles ◽  
Inhibit Tumor Growth ◽  
Cancer Models

scholarly journals Dasatinib Inhibits Lung Cancer Cell Growth and Patient Derived Tumor Growth in Mice by Targeting LIMK1

2020 ◽  
Vol 8 ◽  
Author(s):  
Man Zhang ◽  
Jie Tian ◽  
Rui Wang ◽  
Mengqiu Song ◽  
Ran Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

Lung cancer is a leading cause cancer-related death with diversity. A promising approach to meet the need for improved cancer treatment is drug repurposing. Dasatinib, a second generation of tyrosine kinase inhibitors (TKIs), is a potent treatment agent for chronic myeloid leukemia (CML) approved by FDA, however, its off-targets and the underlying mechanisms in lung cancer have not been elucidated yet. LIM kinase 1 (LIMK1) is a serine/threonine kinase, which is highly upregulated in human cancers. Herein, we demonstrated that dasatinib dose-dependently blocked lung cancer cell proliferation and repressed LIMK1 activities by directly targeting LIMK1. It was confirmed that knockdown of LIMK1 expression suppressed lung cancer cell proliferation. From the in silico screening results, dasatinib may target to LIMK1. Indeed, dasatinib significantly inhibited the LIMK1 activity as evidenced by kinase and binding assay, and computational docking model analysis. Dasatinib inhibited lung cancer cell growth, while induced cell apoptosis as well as cell cycle arrest at the G1 phase. Meanwhile, dasatinib also suppressed the expression of markers relating cell cycle, cyclin D1, D3, and CDK2, and increased the levels of markers involved in cell apoptosis, cleaved caspase-3 and caspase-7 by downregulating phosphorylated LIMK1 (p-LIMK1) and cofilin (p-cofilin). Furthermore, in patient-derived xenografts (PDXs), dasatinib (30 mg/kg) significantly inhibited the growth of tumors in SCID mice which highly expressed LIMK1 without changing the bodyweight. In summary, our results indicate that dasatinib acts as a novel LIMK1 inhibitor to suppress the lung cancer cell proliferation in vitro and tumor growth in vivo, which suggests evidence for the application of dasatinib in lung cancer therapy.

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