scholarly journals Proapoptotic Index Evaluation of Two Synthetic Peptides Derived from the Coneshell Californiconus californicus in Lung Cancer Cell Line H1299

Marine Drugs ◽  
2019 ◽  
Vol 18 (1) ◽  
pp. 10
Author(s):  
Irasema Oroz-Parra ◽  
Carolina Álvarez-Delgado ◽  
Karla Cervantes-Luevano ◽  
Salvador Dueñas-Espinoza ◽  
Alexei F. Licea-Navarro
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Synthetic Peptides ◽  
Cytotoxic Effect ◽  
Defense Mechanism ◽  
Tumor Development ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells

Lung cancer is one of the most common types of cancer, accounting for approximately 15% of all cancer cases worldwide. Apoptosis is the dominant defense mechanism against tumor development. The balance between pro- and antiapoptotic members of the Bcl-2 protein family can determine cellular fate. The venom of predatory marine snails Conus is estimated to have 100–400 toxins called conotoxins. The family of α-conotoxins is known to consist of selective antagonists of nicotinic acetylcholine receptors (nAChRs). Lung cancer cells overexpress several subunits of nAChRs and are considered as an excellent target for new anticancer drugs. We compared the cytotoxic effect of two synthetic peptides derived from Californiconus californicus, Cal14.1a, and Cal14.1b, which only differ by one amino acid in their sequence, and compared their proapoptotic balance by Bax and Bcl-2 mRNA expression. We determined the caspase-3 and -7 activation to demonstrate apoptosis induction. Results showed that Cal14.1a induces a high Bax/Bcl-2 ratio in H1299 (lung cancer cells). Although Cal14.1b has a cytotoxic effect on H1299 cells, reducing cell viability by 30%, it does not increase the Bax/Bcl-2 ratio, which could be explained by the Glu in the 15th residue, which is crucial for the ability of Cal14.1a to induce apoptosis.

scholarly journals Sestrin2 Expression Has Regulatory Properties and Prognostic Value in Lung Cancer

2020 ◽  
Vol 10 (3) ◽  
pp. 109 ◽  
Author(s):  
Hee Sung Chae ◽  
Minchan Gil ◽  
Subbroto Kumar Saha ◽  
Hee Jeung Kwak ◽  
Hwan-Woo Park ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Prognostic Value ◽  
Mammalian Target Of Rapamycin ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Normal Lung ◽  
Therapeutic Modalities

Lung cancer remains the most dangerous type of cancer despite recent progress in therapeutic modalities. Development of prognostic markers and therapeutic targets is necessary to enhance lung cancer patient survival. Sestrin family genes (Sestrin1, Sestrin2, and Sestrin3) are involved in protecting cells from stress. In particular, Sestrin2, which mainly protects cells from oxidative stress and acts as a leucine sensor protein in mammalian target of rapamycin (mTOR) signaling, is thought to affect various cancers in different ways. To investigate the role of Sestrin2 expression in lung cancer cells, we knocked down Sestrin2 in A549, a non-small cell lung cancer cell line; this resulted in reduced cell proliferation, migration, sphere formation, and drug resistance, suggesting that Sestrin2 is closely related to lung cancer progression. We analyzed Sestrin2 expression in human tissue using various bioinformatic databases and confirmed higher expression of Sestrin2 in lung cancer cells than in normal lung cells using Oncomine and the Human Protein Atlas. Moreover, analyses using Prognoscan and KMplotter showed that Sestrin2 expression is negatively correlated with the survival of lung cancer patients in multiple datasets. Co-expressed gene analysis revealed Sestrin2-regulated genes and possible associated pathways. Overall, these data suggest that Sestrin2 expression has prognostic value and that it is a possible therapeutic target in lung cancer.

scholarly journals Human Lung Cancer Cell Line A-549 ATCC Is Differentially Affected by Supranutritional Organic and Inorganic Selenium

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Lérida Liss Flores Villavicencio ◽  
Gustavo Cruz-Jiménez ◽  
Gloria Barbosa-Sabanero ◽  
Carlos Kornhauser-Araujo ◽  
M. Eugenia Mendoza-Garrido ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Nuclear Fragmentation ◽  
Inorganic Selenium

The effects of organic and inorganic forms of selenium (Se) on human cells have been extensively studied for nutritional concentrations; however, to date, little is known about the potential toxicity at supranutritional levels. In the present study we determined the effects of sodium selenite (SSe) and selenomethionine (SeMet) on cell growth and intracellular structures in lung cancer cells exposed at Se concentrations between 0 and 3 mM. Our results showed that SSe affected cell growth more rapidly than SeMet (24 h and 48 h, resp.). After 24 h of cells exposure to 0.5, 1.5, and 3 mM SSe, cell growth was reduced by 10, 50, and 60%, as compared to controls. After 48 h, nuclear fragmentation was evident in cells exposed to SSe, suggesting an induction to cell death. In contrast, SeMet did not affect cell proliferation, and the cells were phenotypically similar to controls. Microtubules and microfilaments structures were also affected by both Se compounds, again SSe being more toxic than SeMet. To our knowledge, this is the first report on the differential effects of organic and inorganic Se in supranutritional levels in lung cancer cells.

scholarly journals Radix Glehniae extract inhibits migration and invasion of lung cancer cells

2018 ◽  
Vol 6 (2) ◽  
pp. 48-53 ◽  
Author(s):  
Wang Zhen-fei ◽  
Liu Li ◽  
Liang Lin ◽  
Hao Qin
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Lung Cancer Cell

Abstract Objective The aim of this study was to investigate the effect of Radix Glehniae on the migration and invasion abilities of lung cancer cells. Methods Normal bronchial cell line 16HBE and lung cancer cell line SK-MES-1 were treated with Radix Glehniae extract. Proliferation, migration, and invasion abilities were determined by Cell Counting Kit (CCK)-8, Transwell, and Matrigel assays, respectively. The expression and secretion levels of tissue inhibitor of metalloproteinases 2 were detected by quantitative PCR and enzyme-linked immunosorbent assay, respectively. Results Radix Glehniae extract inhibited the migration and invasion abilities of SK-MES-1 cells and enhanced TIMP2 expression and secretion by SK-MES-1 cells, without causing toxicity to 16HBE cells. Conclusion Radix Glehniae is useful in lung cancer treatment.

scholarly journals c-Jun N-Terminal Kinase Contributes to Aberrant Retinoid Signaling in Lung Cancer Cells by Phosphorylating and Inducing Proteasomal Degradation of Retinoic Acid Receptor α

2005 ◽  
Vol 25 (3) ◽  
pp. 1054-1069 ◽  
Author(s):  
Harish Srinivas ◽  
Denise M. Juroske ◽  
Shailaja Kalyankrishna ◽  
Dianna D. Cody ◽  
Roger E. Price ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Retinoic Acid Receptor ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Retinoid Signaling ◽  
Phosphopeptide Mapping

ABSTRACT Retinoic acid (RA) is the ligand for nuclear RA receptors (RARs and RXRs) and is crucial for normal epithelial cell growth and differentiation. During malignant transformation, human bronchial epithelial cells acquire a block in retinoid signaling caused in part by a transcriptional defect in RARs. Here, we show that activation of c-Jun N-terminal kinase (JNK) contributes to RAR dysfunction by phosphorylating RARα and inducing degradation through the ubiquitin-proteasomal pathway. Analysis of RARα mutants and phosphopeptide mapping revealed that RARα residues Thr181, Ser445, and Ser461 are phosphorylated by JNK. Mutation of these residues to alanines prevented efficient ubiquitination of RARα and increased the stability of the protein. We investigated the importance of RARα phosphorylation by JNK as a mediator of retinoid resistance in lung cancer. Mice that develop lung cancer from activation of a latent K-ras oncogene had high intratumoral JNK activity and low RARα levels and were resistant to treatment with an RAR ligand. JNK inhibition in a human lung cancer cell line enhanced RARα levels, ligand-induced activity of RXR-RAR dimers, and growth inhibition by RA. These findings point to JNK as a key mediator of aberrant retinoid signaling in lung cancer cells.

Inhibition of mTOR enhances radiosensitivity of lung cancer cells and protects normal lung cells against radiation

2016 ◽  
Vol 94 (3) ◽  
pp. 213-220 ◽  
Author(s):  
Hang Zheng ◽  
Miao Wang ◽  
Jing Wu ◽  
Zhi-Ming Wang ◽  
Hai-Jun Nan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Radiation Therapy ◽  
Cancer Cells ◽  
Cell Line ◽  
Mammalian Target Of Rapamycin ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Normal Lung ◽  
Irradiation Therapy

Radiotherapy has been used for a long time as a standard therapy for cancer; however, there have been no recent research breakthroughs. Radioresistance and various side-effects lead to the unexpected outcomes of radiation therapy. Specific and accurate targeting as well as reduction of radioresistance have been major challenges for irradiation therapy. Recent studies have shown that rapamycin shows promise for inhibiting tumorigenesis by suppressing mammalian target of rapamycin (mTOR). We found that the combination of rapamycin with irradiation significantly diminished cell viability and colony formation, and increased cell apoptosis, as compared with irradiation alone in lung cancer cell line A549, suggesting that rapamycin can enhance the effectiveness of radiation therapy by sensitizing cancer cells to irradiation. Importantly, we observed that the adverse effects of irradiation on a healthy lung cell line (WI-38) were also offset. No enhanced protein expression of mTOR signaling was observed in WI-38 cells, which is normally elevated in lung cancer cells. Moreover, DNA damage was significantly less with the combination therapy than with irradiation therapy alone. Our data suggest that the incorporation of rapamycin during radiation therapy could be a potent way to improve the sensitivity and effectiveness of radiation therapy as well as to protect normal cells from being damaged by irradiation.

The cytotoxic effect of oxymatrine on basic cellular processes of A549 non-small lung cancer cells

2019 ◽  
Vol 121 (6) ◽  
pp. 724-731 ◽  
Author(s):  
Magdalena Izdebska ◽  
Wioletta Zielińska ◽  
Marta Hałas-Wiśniewska ◽  
Klaudia Mikołajczyk ◽  
Alina Grzanka
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cytotoxic Effect ◽  
Lung Cancer Cells ◽  
Cellular Processes

scholarly journals Knockdown of IKKβ Inhibits Tumor Development in a Leptomeningeal Metastasis Mouse Model and Proliferation of Lung Cancer Cells

2020 ◽  
Vol Volume 12 ◽  
pp. 6007-6017
Author(s):  
Yakun Liu ◽  
Yuanyuan Li ◽  
Zhongyao Li ◽  
Chunyan Li ◽  
Junying He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Tumor Development ◽  
Leptomeningeal Metastasis ◽  
Lung Cancer Cells

The Rhizome of Trillium tschonoskii Maxim. Extract Induces Apoptosis in Human Lung Cancer Cells

2011 ◽  
Vol 66 (9-10) ◽  
pp. 477-484 ◽  
Author(s):  
Wenfeng Huang ◽  
Kun Zou ◽  
Bin Xiong
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Butanol Extract ◽  
Human Lung Cancer Cells ◽  
Trillium Tschonoskii

Trillium tschonoskii Maxim. has been used to treat several diseases including cancers in folk medicine. However, the mechanisms responsible for T. tschonoskii extract-induced apoptosis are not clear. This study was mainly undertaken to identify the major biochemical changes in a lung cancer cell line upon treatment with an T. tschonoskii extract (TTME), and to investigate the functional relationship between these changes. The n-butanol extract was used to evaluate the mechanism of induction of apoptosis in A549 human lung cancer cells and its effects on mitochondrial function and production of reactive oxygen species (ROS). The n-butanol extract of T. tschonoskii has cytotoxic, antiproliferative, and morphological effects on the lung cancer cell line. T. tschonoskii mainly leads to apoptosis of cancer cells with a concomitant increase in the release of cytochrome c and a loss of mitochondrial membrane potential in a dose-dependent manner. A rapid increase in the level of intracellular ROS and an accumulation of cells in the G2/M and S phase of the cell cycle were also observed in treated cells. These observations suggest that the n-butanol extract of T. tschonoskii has promising anticancer activities, which could be useful in cancer treatment.

scholarly journals CCL5 production in lung cancer cells leads to an altered immune microenvironment and promotes tumor development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Etienne S. Melese ◽  
Elizabeth Franks ◽  
Rachel A. Cederberg ◽  
Bryant T. Harbourne ◽  
Rocky Shi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Development ◽  
Lung Cancer Cells ◽  
Immune Microenvironment
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