Self-assembled selenium nanoparticles and their application in the rapid diagnostic detection of small cell lung cancer biomarkers

Soft Matter ◽  
2018 ◽  
Vol 14 (4) ◽  
pp. 481-489 ◽  
Author(s):  
Yilin Zhao ◽  
Qiufeng Sun ◽  
Xi Zhang ◽  
Jan Baeyens ◽  
Haijia Su
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Human Lung ◽  
Cancer Biomarkers ◽  
Small Cell ◽  
Selenium Nanoparticles ◽  
Human Lung Cancer ◽  
Small Cell Lung ◽  
Self Assembled ◽  
Diagnostic Detection

Self-assembled selenium nanoparticles are used for rapid serodiagnosis of human lung cancer.

scholarly journals KLF8 overexpression promotes the growth of human lung cancer cells by promoting the expression of JMJD2A

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Dongjie Ma ◽  
Hongsheng Liu ◽  
Yingzhi Qin ◽  
Zhenhuan Tian ◽  
Shanqing Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Colony Formation ◽  
Human Lung ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Small Cell Lung

Abstract Background Non-small-cell lung cancer (lung cancer) has become one of the leading causes worldwide and the underlying mechanism is not fully understood. The transcriptional factor Kruppel like factor 8 (KLF8) is involved in the initiation, progression, transformation, and metastasis of diverse cancers. However, the roles of KLF8 in human non-small cell lung cancer remain unknown. Methods CCK-8 kit and colony formation assay were performed to determine the cell growth of lung cancer cells. Flow cytometry analysis was used to evaluate apoptosis and cell cycle of lung cancer cells. Luciferase reporter assay was used to examine the activation of JMJD2A promoter by KLF8. Chromatin immunoprecipitation assay was performed to evaluate the binding of KLF8 to JMJD2A promoter. Western blot and polymerase chain reaction were applied to analyze the expression of interested genes. Results The mRNA and protein levels of KLF8 in human non-small cell lung cancer tissues were overexpressed compared with the non-cancer tissues. KLF8 was knocked down with lentivirus-mediated short-hairpin RNA (shRNA) in human lung cancer cells (A549 and H1299 cells). The phenotypic results showed that KLF8 knockdown decreased the proliferation rate and colony formation of lung cancer cells. By contrast, lentivirus-mediated KLF8 overexpression promoted the growth of lung cancer cells (A549 and H1299 cells) and non-cancerous bronchial epithelial cell line BEAS-2B. Next, we showed that KLF8 regulated cell cycle at the G0 phase but not regulates cellular apoptosis of lung cancer cells. KLF8 regulated the expression of the cell cycle regulators P21 and CDK4 in a JMJD2A-dependent manner and JMJD2A knockdown significantly blocked the functions of KLF8 in regulating cell cycle and proliferation of lung cancer cells. Finally, we observed that KLF8 bound the promoter of JMJD2A and facilitated the expression of JMJD2A. Conclusions Our evidence demonstrated that KLF8 upregulation in human lung cancer promotes the cell proliferation and colony formation of lung cancer cells. KLF8 binds to the promoter of JMJD2A and subsequently regulates the expression of P21 and CDK4, which contributes to the regulation of cell cycle by KLF8. KLF8 may serve as a target for the treatment of human lung cancer.

Sulindac enhances adenoviral vector expressing mda-7/IL-24–mediated apoptosis in human lung cancer

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Half Life ◽  
Human Lung ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Small Cell Lung

Several studies have shown antitumor activities of themelanoma differentiation–associated gene 7 (mda-7) andthe nonsteroidal anti-inflammatory drug sulindac whenused as a monotherapies against a wide variety of humancancers. However, the combined effects of mda-7 andsulindac have not previously been tested. Therefore, wetested the antitumor activity of an adenoviral vectorexpressing mda-7 (Ad-mda7) in combination with sulindacagainst non–small cell lung cancer cells in vitro andin vivo. When treated with Ad-mda7 in combination withsulindac, human lung cancer cells (A549 and H1299)underwent growth suppression resulting in apoptosis. Thegrowth inhibition induced by Ad-mda7 in combination withsulindac was significantly greater than that observed withAd-mda7 or sulindac alone. Furthermore, the degree ofgrowth inhibition induced using this combination wasdose-dependent for sulindac. Treatment with Ad-mda7 incombination with sulindac had no growth inhibitoryeffects on human normal lung (CCD-16) fibroblasts. Wethen investigated the mechanism by which sulindacenhances Ad-mda7-mediated apoptosis. Sulindac increasedexpression of ectopic MDA-7 protein in tumorcells, thereby increasing the expression of downstreameffectors RNA-dependent protein kinase, p38MAPK,caspase-9, and caspase-3 and enhancing apoptosis ofnon–small cell lung cancer cells. Pulse-chase experimentsshowed that the increased expression of MDA-7 protein insulindac-treated cells was due to increased half-life of theMDA-7 protein. Finally, treatment of human lung tumorxenografts in nude mice with Ad-mda7 plus sulindacsignificantly suppressed growth (P = 0.001) comparedwith Ad-mda7 or sulindac alone. Our results show for thefirst time that combined treatment with Ad-mda7 plussulindac enhances growth inhibition and apoptosis ofhuman lung cancer cells. The increased antitumor activityobserved with the combination treatment is a result ofincreased half-life of MDA-7 protein. Regulation of proteinturnover is a heretofore-unrecognized mechanism of thisnonsteroidal anti-inflammatory drug. [Mol Cancer Ther2005;4(2):291–304]

scholarly journals Expression of tetraspanins in human lung cancer cells: frequent downregulation of CD9 and its contribution to cell motility in small cell lung cancer

Oncogene ◽  
2003 ◽  
Vol 22 (5) ◽  
pp. 674-687 ◽  
Author(s):  
Toshiki Funakoshi ◽  
Isao Tachibana ◽  
Yoshihiko Hoshida ◽  
Hiromi Kimura ◽  
Yoshito Takeda ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Motility ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Human Lung ◽  
Small Cell ◽  
Human Lung Cancer ◽  
Small Cell Lung ◽  
Human Lung Cancer Cells

scholarly journals MRP is frequently expressed in human lung-cancer cell lines, in non-small-cell lung cancer and in normal lung

1996 ◽  
Vol 66 (6) ◽  
pp. 760-767 ◽  
Author(s):  
Giuseppe Giaccone ◽  
Jannette van Ark-Otte ◽  
Gonzalo J. Rubio ◽  
Adi F. Gazdar ◽  
Henk J. Broxterman ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Lung ◽  
Small Cell ◽  
Human Lung Cancer ◽  
Normal Lung ◽  
Lung Cancer Cell ◽  
Small Cell Lung

Biological functions of long noncoding RNAs and circular RNAs in small-cell lung cancer

Epigenomics ◽  
2020 ◽  
Vol 12 (19) ◽  
pp. 1751-1763
Author(s):  
Sachin Kumar ◽  
Monu Pandey ◽  
Surender K Sharawat
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Noncoding Rnas ◽  
Cancer Biomarkers ◽  
Small Cell ◽  
Long Noncoding Rnas ◽  
Circular Rnas ◽  
Small Cell Lung

We aim to discuss comprehensively the role of long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) in small-cell lung cancer (SCLC) biology and their clinical utility as cancer biomarkers. We searched the scientific literature to select articles related to the role of lncRNAs and circRNAs in SCLC biology or as cancer biomarkers. We identified that a number of lncRNAs and circRNAs can regulate key biological processes involved in SCLC development, including cell proliferation, metastasis and chemoresistance mainly acting as miRNA sponges. Also, the expression of a few lncRNAs and circRNAs predicted survival outcome depicting their utility as prognostic biomarkers. Further investigations on the role of lncRNAs and circRNAs in SCLC tumors may yield novel therapeutic targets for SCLC.

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