scholarly journals Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

2010 ◽  
Vol 9 (3) ◽  
pp. 569-580 ◽  
Author(s):  
Som D. Sharma ◽  
Syed M. Meeran ◽  
Santosh K. Katiyar
2009 ◽  
Vol 8 (8) ◽  
pp. 2221-2231 ◽  
Author(s):  
M. Cecilia Crisanti ◽  
Africa F. Wallace ◽  
Veena Kapoor ◽  
Fabian Vandermeers ◽  
Melissa L. Dowling ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148404 ◽  
Author(s):  
Suzanne L. Meredith ◽  
Jennifer L. Bryant ◽  
Muhammad Babur ◽  
Philip W. Riddell ◽  
Roya Behrouzi ◽  
...  

2021 ◽  
Vol 20 ◽  
pp. 153303382199004
Author(s):  
Wei Zhang ◽  
Chao Song ◽  
Xiaona Ren

Background: Drug resistance in cancer cells is a major challenge for anti-cancer therapy. Circular RNA (circRNA) circ_0003998 has been identified as an important regulator in the chemoresistance development of non-small cell lung cancer (NSCLC). The purpose of this study was to investigate the molecular basis underlying the resistance control of circ_0003998 in NSCLC. Methods: The levels of circ_0003998, miR-136-5p and coronin 1C (CORO1C) were gauged by the quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell viability, colony formation and apoptosis were evaluated by the Cell Counting Kit-8 (CCK-8), colony formation and flow cytometry assays, respectively. Targeted relationships among circ_0003998, miR-136-5p and CORO1C were confirmed by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Animal studies were performed to evaluate the function of circ_0003998 in vivo. Results: Our data indicated that circ_0003998 expression was associated with NSCLC resistance to docetaxel (DTX). The knockdown of circ_0003998 promoted DTX sensitivity, suppressed cell colony formation, and enhanced cell apoptosis of A549/DTX and H1299/DTX cells in vitro. Moreover, circ_0003998 knockdown hampered tumor growth and enhanced DTX sensitivity in vivo. Mechanistically, circ_0003998 directly targeted miR-136-5p, and miR-136-5p was a molecular mediator of circ_0003998 function in vitro. Furthermore, CORO1C was a functionally important target of miR-136-5p in regulating DTX-resistant NSCLC cell colony formation, apoptosis and DTX sensitivity in vitro. Additionally, circ_0003998 modulated CORO1C expression by working as a miR-136-5p sponge. Conclusion: Our present work identified that circ_0003998 regulated DTX-resistant NSCLC cell colony formation, apoptosis and DTX sensitivity at least partially by controlling CORO1C expression by sponging miR-136-5p, illuminating a rationale for developing circ_0003998 as a therapeutic target of chemoresistant NSCLC.


2015 ◽  
Vol 356 (2) ◽  
pp. 985-993 ◽  
Author(s):  
Mao-Bin Meng ◽  
Huan-Huan Wang ◽  
Wen-Hao Guo ◽  
Zhi-Qiang Wu ◽  
Xian-Liang Zeng ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Lei Song ◽  
Liping Peng ◽  
Shucheng Hua ◽  
Xiaoping Li ◽  
Lianjun Ma ◽  
...  

MicroRNAs (miRNAs or miRs) regulate gene expression at the posttranscriptional level and are involved in many biological processes such as cell proliferation and migration, stem cell differentiation, inflammation, and apoptosis. In particular, miR-144-3p is downregulated in various cancers, and its overexpression inhibits the proliferation and metastasis of cancer cells. However, the role of miR-144-5p in non-small-cell lung cancer (NSCLC), especially radiosensitivity, is unknown. In this study, we found that miR-144-5p was downregulated in NSCLC clinical specimens as well as NSCLC cell lines exposed to radiation. Enhanced expression of miR-144-5p promoted the radiosensitivity of NSCLC cells in vitro and A549 cell mouse xenografts in vivo. Furthermore, we identified activating transcription factor 2 (ATF2) as the direct and functional target of miR-144-5p using integrated bioinformatics analysis and a luciferase reporter assay. In addition, restoration of ATF2 expression inhibited miR-144-5p-induced NSCLC cell sensitivity to radiation in vitro and in vivo. Our findings suggest that deregulation of the miR-144-5p/ATF2 axis plays an important role in NSCLC cell radiosensitivity, thus representing a new potential therapeutic target for NSCLC.


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