Investigation on Potential Correlation Between the RNA-Binding Protein of Evolutionarily Conserved MEX3 Family and Non–Small-Cell Lung Cancer

Ming Zhang ◽  
Hualiang Zhang ◽  
Linfeng Cao ◽  
Gouxin Hou ◽  
Chao Lu ◽  

Abstract Background As mRNA binding proteins, MEX3 (muscle excess 3) family highlights its unique characteristics and plays an emerging role in post-transcriptionally regulating programmed of biological processes, including tumor cell death and immunological relevance. These have been shown to be involved in various diseases, however, the role of MEX3 in non-small-cell lung cancer (NSCLC) has not been fully elucidated. Results In this study, we found that the sequence or copy number of MEX3 gene did not change significantly, which can explain the stability of malignant tumor development through the COSMIC database. Further, gene expression in NSCLC was examined using the Oncomine™ database, and the prognostic value of each gene was analyzed by Kaplan-Meier analysis. The results showed that overexpressed of MEX3A, MEX3B, MEX3C and MEX3D were associated with significantly lower OS in patients with NSCLC and LUAD, while overexpressed of MEX3D was associated with significantly poorer OS in patients with LUSC. We also applied the Tumor Immune Estimation Resource (TIMER) tool to assess the correlations between distinct MEX3 and the infiltrating immune cell landscape. Conclusion On this subject, we have learned about the complexity and heterogeneity of NSCLC through MEX3. We found that most of MEX3 is highly expressed in NSCLC. High expression indicates a poor prognosis and has a certain immune correlation. Therefore, these conclusions can lay a framework for the prognosis of NSCLC patients and the development of treatment strategies in the future.

2018 ◽  
Vol 98 (12) ◽  
pp. 1562-1574 ◽  
Elena Martínez-Terroba ◽  
Teresa Ezponda ◽  
Cristina Bértolo ◽  
Cristina Sainz ◽  
Ana Remírez ◽  

Lung Cancer ◽  
2002 ◽  
Vol 36 (1) ◽  
pp. 27-32 ◽  
Fumihiro Tanaka ◽  
Tetsuya Takata ◽  
Tomoko Yamada ◽  
Kazuhiro Yanagihara ◽  
Yosuke Otake ◽  

2019 ◽  
Vol 10 (4) ◽  
pp. 585-586 ◽  
Meng Lu ◽  
Yanjun Su

2020 ◽  
Vol 19 ◽  
pp. 117693512094221
Shahab Bakhtiari ◽  
Sadegh Sulaimany ◽  
Mehrdad Talebi ◽  
Kabmiz Kalhor

Genetic variations such as single nucleotide polymorphisms (SNPs) can cause susceptibility to cancer. Although thousands of genetic variants have been identified to be associated with different cancers, the molecular mechanisms of cancer remain unknown. There is not a particular dataset of relationships between cancer and SNPs, as a bipartite network, for computational analysis and prediction. Link prediction as a computational graph analysis method can help us to gain new insight into the network. In this article, after creating a network between cancer and SNPs using SNPedia and Cancer Research UK databases, we evaluated the computational link prediction methods to foresee new SNP-Cancer relationships. Results show that among the popular scoring methods based on network topology, for relation prediction, the preferential attachment (PA) algorithm is the most robust method according to computational and experimental evidence, and some of its computational predictions are corroborated in recent publications. According to the PA predictions, rs1801394-Non-small cell lung cancer, rs4880-Non-small cell lung cancer, and rs1805794-Colorectal cancer are some of the best probable SNP-Cancer associations that have not yet been mentioned in any published article, and they are the most probable candidates for additional laboratory and validation studies. Also, it is feasible to improve the predicting algorithms to produce new predictions in the future.

2016 ◽  
Vol 21 (8) ◽  
pp. 910-921 ◽  
Leora Horn ◽  
Martin Reck ◽  
David R. Spigel

2009 ◽  
Vol 101 (4) ◽  
pp. 237-247 ◽  
Céline Delloye-Bourgeois ◽  
Elisabeth Brambilla ◽  
Marie-May Coissieux ◽  
Céline Guenebeaud ◽  
Rémy Pedeux ◽  

2013 ◽  
Vol 9 (8) ◽  
pp. 1065-1068
Niki Karachaliou ◽  
Rafael Rosell

2020 ◽  
Vol 80 (22) ◽  
pp. 5051-5062
Kee-Beom Kim ◽  
Youngchul Kim ◽  
Christopher J. Rivard ◽  
Dong-Wook Kim ◽  
Kwon-Sik Park

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Han-Lin Chou ◽  
Yao Fong ◽  
Hsin-Hsien Lin ◽  
Eing Mei Tsai ◽  
Jeff Yi-Fu Chen ◽  

In recent years, combination chemotherapy is a primary strategy for treating lung cancer; however, the issues of antagonism and side effects still limit its applications. The development of chemosensitizer aims to sensitize chemoresistant cancer cells to anticancer drugs and therefore improve the efficacy of chemotherapy. In this study, we examined whether N-[2-(morpholin-4-yl)phenyl]-2-{8-oxatricyclo[,2,7]trideca-1(9),2(7),3,5,10,12-hexaen-4-yloxy}acetamide (NPOA), an acetamide derivative, sensitizes human non-small-cell lung cancer (NSCLC) H1299 cells towards camptothecin- (CPT-) induced apoptosis effects. Our results demonstrate that the combination of CPT and NPOA enhances anti-lung-cancer effect. The cytometer-based Annexin V/propidium iodide (PI) staining showed that CPT and NPOA cotreatment causes an increased population of apoptotic cells compared to CPT treatment alone. Moreover, Western blotting assay showed an enhancement of Bax expression and caspase cascade leading to cell death of H1299 cells. Besides, CPT and NPOA cotreatment-mediated disruption of mitochondrial membrane potential (MMP) in H1299 cells may function through increasing the activation of the stressed-associated c-Jun N-terminal kinase (JNK). These results showed that NPOA treatment sensitizes H1299 cells towards CPT-induced accumulation of cell cycle S phase and mitochondrial-mediated apoptosis through regulating endogenous ROS and JNK activation. Accordingly, NPOA could be a candidate chemosensitizer of CPT derivative agents such as irinotecan or topotecan in the future.

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 690 ◽  
Arik Bernard Schulze ◽  
Georg Evers ◽  
Andrea Kerkhoff ◽  
Michael Mohr ◽  
Christoph Schliemann ◽  

Lung cancer is the leading cause of cancer-related deaths worldwide. With a focus on histology, there are two major subtypes: Non-small cell lung cancer (NSCLC) (the more frequent subtype), and small cell lung cancer (SCLC) (the more aggressive one). Even though SCLC, in general, is a chemosensitive malignancy, relapses following induction therapy are frequent. The standard of care treatment of SCLC consists of platinum-based chemotherapy in combination with etoposide that is subsequently enhanced by PD-L1-inhibiting atezolizumab in the extensive-stage disease, as the addition of immune-checkpoint inhibition yielded improved overall survival. Although there are promising molecular pathways with potential therapeutic impacts, targeted therapies are still not an integral part of routine treatment. Against this background, we evaluated current literature for potential new molecular candidates such as surface markers (e.g., DLL3, TROP-2 or CD56), apoptotic factors (e.g., BCL-2, BET), genetic alterations (e.g., CREBBP, NOTCH or PTEN) or vascular markers (e.g., VEGF, FGFR1 or CD13). Apart from these factors, the application of so-called ‘poly-(ADP)-ribose polymerases’ (PARP) inhibitors can influence tumor repair mechanisms and thus offer new perspectives for future treatment. Another promising therapeutic concept is the inhibition of ‘enhancer of zeste homolog 2’ (EZH2) in the loss of function of tumor suppressors or amplification of (proto-) oncogenes. Considering the poor prognosis of SCLC patients, new molecular pathways require further investigation to augment our therapeutic armamentarium in the future.

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