ABSTRACT
Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiRNA-488-3p inhibits malignant progression of NSCLC by modulating ADAM9, by Y. Wu, Y. Wu, X.-Y. Chen, Y.-X. Niu, F.-Z. Lv, W. Gao, published in Eur Rev Med Pharmacol Sci 2020; 24 (17): 8893-8901-DOI: 10.26355/eurrev_202009_22830-PMID: 32964979" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/22830.
ABSTRACT
OBJECTIVE: The purpose of this study was to investigate the role of microRNA-488-3p in the proliferation, invasion and migration of lung cancer cells and to further explore the potential regulatory mechanisms. PATIENTS AND METHODS: MicroRNA-488-3p expression in 46 pairs of tumor tissue and paracancerous tissue specimens collected from non-small cell lung cancer (NSCLC) patients were measured through quantitative real-time polymerase chain reaction (qRT-PCR) method, and the interplay between microRNA-488-3p expression and some clinical indicators of these subjects was also analyzed. In addition, microRNA-488-3p overexpression models were constructed in NSCLC cell lines, and then Cell Counting Kit-8 (CCK-8) test and transwell assays were carried out to evaluate the effect of microRNA-488-3p on the NSCLC cell functions. Furthermore, bioinformatics analysis and luciferase reporter gene assay were carried out to uncover the potential interaction between microRNA-488-3p and its downstream gene ADAM9. RESULTS: QPCR results revealed that microRNA-488-3p showed a significant lower expression in NSCLC tissue samples than in adjacent normal ones. In comparison to patients with high expression of microRNA-488-3, patients with low expression of microRNA-488-3 exhibited higher incidence of lymph node or distant metastasis and lower survival rate. In vitro cell experiments showed that, in comparison to control group, overexpression of microRNA-488-3p significantly weakened the proliferation ability as well as the invasion and migration of NSCLC cells. Subsequently, a significant increase in ADAM9 expression in NSCLC tissue samples was found, which indicated its negative correlation with microRNA-488-3p. In addition, cell recovery experiment demonstrated that overexpression of ADAM9 could counteract the impact of microRNA-488-3p upregulation on the proliferation and invasion ability of NSCLC cells, and the two may thus together affect the malignant progression of NSCLC. CONCLUSIONS: It can be concluded that microRNA-488-3p, which is associated with the incidence of metastasis in NSCLC patients, can inhibit the malignant progression of NSCLC cells by modulating ADAM9 expression.
Subject(s)
ADAM Proteins/metabolism , Carcinoma, Non-Small-Cell Lung/metabolism , Lung Neoplasms/metabolism , Membrane Proteins/metabolism , MicroRNAs/metabolism , ADAM Proteins/genetics , Aged , Aged, 80 and over , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line , Female , Humans , Lung Neoplasms/pathology , Male , Membrane Proteins/genetics , MicroRNAs/genetics , Middle AgedABSTRACT
OBJECTIVE: Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer, with an unfavorable prognosis of 5-year survival rates. It is of great clinical significance to further search for more efficacious and novel targets for diagnosis and therapeutic strategies. This study aimed at clarifying the role of long non-coding RNA (lncRNA) NORAD in proliferation, invasion and migration and tumor growth of NSCLC. MATERIALS AND METHODS: In this study, mRNA levels of lncRNA NORAD were examined by RT-PCR. CCK-8 assay was applied to test cell viability. Furthermore, wound healing assay and transwell assay were performed to detect the migration and invasion of A549 cells, respectively. Immunohistochemistry was applied to assess the levels of CXC chemokine receptor (CXCR) 4 and CXC chemokine ligand (CXCL) 12. Mice models of NSCLC in vivo were exploited to further examine the potential role of NORAD in tumor growth. Key proteins related to Ras homolog gene family member A (RhoA) GTPase/Rho-associated kinase (RhoA/ROCK) pathway were determined by Western blot. RESULTS: NORAD has elevated the levels in NSCLC tissues and cells. NORAD interference dramatically inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion by downregulating CXCR4 and CXCL12 expression. RhoA/ROCK signaling pathway was activated in NSCLC. CONCLUSIONS: This study revealed that the downregulation of lncRNA NORAD could slow down the progression of NSCLC by regulating CXCR4 and RhoA/ROCK signaling pathway.
Subject(s)
Carcinoma, Non-Small-Cell Lung/metabolism , Cell Movement , Gene Expression Regulation, Neoplastic , Lung Neoplasms/metabolism , RNA, Long Noncoding/metabolism , Receptors, CXCR4/metabolism , rho-Associated Kinases/metabolism , rhoA GTP-Binding Protein/metabolism , Carcinoma, Non-Small-Cell Lung/pathology , Cell Proliferation , Humans , Lung Neoplasms/pathology , Neoplasm Invasiveness , RNA, Long Noncoding/genetics , Signal Transduction , Tumor Cells, CulturedABSTRACT
OBJECTIVE: To investigate the role of TNF-alpha and ICAM-1 in the pathogenesis of cerebral malaria. METHODS: Immunohistochemical method and ELISA were employed to examine the expression of ICAM-1 on the brain microvessel endothelium and to detect the production of serum TNF-alpha in P. berghei ANKA strain infected-CBA/J mice. RESULTS: Serum TNF-alpha levels of mice were apparently higher and the ICAM-1 expression was more evident in P. berghei ANKA infected-CBA/J mice than in control groups. rTNF-alpha i.p. injection could enhance the development of CM and the expression of ICAM-1 on brain endothelial cells(EC). CONCLUSION: Excessive production of TNF-alpha may mediate the expression of ICAM-1 on brain EC and hence cause the development of CM.
