Accumulating evidence suggests that the dysregulation of long non-coding RNAs (lncRNAs) serves vital roles in the incidence and progression of lung cancer. However, the molecular mechanisms of LINC00968, a recently identified lncRNA, remain unknown. The objective of present study was to investigate the role of a prospective lncRNA-miRNA‑mRNA network regulated by LINC00968 in non-small cell lung cancer cells. Following the transfection of lentiviruses carrying LINC00968 into A549 cells, the microRNA (miRNA) expression profile of the cells in response to the overexpression of LINC00968 was detected using an miRNA microarray. Five differentially expressed miRNAs (DEMs) with LINC00968 overexpression were obtained, including miR-9-3p, miR‑22-5p, miR-668-3p, miR‑3675-3p and miR-4536-3p. Five target prediction algorithms and three target validation algorithms were used to obtain 1,888 prospective target genes of the five DEMs. The result of Gene Ontology analysis suggested that these five DEMs were involved in complex cellular pathways, which included intracellular transport, organelle lumen and nucleotide binding. Furthermore, analysis of Kyoto Encyclopedia of Genes and Genomes pathways indicated that the five DEMs were important regulators in the adherens junction and focal adhesion. An lncRNA-miRNA-mRNA regulatory network and a protein-protein interaction network were then constructed. Eventually, a prospective lncRNA‑miRNA-mRNA regulatory network of LINC00968, three miRNAs (miR-9, miR-22 and miR-4536) and two genes (polo-like kinase 1 and exportin-1) was obtained following validation in the Cancer Genome Atlas database. These results may provide novel insights to support future research into lncRNA in lung cancer.

Download full-text PDF

Source
http://dx.doi.org/10.3892/ijmm.2017.3187DOI Listing

Publication Analysis

Top Keywords

lung cancer
16
regulatory network
12
lncrna-mirna-mrna regulatory
8
long non-coding
8
linc00968 non-small
8
non-small cell
8
cell lung
8
a549 cells
8
mirna microarray
8
linc00968
7

Similar Publications

Lung cancer is correlated with a high death rate, with approximately 1.8 million mortality cases reported worldwide in 2022. Despite development in the control of lung cancer, most cases are detected at higher stages with short survival rates.

View Article and Find Full Text PDF

MicroRNA abundance as a particular biomarker for precisely identifying cancer metastases has emerged in recent years. The expression levels of miRNA are analyzed to get insights into cancer tissue detection and subtypes. Similar to other cancer types, the miRNA shows high levels of target mRNA dysregulation in association with non-small cell lung carcinoma (NSCLC).

View Article and Find Full Text PDF

Novel Ru(II) Complexes as Type-I/-II Photosensitizers for Multimodal Hypoxia-Tolerant Chemo-Photodynamic/Immune Therapy.

Mol Pharm

January 2025

School of Pharmacy, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong 226001, Jiangsu Province, China.

Photodynamic therapy (PDT) is increasingly regarded as an attractive approach for cancer treatment due to its advantages of low invasiveness, minimal side effects, and high efficiency. Here, two novel Ru(II) complexes , were designed and synthesized by coordinating phenanthroline and biquinoline ligands with Ru(II) center, and their chemo-photodynamic therapy and immunotherapy were explored. Both and exhibited significant phototoxicity against A549 and 4T1 tumor cells type-I/-II PDT.

View Article and Find Full Text PDF

Microenvironmental β-TrCP negates amino acid transport to trigger CD8 T cell exhaustion in human non-small cell lung cancer.

Cell Rep

January 2025

The Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, China; Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China. Electronic address:

CD8 T cell exhaustion (Tex) has been widely acknowledged in human cancer, while the underlying mechanisms remain unclear. Here, we demonstrate that reduced amino acid (aa) metabolism and mTOR inactivation are accountable for Tex in human non-small cell lung cancer (NSCLC). NSCLC cells impede the T cell-intrinsic transcription of SLC7A5 and SLC38A1, disrupting aa transport and consequently leading to mTOR inactivation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!