Abstract
Long noncoding RNA (LncRNA) is a new type of regulatory RNA. LncRNA HOX antisense intergenic RNA (HOTAIR), as an oncogene in non-small cell lung cancer (NSCLC), is one of the key determinants of tumor progression. However, its possible molecular mechanism and the immunomodulatory pathway involved in NSCLC are still unclear. This study aims to explore whether HOTAIR promotes proliferation, migration and invasion of the NSCLC cells by inhibiting the expression of C-C Motif Chemokine Ligand 22 (CCL22). We collected 30 clinical samples of cancer and adjacent normal tissues from the patients with NSCLC, using real-time quantitative polymerase chain reaction (RT-qPCR) to detect the LncRNA HOTAIR and CCL22 mRNA expression in tissues. Immunohistochemistry was used to detect the protein expression of CCL22 in cancer and adjacent normal tissues. Cell experiments were conducted to verify that LncRNA HOTAIR regulates the expression of CCL22 and participates in the progress of NSCLC. The antisense oligonucleotide (ASO) probe interfering with LncRNA HOTAIR and the interference fragment of CCL22 (si-CCL22) were constructed. A549 cells were co-transfected with ASO-HOTAIR and si-CCL22. We used RT-qPCR to detect the expression of LncRNA HOTAIR and CCL22 mRNA in the cells, enzyme-linked immunosorbent assay (ELISA) used to detect the CCL22 protein level in the cell supernatant. 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was applied to detect cell proliferation, the Flow cytometry to detect cell apoptosis. Finally, the Transwell test was utilized to detect cell migration and invasion. In conclusion, this study suggests that HOTAIR may promote proliferation, migration and invasion of the NSCLC cells by inhibiting CCL22 expression, which may play a key role in NSCLC cell immunity.
Highlights
Lung cancer is a malignant tumor that seriously threatens human health and life nowadays, whose incidence is increasing in many countries [1]
The high expression of chemotactic factor C Motif Chemokine Ligand 22 (CCL22) and CCL22 can recruit regulatory T cells (Treg) to the tumor site of Non-small cell lung cancer (NSCLC) [10, 11]. These results suggest that CCL22 inhibits the proliferation, migration, and invasion of the NSCLC cells
The real-time quantitative polymerase chain reaction (RT-qPCR) results showed that, the expression of Long noncoding RNA (LncRNA) HOTAIR was up-regulated, while the expression of CCL22 mRNA was down-regulated in the non-small cell lung cancer clinical samples compared with adjacent normal tissues (Fig 1A and 1B)
Summary
Lung cancer is a malignant tumor that seriously threatens human health and life nowadays, whose incidence is increasing in many countries [1]. Non-small cell lung cancer (NSCLC) is the most common histology in lung cancer, accounting for 80%-85% of lung cancer [2]. The website of Zhongshan Science and Technology Bureau was listed as follow: http://kj. Zs.gov.cn/ The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript The website of Zhongshan Science and Technology Bureau was listed as follow: http://kj. zs.gov.cn/ The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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