Abstract
Background: Non-small cell lung cancer (NSCLC) is a highly malignant tumor. Accumulating evidence suggested that prostate cancer non-coding RNA 1 (PRNCR1) participated in the pathogenesis of NSCLC, whereas the elaborate mechanism remains unclear. Hence, the role of PRNCR1 in the progression of NSCLC was investigated.Methods: Levels of PRNCR1, microRNA-126-5p (miR-126-5p), and metadherin (MTDH) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was measured using Cell Counting Kit-8 (CCK-8). Flow cytometry was conducted to determine cell apoptosis. Besides, transwell assay was performed to detect cell migration and invasion in NSCLC cells. The expression levels of E-cadherin, N-cadherin, Vimentin, and MTDH were detected via Western blot. Dual-luciferase reporter, RNA immunoprecipitation, and RNA pull down assays were employed to verify the relationship between miR-126-5p and PRNCR1 or MTDH.Results: PRNCR1 and MTDH levels were highly expressed, while miR-126-5p expression was lowly expressed in NSCLC tissues and cell lines. Knockdown of PRNCR1 promoted cell apoptosis, impeded proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in NSCLC cells, and these effects were abrogated by its target gene of miR-126-5p inhibitor. Moreover, MTDH as the target of PRNCR1, its overexpression reversed the impacts of miR-126-5p mimic on cell behaviors and EMT in vitro. Finally, PRNCR1 and miR-126-5p regulated MTDH expression.Conclusion: PRNCR1 modified cell behaviors and EMT via miR-126-5p/MTDH axis in NSCLC cells, providing a novel thinking for clinical treatment of NSCLC.
Highlights
Lung cancer is the respiratory tract cancer with high malignancy [1], of which non-small cell lung cancer (NSCLC) is the significant member and approximately occupies 85% of lung cancer [2], while the 5-year survival rate of Non-small cell lung cancer (NSCLC) patients is relatively low [3]
The level of prostate cancer non-coding RNA 1 (PRNCR1) and miR-126-5p was detected by quantitative real-time polymerase chain reaction (qRT-PCR), and the results showed that there was the same tendency of PRNCR1 and miR-126-5p levels in NSCLC tissues and cell lines (Figure 1C,D)
These data emerged that the level of PRNCR1 was increased, whereas miR-126-5p expression was impeded in NSCLC tissues and cell lines
Summary
Lung cancer is the respiratory tract cancer with high malignancy [1], of which non-small cell lung cancer (NSCLC) is the significant member and approximately occupies 85% of lung cancer [2], while the 5-year survival rate of NSCLC patients is relatively low [3]. It is expected to find the effective therapeutic methods via curbing cell proliferation and metastasis in NSCLC. Non-small cell lung cancer (NSCLC) is a highly malignant tumor. Transwell assay was performed to detect cell migration and invasion in NSCLC cells. Results: PRNCR1 and MTDH levels were highly expressed, while miR-126-5p expression was lowly expressed in NSCLC tissues and cell lines. Knockdown of PRNCR1 promoted cell apoptosis, impeded proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in NSCLC cells, and these effects were abrogated by its target gene of miR-126-5p inhibitor. MTDH as the target of PRNCR1, its overexpression reversed the impacts of miR-126-5p mimic on cell behaviors and EMT in vitro. Conclusion: PRNCR1 modified cell behaviors and EMT via miR-126-5p/MTDH axis in NSCLC cells, providing a novel thinking for clinical treatment of NSCLC
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