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Published on: January 19, 2019
miR-142-5p regulates CD4+ T cells in human non-small cell lung cancer through PD-L1 expression via the PTEN pathway
Jun Wan1, Xiean Ling1, Bin Peng1
1Department of Thoracic Surgery, The Shenzhen People's Hospital, The Second Clinical Medicine College of Jinan University, Shenzhen, Guangdong 518020, P.R. China.
Abstract:
The present study aimed to evaluate the function of microRNA (miR)-142-5p on cancer immunity to induce apoptosis in human non-small cell lung cancer (NSCLC) and its mechanism. miR-142-5p expression was upregulated, and CD4+ T cell levels were reduced in patients with NSCLC. Overexpression of miR-142-5p expression inhibited the cancer effects of CD4+ T cells on NSCLC cell lines, and downregulation of miR-142-5p increased the cancer effects of CD4+ T cells on NSCLC cell lines, compared with the control group. In addition, we found that overexpression of miR-142-5p suppressed PTEN protein expression and induced PI3K, p-Akt and PD-L1 protein expression in an in vitro model of NSCLC. Downregulation of miR-142-5p induced PTEN and PD-L1 protein expression and suppressed PI3K and p-Akt and protein expression in an in vitro model of NSCLC. The suppression of PD-L1 reduced the cancer effects of CD4+ T cells on NSCLC cell lines following miR-142-5p downregulation. The inhibition of PTEN also reduced the cancer effects of CD4+ T cells on NSCLC cell lines following miR-142-5p downregulation. Therefore, our study demonstrated that miR-142-5p regulated CD4+ T cells in human NSCLC through PD-L1 expression via the PTEN pathway.
Insights
MicroRNA-142-5p impacts non-small cell lung cancer immunity by affecting CD4+ T cells. It regulates cancer cell apoptosis via the PTEN/PD-L1 pathway, offering potential therapeutic targets.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related deaths.
- MicroRNAs (miRNAs) play crucial roles in cancer development and immune regulation.
- The specific role of miR-142-5p in NSCLC immunity remains to be fully elucidated.
Purpose of the Study:
- To investigate the function of miR-142-5p in NSCLC immunity.
- To elucidate the underlying molecular mechanisms involving CD4+ T cells, PTEN, and PD-L1.
- To assess the potential of miR-142-5p as a therapeutic target in NSCLC.
Main Methods:
- Analysis of miR-142-5p expression and CD4+ T cell levels in NSCLC patients.
- In vitro experiments involving overexpression and downregulation of miR-142-5p in NSCLC cell lines.
- Assessment of protein expression levels of PTEN, PI3K, p-Akt, and PD-L1.
- Evaluation of the impact of miR-142-5p modulation on CD4+ T cell-mediated anti-cancer effects.
Main Results:
- miR-142-5p expression was upregulated, and CD4+ T cell levels were reduced in NSCLC patients.
- Overexpression of miR-142-5p inhibited CD4+ T cell anti-cancer activity, while downregulation enhanced it.
- miR-142-5p modulated PTEN, PI3K, p-Akt, and PD-L1 protein expression in vitro.
- Modulation of PD-L1 and PTEN affected CD4+ T cell-mediated anti-cancer effects in NSCLC.
Conclusions:
- miR-142-5p plays a significant role in regulating anti-tumor immunity in NSCLC.
- The mechanism involves the regulation of CD4+ T cell function through the PTEN/PD-L1 pathway.
- miR-142-5p represents a potential therapeutic target for enhancing anti-cancer immunity in NSCLC.
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