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Air-Liquid Interface Microfluidic Monitoring Sensor Platform for Studying Autophagy Regulation after PM2.5 Exposure
Lulu Zheng1, Zhijin Yang1, Zhiwei Xue1
1Engineering Research Center of Optical Instrument and System, The Ministry of Education, Shanghai Key Laboratory of Modern Optical System, University of Shanghai for Science and Technology, Shanghai 200093, P. R. China.
Abstract:
Undoubtedly, a deep understanding of PM2.5-induced tumor metastasis at the molecular level can contribute to improving the therapeutic effects of related diseases. However, the underlying molecular mechanism of fine particle exposure through long noncoding RNA (lncRNA) regulation in autophagy and, ultimately, lung cancer (LC) metastasis remains elusive; on the other hand, the related monitoring sensor platform used to investigate autophagy and cell migration is lacking. Herein, this study performed an air-liquid interface microfluidic monitoring sensor (AIMMS) platform to analyze human bronchial epithelial cells after PM2.5 stimulation. The multiomics analysis [RNA sequencing (RNA-seq) on lncRNA and mRNA expressions separately] showed that MALAT1 was highly expressed in the PM2.5 treatment group. Furthermore, RNA-seq analysis demonstrated that autophagy-related pathways were activated. Notably, the main mRNAs associated with autophagy regulation, including ATG4D, ATG12, ATG7, and ATG3, were upregulated. Inhibition or downregulation of MALAT1 inhibited autophagy via the ATG4D/ATG12/ATG7/ATG3 pathway after PM2.5 exposure and ultimately suppressed LC metastasis. Thus, based on the AIMMS platform, we found that MALAT1 might become a promising therapeutic target. Furthermore, this low-cost AIMMS system as a fluorescence sensor integrated with the cell-monitor module could be employed to study LC migration after PM2.5 exposure. With the fluorescence cell-monitoring module, the platform could be used to observe the migration of LC cells and construct the tumor metastasis model. In the future, several fluorescence probes, including nanoprobes, could be used in the AIMMS platform to investigate many other biological processes, especially cell interaction and migration, in the fields of toxicology and pharmacology.
Insights
Fine particle (PM2.5) exposure promotes lung cancer metastasis by upregulating MALAT1, which activates autophagy. Inhibiting MALAT1 suppressed metastasis, identifying it as a therapeutic target. A novel sensor platform was also developed.
Area of Science:
- Environmental toxicology
- Molecular oncology
- Biomedical engineering
Background:
- Particulate matter (PM2.5) exposure is linked to lung cancer (LC) metastasis, but the molecular mechanisms involving long noncoding RNAs (lncRNAs) and autophagy remain unclear.
- Existing methods for studying autophagy and cell migration in response to PM2.5 are limited, hindering mechanistic investigations.
Purpose of the Study:
- To elucidate the molecular mechanism of PM2.5-induced lung cancer metastasis via lncRNA regulation of autophagy.
- To develop and utilize an air-liquid interface microfluidic monitoring sensor (AIMMS) platform for analyzing cellular responses to PM2.5.
- To identify potential therapeutic targets for mitigating PM2.5-driven lung cancer progression.
Main Methods:
- Human bronchial epithelial cells were stimulated with PM2.5 and analyzed using an AIMMS platform.
- Multiomics analysis, including RNA sequencing (RNA-seq) for lncRNA and mRNA expression, was performed.
- The role of MALAT1 and its downstream autophagy pathway (ATG4D/ATG12/ATG7/ATG3) in PM2.5-induced cell migration and metastasis was investigated through inhibition and downregulation studies.
Main Results:
- PM2.5 exposure significantly upregulated the expression of MALAT1 and key autophagy-related mRNAs (ATG4D, ATG12, ATG7, ATG3).
- Activation of autophagy pathways was observed following PM2.5 stimulation.
- Inhibition of MALAT1 effectively suppressed PM2.5-induced autophagy and subsequently reduced lung cancer cell metastasis.
- The developed AIMMS platform successfully monitored cell migration and autophagy in response to PM2.5.
Conclusions:
- MALAT1 plays a critical role in PM2.5-induced lung cancer metastasis by promoting autophagy via the ATG4D/ATG12/ATG7/ATG3 pathway.
- MALAT1 represents a promising therapeutic target for preventing or treating lung cancer metastasis driven by PM2.5 exposure.
- The low-cost AIMMS system offers a valuable tool for studying lung cancer cell migration and other biological processes in toxicology and pharmacology.
