Background Chronic obstructive pulmonary disease (COPD) is a disease that causes obstructed airways and abnormal inflammatory responses in the lungs. Early growth response 3 (EGR3) has been revealed to play a vital role in the regulation of the inflammatory response in certain diseases. We aimed to explore the role of EGR3 and its upstream mechanism in COPD. Methods and result In the present study, 16HBE cells were treated with cigarette smoke extract (CSE) to mimic the inflammatory response in vitro. RT-qPCR revealed that the expression of EGR3 was upregulated in lungs from COPD patients. EGR3 expression in 16HBE cells was increased by CSE treatment. Moreover, flow cytometry analysis and western blot analysis showed that EGR3 downregulation inhibited 16HBE cell apoptosis. EGR3 silencing decreased the protein levels of IL-6, TNF-α, IL-1β and COX2 in CSE-stimulated 16HBE cells. In addition, EGR3 was targeted by microRNA-200c-3p (miR-200c-3p) in 16HBE cells. MiR-200c-3p expression was significantly decreased in lung tissues from COPD patients compared to that in healthy controls. Furthermore, miR-200c-3p bound to lncRNA X-inactive specific transcript (XIST) in 16HBE cells. Additionally, XIST expression was elevated in lung tissues from COPD patients. Rescue assays indicated that EGR3 overexpression counteracted the effects of XIST downregulation on apoptosis and inflammation in CSE-stimulated 16HBE cells. Conclusion The XIST/miR-200c-3p/EGR3 axis facilitated apoptosis and inflammation in CSE-stimulated 16HBE cells. These findings may provide novel insight for treating COPD by alleviating lung inflammation.

The aberrant expression of microRNA is an important regulator in the tumorigenesis of non-small cell lung cancer. In this study, we found that miR-499a-5p was notably downregulated in non-small cell lung cancer tissues and cell lines. Decreased miR-499a-5p expression was associated with larger tumor size and higher TNM stage. Non-small cell lung cancer patients with low expression of miR-499a-5p exhibited a worse overall survival rate compared with those patients with high expression of miR-499a-5p. Ectopic expression of miR-499a-5p significantly suppressed non-small cell lung cancer cell proliferation and colony formation, and hampered cell cycle at G0/G1 phase in vitro. Conversely, knockdown of miR-499a-5p promoted non-small cell lung cancer cell proliferation and colony formation, and induced cell cycle at S phase. Furthermore, in vivo experiments revealed that overexpression of miR-499a-5p inhibited the tumor formation in a nude mouse xenograft model. Mechanistic studies showed that fibroblast growth factor 9 was a direct target gene of miR-499a-5p. miR-499a-5p directly bound to fibroblast growth factor 9 mRNA 3’-UTR, therefore led to the reduction in fibroblast growth factor 9 protein expression. Finally, rescue experiments confirmed that silencing of fibroblast growth factor 9 partially reversed the phenotypes of miR-499a-5p knockdown on non-small cell lung cancer cell proliferation. In conclusion, our study demonstrates that downregulation of miR-499a-5p predicts a worse prognosis of patients with non-small cell lung cancer and restrains the tumorigenesis by targeting fibroblast growth factor 9. These findings may provide valuable clues for the future development of therapeutic strategies against this cancer.

As one of the most common cause of cancer death in the world, lung cancer causes approximately 1.6 million deaths annually. Among them, NSCLC accounts for approximately 85% of patients in whole lung cancer patients. Ginsenoside Rg1 has been confirmed to play an important role in various diseases including cancer. As one of miRNAs, miR-126 closely involves in pathogenesis of the several types of cancers including colorectal, prostate, bladder and gastric cancer, and so on. Thus, the present study aims to investigate effects of the Ginsenoside Rg1 on NSCLC and underlying mechanism. In the study, two lung cancer cell lines including A549 and H1650 were used. It was found that expression of miR-126 was decreased in PBMC of NSCLC patients compared to healthy control. Expression of miR-126 was decreased in cancer tissue compared to paracancerous tissues in NSCLC patients. Importantly, it was found Ginsenoside Rg1 could inhibit growth of lung cancer cells. miR-126 KD remarkably increased the expression of apoptosis genes including caspase 3 and caspase 9 and decreased cell viability in lung cancer cells including A549 and H1650 cells. Interesting, in silico analysis indicated that miR-126 could target PI3K signaling pathway, which was confirmed by WB assay. KD of PI3KR2 compromised promotion of miR-126 on cell apoptosis. Similarly, it was found that KD of mTOR compromised promotion of miR-126 on cell apoptosis. Inhibition of Ginsenoside Rg1 on growth of lung cancer cells was through miR-126 and mTOR. Thus, the present study confirmed that Ginsenoside Rg1 remarkably inhibit lung cancer, which is through microRNA-126-PI3K-AKT-mTOR pathway.

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The formation of p−n junctions has attracted much attention for improving the gas-sensing performances in the field of gas detection. Although the p−n heterojunctions with a defined interfacial contact are crucial in investigating their roles on gas-sensing properties, the design of such well-defined p−n heterojunctions has been sparse until now. Herein, a p−n heterostructure composed of well-defined {001}-faceted Co 3 O 4 as backbones and Fe 2 O 3 nanorods as shells was synthesized using a simple hydrothermal method without the requirement of seed crystals. During the reaction, it was demonstrated that the acetic acid holds the key to the epitaxial growth of Fe 2 O 3 nanorods on the surface of Co 3 O 4 nanocubes. The response of this as-designed Fe 2 O 3 @Co 3 O 4 composite (R a /R g = 134.9) toward 100 ppm triethylamine was about 6 times higher than that of pristine Co 3 O 4 (R a /R g = 23.1) and 5 times higher than that of pristine Fe 2 O 3 (R a /R g = 28.9). The highly boosted gas-sensing performances were attributed to the positive effects of the heterointerface on the gas adsorption process that were revealed through the firstprinciples method based on the defined heterointerfacial contacts, as well as the enlarged signal of gas−solid reactions through the heterojunctions. This work not only provides a strategy to improve gas-sensing performances but also provides guidance for the investigation of the effects of p−n heterojunctions on gas-sensing properties by designing interfacial contact with defined crystal facets.