PERP May Affect the Prognosis of Lung Adenocarcinoma by Inhibiting Apoptosis.

Background: PERP, a member of the peripheral myelin protein gene family, is a new therapeutic target in cancer. The relationships between PERP and immune cell infiltration in lung cancer have not been studied. Therefore, the role of PERP in the tumour microenvironment (TME) of lung cancer needs to be further explored. Methods: In this study, we explored the association between PERP expression and clinical characteristics by analysing data from the TCGA database. Cox regression and Kaplan‒Meier methods were used to investigate the relationship between the expression of PERP and overall survival in patients with lung adenocarcinoma (LUAD). The relationship between PERP expression and the degree of infiltration of specific immune cell subsets in LUAD was evaluated using the TIMER database and GEPIA. We also performed GO enrichment analysis and KEGG enrichment analysis to reveal genes coexpressed with PERP using the Coexpedia database. Finally, we verified the expression and function of PERP in LUAD tissues and the A549 cell line by RT‒PCR, Western blot, CCK-8, IHC, and wound healing assays. The mouse model was used to study the in vivo effects of PERP. Results: According to our results, PERP expression was significantly higher in LUAD tissues and associated with the clinical characteristics of the disease. Survival was independently associated with PERP in LUAD patients. We further verified that PERP might regulate B-cell infiltration in LUAD to affect the prognosis of LUAD. To identify PERP-related signalling pathways in LUAD, we performed a genome-aggregation analysis (GSEA) between low and high PERP expression datasets. LUAD cells express higher levels of PERP than paracarcinoma cells, and PERP inhibits the proliferation and metastasis of A549 cells through apoptosis. Conclusion: PERP may affect the prognosis of lung adenocarcinoma by inhibiting apoptosis and is associated with immune cell infiltration.

An elastic MOF/graphene aerogel with high photothermal efficiency for rapid removal of crude oil.

Due to the frequent spill accidents during crude oil exploration and transport, to rapidly cleanup crude oil and eliminate the environmental pollution of oil spill is in high demand. In this work, a three-dimensional graphene aerogel (MEGA) with high elasticity, photothermal conversion capacity and adsorption capacity was prepared for rapid removal of crude oil. The results showed that the as-prepared MEGA exhibited a layered structure, the octahedral HKUST-1 nanoparticles and hydrophobic polydimethylsiloxane (PDMS) coatings were uniformly deposited on the surface. Such a hierarchical micro-nano porous structure not only improved the aerogel's hydrophobicity (water contact angle in air up to 152.7°), but also endowed it with strong oil adsorption capacity (41-118 times of its own weight). Especially, the MEGA showed excellent photothermal conversion capacity. Under light irradiation, its temperature raised to 80 â„ƒ from room temperature in 100 s. As a result, the adsorption for one drop of crude oil by MEGA was shortened from 5 h to 40 s, comparing with that in dark condition. In addition, the MEGA showed remarkable elasticity and mechanical stability, it could maintain more than 90% efficiency after 10 adsorption-compression cycles. This study suggests that the prepared MEGA has great potential for rapid removal of crude oil.

miR-193a-5p promotes pancreatic cancer cell metastasis through SRSF6-mediated alternative splicing of OGDHL and ECM1.

MicroRNAs (miRNAs) are short and non-coding RNAs binding to 3'UTR of target mRNAs to downregulate their expression. Recent studies have shown that miRNAs indirectly regulated alternative splicing (AS) by targeting splicing factors and caused shifts in splicing patterns of target genes. However, the roles of miRNA-regulating splicing factors in pancreatic cancer progression remain unknown. Herein, we reported that miR-193a-5p was markedly upregulated in pancreatic cancer tissues and cells and correlated with clinical outcomes of pancreatic cancer patients. Overexpression of miR-193a-5p contributed to the metastasis of pancreatic cancer cells both in vitro and in vivo. The mechanistic investigation suggested that miR-193a-5p modulated oxoglutarate dehydrogenase-like (OGDHL) and extracellular matrix protein 1 (ECM1) AS by targeting serine/arginine-rich splicing factor 6 (SRSF6), leading to the activation of the epithelial-to-mesenchymal transition (EMT) process. Together, our findings highlighted the role of miR-193a-5p-targeting SRSF6 in pancreatic cancer metastasis, which may serve as a novel target for pancreatic cancer diagnosis and therapy.

Correction: Protease Nexin I is a feedback regulator of EGF/ PKC/MAPK/EGR1 signaling in breast cancer cells metastasis and stemness.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Protease Nexin I is a feedback regulator of EGF/PKC/MAPK/EGR1 signaling in breast cancer cells metastasis and stemness.

Breast cancer is the most prevalent cancer in women worldwide, which remains incurable once metastatic. Breast cancer stem cells (BCSCs) are a small subset of breast cancer cells, which are the radical cause of drug resistance, tumor relapse, and metastasis in breast cancer. The extracellular serine protease inhibitor serpinE2, also named protease nexin-1 (PN-1), contributes to enhanced metastasis of cancer cells mainly by remodeling the tumor matrix. In this study, we found that PN-1 was up-regulated in breast cancer, which promoted cell invasion, migration and stemness. Furthermore, by using specific inhibitors, we discovered that epidermal growth factor (EGF) up-regulated PN-1 in breast cancer cells through cascade activation of epidermal growth factor receptor (EGFR) to the activation of protein kinase Cδ (PKCδ), mitogen-activated protein kinase (MEK) and extracellular signal-related kinase (ERK), which finally led to the up-regulation of early growth response protein 1 (EGR1). Moreover, EGF signaling was further activated as a feedback of PN-1 up-regulation through PN-1 blocking HtrA1. Taken together, our findings revealed a novel signaling axis that up-regulated PN-1 expression in breast cancer cells, and the new mechanism of PN-1-promoted breast cancer metastasis, which may provide new insights into identifying novel therapeutic targets for breast cancer.