Cancer is the leading cause of morbidity and mortality worldwide, particularly lung cancer. Heat shock proteins and their upstream heat shock factors are involved in the occurrence of cancer and have been widely researched. However, the role of heat shock factor 2 (HSF2) in lung cancer remains unclear. In the present study, expression levels of HSF2 in lung cancer tissues from 50 lung cancer patients were detected by reverse transcription quantitative polymerase chain reaction, and 76% (38/50) were upregulated compared with the matched normal tissues. This suggested possible involvement of HSF2 in lung cancer. To additionally investigate the role of HSF2 in lung cancer occurrence, a plasmid encoding HSF2 was constructed. HSF2 was over expressed in normal lung epithelial BEAS-2B cells and lung cancer A549 cells. The results showed that HSF2 overexpression promoted cell proliferation and cell migration in BEAS-2B and A549 cells. Additional experiments showed that the HSF2-induced cell proliferation and cell migration were dependent on induction of HSPs, particularly HSP27 and HSP90, as co-transfection of HSP27 small interfering RNA (siRNA) or HSP90 siRNA attenuated HSF2-induced cell growth and migration. In conclusion, the present study showed that HSF2 is aberrantly expressed in lung cancer, and it may be an upstream regulator of HSPs, which may strongly affect cell growth and cell migration. Additional studies are required to explain the detailed mechanism between lung cancer, HSF2, HSPs and other possible signaling pathways.
Serine/threonine kinase 33 (STK33) is a novel protein that has attracted considerable interest in recent years. Previous research has revealed that STK33 expression plays a special role in cancer cell proliferation. However, the mechanisms of STK33 induction of cancer cells remain largely unknown. In this study, it is demonstrated that STK33 expression varies in NL9980 and L9981 cells which are homogeneous cell lines with similar genetic backgrounds. STK33 can promote cell migration and invasion and suppress p53 gene expression in the NL9980 and L9981 cells. In addition, this protein also promotes epithelial-mesenchymal transition (EMT). Moreover, STK33 knockdown decreases tumor-related gene expression and inhibits cell migration, invasion, and EMT, suggesting that STK33 may be a mediator of signaling pathways that are involved in cancer. In conclusion, our results suggest that STK33 may be an important prognostic marker and a therapeutic target for the metastatic progression of human lung cancer.
The multi-energy system (MES) is believed to have bright prospects in the future for its advantages of high energy efficiency, flexible operation condition, and environmentally friendly. The heating network and the heat load play an important role in the MES and have great potentials in improving the system performance. In this paper, an optimal planning method is proposed for the MES that considers the thermal storage capacity of the heating network and the heat load. The objective includes the investment cost, the fuel cost, the grid cost, the maintenance cost, and the environmental cost. The constraints of the cogeneration, the heating network, and the heat load are all taken into consideration. The simulation based on the typical working conditions in annual operation is performed to verify the effectiveness of the proposed planning method. Four cases are set in order to comprehensively investigate the effect of the thermal storage capacity of the heating network and the heat load on the MES planning. The results indicate that the proposed method can decrease the capacity of the devices and reduce the fuel cost.INDEX TERMS Heat load, heating network, multi-energy system (MES), optimal planning, thermal storage capacity.
Lung cancer is the most common cause of cancer-related death in the world. Long non-coding RNAs (lncRNAs) are longer than 200 nucleotides transcripts which are not translated into protein. Linc00662 is overexpressed in lung cancer. However, the roles of linc00662 involved in lung cancer progression are still unknown. In our study, we found that linc00662 was overexpressed in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) by analyzing the TCGA data. We knockdown the linc00662 expression using siRNAs and found that silencing linc00662 significantly inhibited the proliferation and colony formation of A549 and H460 cells. We further found that knockdown of linc00662 increased the miR-145-5p expression and decreased PAFAH1B2 expression. We further showed that linc00662 could bind with miR-145-5p, and miR-145-5p could bind to the 3’UTR of PAFAH1B2. miR-145-5p could negatively regulate PAFAH1B2 both in the mRNA and protein levels. Loss of miR-145-5p could abolish the inhibitory effects of silencing linc00662 on the proliferation and colony formation of A549 and H460 cells. All these findings revealed that linc00662 functioned as an oncogene by acting as competing endogenous RNA (ceRNA) to sponge and regulate miR-145-5p in lung cancer and may provide a potential target of lung cancer treatment.
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