Gastric cancer (GC) is one of the major global health problems, especially in Asia. Nowadays, long non-coding RNA (lncRNA) has gained significant attention in the current research climate such as carcinogenesis. This research desires to explore the mechanism of Prader-Willi region non-protein coding RNA 1 (PWRN1) on regulating GC process. Differentially expressed lncRNAs in GC tissues were screened out through microarray analysis. The RNA and protein expression level were detected by quantitative real-time PCR (qRT-PCR) and Western blot. Cell proliferation, apoptosis rate, metastasis abilities were respectively determined by cell counting kit 8 (CCK8), flow cytometry, wound healing, and transwell assay. The luciferase reporter system was used to verify the targetting relationships between PWRN1, , and phosphatase and tensin homolog (). RNA-binding protein immunoprecipitation (RIP) assay was performed to prove whether PWRN1 acted as a competitive endogenous RNA (ceRNA) of Tumor xenograft model and immunohistochemistry (IHC) were developed to study the influence of PWRN1 on tumor growth Microarray analysis determined that PWRN1 was differently expressed between GC tissues and adjacent tissues. qRT-PCR revealed PWRN1 low expression in GC tissues and cells. Up-regulated PWRN1 could reduce proliferation and metastasis and increase apoptosis in GC cells, while had reverse effects. The RIP assay indicated that PWRN1 may target an oncogene, The tumor xenograft assay found that up-regulated PWRN1 suppressed the tumor growth. The bioinformatics analysis, luciferase assay, and Western blot indicated that PWRN1 affected /// axis via suppressing Our findings suggested that PWRN1 functioned as a ceRNA targetting and suppressed GC development via p53 signaling pathway.

Gastric cancer (GC) is one of the most common cancers worldwide and is thus a global cancer burden. Here, we focused on a novel circular RNA hsa_circ_0092306 and explored the potential molecular mechanism to provide a new target for and novel insights into GC treatment. The GEO microarray was mined and analyzed with R software. Sanger sequencing and RNase R assay were applied to verify the identification of hsa_circ_0092306. Quantitative real-time PCR and western blot were performed to measure the mRNA and protein levels. Pull-down and luciferase reporter assays were conducted to confirm the target relationships. Annexin V-PI apoptosis flow cytometry, 3-(4,5Dimethylthiazol- yl)-2,5Dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT), wound healing, and Transwell assays were applied to detect cell apoptosis, viability, migration, and invasion in MKN-45 cells, respectively. A xenograft in vivo experiment was conducted to confirm the cell experiment results. hsa_circ_0092306 was upregulated in GC tissues and GC cells, and promoted GC development in MKN-45 cells. hsa_circ_0092306 inhibited tumor suppressor miR-197-3p expression but promoted tumor promotor protein kinase C beta (PRKCB) expression in MKN-45 cells. hsa_circ_0092306 and PRKCB had a common target (miR-197-3p) and were negatively related to miR-197-3p expression. hsa_circ_0092306 promoted the development of GC by regulating the pathway of miR-197-3p/PRKCB in MKN-45 cells.

Lung cancer is the leading cause of global cancer-associated mortality, therefore it is important to reveal the molecular mechanisms of lung cancer progression and to develop novel therapeutic targets. The results of the present study identified that manganese-12 acetate (Mn12Ac) was able to significantly inhibit the migration and invasion of A549 cells. Western blotting demonstrated that treatment with Mn12Ac was able to upregulate E-cadherin, and downregulate N-cadherin and vimentin. It was also identified by a quantitative polymerase chain reaction analysis that Mn12Ac was able to reduce the mRNA expression levels of EMT-associated transcription factors Snail, Slug, Twist-related protein 1 and zinc finger E-box-binding homeobox 1. It was also demonstrated that Mn12Ac was able to reduce the expression levels of Wnt and β-catenin proteins, and suppress the phosphorylation of phosphoinositide 3-kinase (PI3K) and AKT in A549 cells. Notably, it was revealed that Mn12Ac was able to decrease the mRNA and protein expression levels of programmed death ligand-1. Taken together, the results suggested that Mn12Ac is able to inhibit cell migration, invasion and EMT in lung cancer cells by regulating the Wnt/β-catenin and PI3K/AKT signaling pathways.

The zinc finger homeodomain (ZF-HD) genes belong to the homeobox gene family, playing critical roles in flower development and stress response. Despite their importance, however, to date there has been no genome-wide identification and characterization of the ZF-HD genes that are probably involved in stress responses in maize. In this study, 24 ZF-HD genes were identified, and their chromosomal locations, protein properties, duplication patterns, structures, conserved motifs and expression patterns were investigated. The results revealed that the ZF-HD genes are unevenly distributed on nine chromosomes and that most of these genes lack introns. Six and two ZF-HD genes have undergone segmental and tandem duplication, respectively, during genome expansion. These 24 ZF-HD transcription factors were classified into six major groups on the basis of protein molecular evolutionary relationship. The expression profiles of these genes in different tissues were evaluated, resulting in producing two distinct clusters. ZF-HD genes are preferentially expressed in reproductive tissues. Furthermore, expression profiles of the 24 ZF-HD genes in response to different kinds of stresses revealed that ten genes were simultaneously up-regulated under ABA, salt and PEG treatments; meanwhile four genes were simultaneously down-regulated. These findings will pave the way for deciphering the function and mechanism of ZF-HD genes on how to implicate in abiotic stress.

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