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SummaryErbin is an ErbB2 binding protein, which belongs to the LAP (leucine-rich repeat (LRR) and PDZ domain) protein family. We previously reported that Tax1, a protein of the human T-cell leukemia virus type I (HTLV-I), associated with Erbin by using Erbin PDZ domain as a bait to screen a human T lymphocyte cDNA library by a yeast two hybrid strategy. In the present study, we demonstrated that Tax1 enhances cancer cell proliferation via Ras-Raf-MEK-ERK signaling pathway by using molecular section strategy. The pull-down assay showed that the four amino acid domain, that is, Tax1 350-353, might specifically interact with Erbin, but not any other Tax1

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Chitosan could form nanoparticles with DNA through electrostatic interaction, and hence protect the DNA from enzymatic degradation. Numerous studies have been working on modifying chitosan aiming at improving its transgenic efficacy. While the modification of chitosan with alkyl group has been shown to significantly improve the cell transfection efficiency, little is known about its impact on its biocompatibility. The current study was performed to investigate the impact of alkylated-chitosan/DNA nanoparticles on the function of the murine macrophage through observing its phagocytic activity and production of pro-inflammatory cytokines (IL-1beta, IL-6, IL-10, IL-12 and TNF-alpha). Our results demonstrated that the alkylated-chitosan/DNA nanoparticles at the concentration of 20 microg/ml DNA content had no significant impact on the production of cytokines and phagocytic activity of the macrophages as compared with the unmodified chitosan/DNA nanoparticles and negative control even after 24 h co-incubation. It suggested that the modification of chitosan with alkyl group should not have negative impact on the function of the macrophages.

Purpose The goal of this study was to identify the crucial autophagy-related genes (ARGs) in periodontitis and construct mRNA-miRNA-lncRNA networks to further understand the pathogenesis of periodontitis. Methods We used the Gene Expression Omnibus (GEO) database and Human Autophagy Database (HADb) to identify differentially expressed mRNAs, miRNAs, and ARGs. These ARGs were subjected to Gene Ontology (GO), KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway, and PPI (protein–protein interaction) network analysis. Two databases (miRDB and StarBase v2.0) were used to reverse-predict miRNAs while the miRNA-lncRNA interaction was predicted using the StarBase v2.0 and LncBase Predicted v.2 databases. After excluding the lncRNAs only present in the nucleus, a competing endogenous RNA (ceRNA) network was built. Finally, we used quantitative real-time PCR (qRT-PCR) to confirm the levels of mRNA expression in the ceRNA network. Results The differential expression analysis revealed 10 upregulated and 10 downregulated differentially expressed ARGs. After intersecting the reverse-predicted miRNAs with the differentially expressed miRNAs, a ceRNA network consisting of 4 mRNAs (LAMP2, NFE2L2, NCKAP1, and EGFR), 3 miRNAs (hsa-miR-140-3p, hsa-miR-142-5p, and hsa-miR-671-5p), and 30 lncRNAs was constructed. In addition, qRT-PCR results revealed that EGFR expression was downregulated in diseased gingival tissue of periodontitis patients. Conclusion Four autophagy-related genes, especially EGFR, may play a key role in periodontitis progression. The novel ceRNA network may aid in elucidating the role and the mechanism of autophagy in periodontitis, which could be important in developing new therapeutic options.

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Lung cancer metastasis is the leading cause of poor prognosis and death for patients. Long noncoding RNAs (lncRNAs) have been validated the close correlation with lung cancer metastasis, but few comprehensive analyses have reported the specific association between lncRNA and cancer metastasis, especially via both competing endogenous RNA (ceRNA) regulatory relationships and functional regulatory networks. Here, we constructed primary and metastatic ceRNA networks, identified 12 and 3 candidate lncRNAs for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) respectively and excavated some drugs that might have potential therapeutic effects on lung cancer progression. In summary, this study systematically analyzed the competitive relationships and regulatory mechanism of the repeatedly dysregulated lncRNAs in lung cancer carcinogenesis and metastasis, and provided a new idea for screening potential therapeutic drugs for lung cancer.

Organisms evolved into different species to adapt to the environment according to the laws of Darwinian evolution. In a single life, prostate cancer cells can also evolve into tumor stem cells to adapt to the microenvironment, such as different chemotherapeutic drugs. These cancer cells become an unrestricted growth group relatively independent of the individual. The present review attempts to establish evidence that prostate cancer cells may survive by hormonotherapy and chemotherapy by gene amplification, mutation, and alternative splicing. Simultaneously, novel treatment strategies have been cited and evaluated, avoiding the resistance mechanisms.