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Metabolo-epigenetics: The particular interplay associated with metabolism and epigenetics during early on inspiring seed cellular material growth.
Results β-arrestin1 was aberrantly upregulated in human ESCC tissues, ESCC cell lines and animal model of ESCC. β-arrestin1 downregulation inhibited cell proliferation, migration, invasion and EMT of ESCC in vitro and vivo. β-arrestin downregulation also suppressed tumor growth in vivo model of ESCC. In addition, the inhibitory effects of β-arrestin1 downregulation were exerted via AKT/GSK3β/β-catenin signaling pathway. Discussion The results in the present study together confirmed the truth that β-arrestin1 interference may suppress ESCC cell proliferation, migration, invasion, EMT and tumor growth via AKT/GSK3β/β-catenin signaling pathway. © 2020 Tan et al.[This corrects the article DOI 10.2147/OTT.S216620.]. © 2020 Xia and Wang.Background Recent studies showed that aberrant expression of miRNAs causes tumor-suppressing or promoting effects in various cancers including gastric cancer (GC). Our previous studies showed that lots of miRNAs and mRNA expressed differentially in GC and normal tissues. However, the critical miRNAs and mRNA need to be clarified. Materials and Methods Microarray sequencing was used to profile the differential expression of miRNAs and mRNA in GC and normal tissues. Bioinformatics analysis and database prediction were used to search the critical miRNAs and mRNA. Real-time quantitative polymerase chain reaction (RT-qPCR), luciferase reporter assay, immunohistochemistry (IHC), wound healing assay and transwell assay were used to clarify the relationship between the target miRNAs and mRNA. Statistical analysis was used to seek their value of diagnosis and prognosis. Results We identified microRNA-6165 (miR-6165) as a novel cancer-related miRNA in GC through high-throughput microarray sequencing. By bioinformatics analysis and luciferase reporter assay, we found STRN4 was the target of miR-6165. Via a series of cell experiments, we determined that miR-6165 suppressed GC cells migration and invasion by targeting STRN4. Also, we discovered the potential diagnosis and prognosis value of miR-6165 and STRN4. Conclusion It was found that miR-6165 might suppress GC migration and invasion by targeting STRN4 in vitro, and the further research should focus more on the potential diagnosis and prognosis value of miR-6165 and STRN4 in gastric cancer patients. © 2020 Wang et al.Currently, women with metastatic or recurrent cervical cancer still have very limited treatment options. Despite the rapid advancements in targeted therapies, no targeted therapy was approved for cervical cancer, except for bevacizumab. In the present study, we reported a 52-year-old heavily pre-treated EGFR amplified patient with metastatic cervical squamous cancer who benefited from afatinib with a progression-free survival (PFS) of 5.5 months. The patient was administered with a first-line treatment of chemotherapy and bevacizumab with a PFS of 4.3 months. Subsequently the patient was treated with a second-line regimen of angiogenesis inhibitor apatinib plus chemotherapy and a third-line treatment of pembrolizumab. Genomic profiling revealed significant EGFR amplification in both primary (copy number [CN] =15.9) and metastatic lesions (CN =18). Afatinib monotherapy was then administered as the fourth-line regimen. She achieved partial response (PR) with a PFS of 5.5 months. At disease progression, the CN of EGFR was elevated to 39.9 accompanied by the emergence of PIK3CA amplification (CN =4.2). The patient was treated with everolimus and afatinib and achieved stable disease (SD) after 3 months. To the best of our knowledge, this is the first clinical evidence of an EGFR-amplified metastatic cervical cancer patient benefiting from afatinib as a single agent. © 2020 Chen et al.Purpose Glioma is an aggressive tumor from the nervous system, which causes more than 70% of primary malignant brain tumors. Considering its severe malignancy, there is an urgent need to investigate more practical markers to understand the pathogenesis of glioma, and potential treatment methods for glioma patients. In the paper, we are focused on examining the roles of LINC01140, miR-199a-3p, and ZHX1 in the progression of gliomas, as well as their inner associations and modulation mechanisms. Methods qRT-PCR was employed to examine the expression levels of LINC01140 and miR-199a-3p. We measured the expressions of ZHX1 via qRT-PCR and Western blotting. CCK8 assays, migration assays, and invasion assays were carried out to determine the cell viabilities and abilities of migration and invasion. We also conducted in vivo tumor growth experiments to investigate the roles of LINC01140 in glioma developments. Results The expressions of LINC01140 were promoted in glioma. Silencing LINC01140 could inhibit glioma cell viabilities, migration, and invasion. In our experiments, miR-199a-3p was inhibited in glioma. LINC01140 negatively regulated the expressions of miR-199a-3p in glioma. MiR-199a-3p could target ZHX1 to inhibit its expression in glioma cells. Conclusion LINC01140 could promote glioma developments by modulating the miR-199a-3p/ZHX1 axis. © 2020 Xin et al.Objective It has been verified that long non-coding RNAs (lncRNAs) play critical roles in the development of human cancers. Increasing evidence indicates that lncRNA human plasmacytoma variant translocation1 (PVT1) was dysregulated in non-small cell lung cancer (NSCLC) which is the leading cause of cancer-related death. However, the precise mechanism underlying the effect of PVT1 remains elusive. Our research focused on the correlation of PVT1 to miR-148 and RAB34 in NSCLC. Methods The quantitative real-time PCR (qRT-PCR) and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro. Results In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo. Conclusion Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets. © 2020 Xi et al.Background Liver cancer (LC) is the sixth most common cancer and the second leading cause of cancer mortality worldwide, and its incidence rate is high in China. Methods In this study, we aimed to investigate the contribution of MIR137HG (MIR137 Host Gene) polymorphisms to LC risk in a case-control study with 432 LC patients and 430 healthy controls. A logistic recession model was used to evaluate the effects of candidate single nucleotide polymorphisms (SNPs) on LC risk. HaploReg v 4.1 database was conducted to predict the potential functionality of SNPs. Results The results revealed that rs17371457 and rs7554283 in the MIR137HG gene were correlated with an enhanced LC risk under the allele (P = 0.001 and P = 0.043, respectively) and genetic models (P 55 years (P less then 0.05); rs17371457 was related to higher LC risk in males (P less then 0.05). Similarly, the haplotype AG constituted by rs12333983 and rs3735451 significantly increased LC risk in Chinese Li population (P = 0.043). Six SNPs distributed in MIR137HG were successfully predicted as regulatory SNPs with different biological functions. Conclusion Our research firstly showed that MIR137HG gene polymorphisms were implicated in LC susceptibility among Chinese Li population. © 2020 Wang et al.Gastric cancer is one of the most common malignant tumors, and it is also one of the leading causes of cancer death worldwide. Because of its insidious symptoms and lack of early dictation screening, many cases of gastric cancer are at late stages which make it more complicated to cure. For these advanced-stage gastric cancers, combination therapy of surgery, chemotherapy, radiotherapy and target therapy would bring more benefit to the patients. However, the drug-resistance to the chemotherapy restricts its effect and might lead to treatment failure. In this review article, we discuss the mechanisms which have been found in recent years of drug resistance in gastric cancer. And we also want to find new approaches to counteract chemotherapy resistance and bring more benefits to the patients. © 2020 Ruan et al.Background Cervical cancer (CC) ranks as the second most common malignancy in women, accounting for more two 2 million deaths every year in the world. Recently, circular RNAs (circRNAs) have been reported to regulate the progression of multiple human tumors; however, whether it involves in CC remains largely elusive. Materials and Methods Two GEO circRNA expression profiles (GSE102686, GSE113696) were downloaded to analyze the differentially expressed circRNAs using bioinformatics methods. Expression of circ_103973, miR-335 and PPP6C in CC tissues and cell lines were examined by qRT-PCR. Cell apoptosis was assessed with PI/Annexin-V double staining followed by the analysis of flow cytometry. Cell proliferation was evaluated by MTT and colony formation assays. Interaction between circ_103973 and miR-335, as well as miR-335 and PPP6C, were verified by dual-luciferase reporter assay. Results Circ_103973 was found to be highly expressed in both GSE102686 and GSE113696 datasets as well as in CC tissue samples and cell lines. Higher levels of circ_103973 were correlated to a worse outcome of CC patients. Knockdown of circ_103973 significantly promoted CC cell apoptosis and inhibited CC cell proliferation in vitro. Mechanistically, we demonstrated that circ_103973 served as a sponge of miR-335, which directly targeted PPP6C in CC cells. miR-335 was found to be decreased in CC, while PPP6C was found to be increased in CC. Moreover, anti-miR-335 could reverse the inhibitory effects of circ_103973 knockdown on CC cell proliferation, and this phenomenon could be blocked by si-PPP6C. Conclusion Circ_103973 promoted CC cell proliferation in vitro by physically binding miR-335, which further targeted and regulated PPP6C. selleck chemicals llc © 2020 Zhu et al.Background Informed consent is an obligatory requirement for research engaging human subjects. Informed consent form (ICF) should be provided for human subjects to confirm their willingness for voluntary participation in a study. Ethical and legal obligations necessitate the presence of informed consent essential items to be built into the ICF. Objective To evaluate the content of ICFs obtained from different genetic studies accomplished in Jordan and their adherence to ethical guidelines proposed by the International Conference on Harmonization-Good Clinical Practice (ICHGCP). Methods and Measures A total of 44 ICFs obtained from master theses and grant proposals at two major universities in Jordan were analyzed according to the good clinical practice criteria proposed by ICHGCP. ICFs were scored for the presence or absence of ICF main items/categories. Results Results show inadequate information present in the examined ICFs. The highest information score was 17 out of 20, while the lowest score was one out of 20.
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