Notes

Targeted transcriptomic looks at involving RNA isolated coming from formalin-fixed as well as paraffin-embedded human being menisci.
hondrial dysfunction in the A2780 cells and enhanced apoptosis induced by cisplatin in the ovarian cancer cell line A2780. But this process was not related to endoplasmic reticulum apoptotic pathway.
Glioma is the most aggressive human brain tumor. Recent studies revealed that microRNAs play vital roles in glioma. However, the function of microRNA-525-5p (miR-525-5p) in glioma remains unclear.

qRT-PCR and Western blotting were used to evaluate mRNA and protein levels in glioma tissues and cells. Colony formation, CCK-8, and Edu assays evaluated the growth of glioma cells. Wound-healing, transwell, and 3D invasion assays examined the migration and invasion activities of glioma cells. Luciferase reporter assays assessed the regulatory relationship interaction between miR-525-5p and Stat-1. A mouse xenograft model was used to examine the effect of miR-525-5p on glioma in vivo.

miR-525-5p expression was downregulated in glioma tissues and cells. Overexpressing miR-525-5p decreased the growth of glioma cells and reduced the migration, invasion, and epithelial-mesenchymal transition of glioma cells. Bioinformatics analysis identified Stat-1 as a potential target of miR-525-5p, and dual luciferase reporter assays revealed that miR-525-5p negatively regulates Stat-1. Decreased Stat-1 led to the inhibition of FOXM1, affecting NF-κB signaling activity. Go6976 Overexpressing miR-525-5p reduced tumor development in vivo.

miR-525-5p negatively regulates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in glioma, and Stat 1 is a target of miR-525-5p. miR-525-5p may be a potential target for glioma treatment.
miR-525-5p negatively regulates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in glioma, and Stat 1 is a target of miR-525-5p. miR-525-5p may be a potential target for glioma treatment.[This retracts the article DOI 10.2147/OTT.S232594.].[This retracts the article DOI 10.2147/OTT.S254925.].
Referring to global cancer statistics, the incidence of gastric cancer (GC) was ranked sixth; however, detailed mechanisms underlying its development were not thoroughly investigated. Previous studies have reported that inhibition of ubiquitin-specific peptidase 8 (USP8) induced degradation of several receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR), embryonic stem cells (ESCs), etc. Nevertheless, the regulation of HER-2 by USP8 and the molecular mechanisms controlling their role in the pathogenesis of GC remain unknown.

A total of 69 patients with histologically confirmed GC were recruited to satisfy the purpose of this study. Initially, tumor samples and GC cell lines were used to detect USP8 and HER-2 levels. Next, MTT and colony formation assays were applied to analyze cell proliferation capability. Cell migration and invasion ability were examined by transwell assays. To examine related mRNA and protein expressions, Western blot assays and quantitative real-time PCR (qRT-PCRein-serine-threonine kinase (PI3K/AKT) pathway.

The USP8 inhibited HER-2 positive GC cell proliferation and migration in vivo and in vitro and probably served as a novel potential therapeutic biomarker for HER-2 positive GC.
The USP8 inhibited HER-2 positive GC cell proliferation and migration in vivo and in vitro and probably served as a novel potential therapeutic biomarker for HER-2 positive GC.
Long non-coding RNA (lncRNA) NCK1-AS1 could regulate multiple cancer progression. However, little is known regarding the roles and acting mechanisms of NCK-AS1 in gastric cancer (GC) progression. This work was aimed to explore the relationship between NCK1-AS1 and GC progression to illustrate the mechanisms of NCK1-AS1.

NCK1-AS1 expression level in GC tissues and cells was measured with a quantitative real-time PCR method. In vitro experiments including cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were employed to detect biological roles of NCK1-AS1 in GC progression. In vivo experiments were performed to analyze the roles of NCK1-AS1 on GC malignant phenotype. Moreover, mechanisms behind the biological roles of NCK1-AS1 in GC were investigated using bioinformatic analysis, luciferase activity reporter assay, RNA immunoprecipitation assay, and rescue experiments.

NCK1-AS1 was found to have elevated expression in GC tissues and cells in comparison with normal counterparts. Loss-of-function experiments showed knockdown of NCK1-AS1 refrained GC cell proliferation, colony formation, migration, and invasion in vitro. Animal experiments showed silence of NCK1-AS1 suppresses tumor growth in vivo. Functionally, NCK1-AS1 serves as a sponge for microRNA-137 (miR-137) to upregulate nucleoporin 43 (NUP43) expression in GC. Rescue experiments proved the carcinogenic role of NCK1-AS1/miR-137/NUP43 axis in GC progression.

In conclusion, the NCK1-AS1/miR-137/NUP43 axis was identified that could contribute to GC malignancy behaviors.
In conclusion, the NCK1-AS1/miR-137/NUP43 axis was identified that could contribute to GC malignancy behaviors.
Long intergenic non-coding RNAs (lincRNAs) are associated with the progression of glioblastoma (GBM). However, how linc01094 contributes to the growth and metastatic phenotypes of GBM remains not fully studied.

The expression levels of linc01094 and miR-126-5p in GBM tissues and cell lines were analyzed using qRT-PCR. Loss-of-function experiments were performed to detect the biological activity of linc01094 in GBM. Glioblastoma tumor model was constructed to explore the impact of linc01094 on GBM cell growth in vivo. Linc01094-sponged miR-126-5p was certified by luciferase reporter assay and RNA immunoprecipitation (RIP). The protein expression of miRNA target gene, dynactin subunit 4 (DCTN4) was detected using Western blotting assay.

Herein, we observed that the level of linc01094 was higher in GBM tissues. Silencing of linc01094 restrained the growth and invasive abilities of GBM cell. Moreover, linc01094 level was negatively associated with miR-126-5p level in GBM and linc01094 acted as a "sponge" for miR-126-5p.
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