Notes

Discerning concentrating on regarding NaV1.6 by means of inhibition of the CRMP2-Ubc9 conversation reduces discomfort within rodents.
th adding DDX53 si-DDX53-CNE1-TR exosomes, and the increased IC50 to Taxol was obviously reversed.

This study firstly discovered that DDX53 was highly expressed in Taxol-resistant NPC cells, which could be transferred into normal NPC cells via exosome secretion. The transferred DDX53 could upregulate the expression of MDR1 in NPC cells to promote the resistant capacity to Taxol, which provided a novel insight for understanding NPC and might be a potential therapeutic target for NPC.
This study firstly discovered that DDX53 was highly expressed in Taxol-resistant NPC cells, which could be transferred into normal NPC cells via exosome secretion. The transferred DDX53 could upregulate the expression of MDR1 in NPC cells to promote the resistant capacity to Taxol, which provided a novel insight for understanding NPC and might be a potential therapeutic target for NPC.
Dysregulated lipid metabolism has been reported in the progression of hepatocellular carcinoma (HCC). In the present study, we investigated the molecular characteristics of lipid-metabolism-related genes (IMRGs) as prognostic markers for HCC.

Multi-dimensional bioinformatics analyses were performed to comprehensively analyze IMRGs, and to construct prognostic prediction signatures.

Data of 770 HCC patients and their corresponding 776 IMRGs were downloaded from three databases. Patients were classified into 2 molecular clusters that were associated with overall survival, clinical characteristics, and immune cells. The biological functions of the IMRGs differentially expressed between the 2 clusters were associated with tumor-related metabolic pathways. A 6 IMRG signature (6-IS), consisting of FMO3, SLC11A1, RNF10, KCNH2, ME1, and ZIC2, was established as an independent prognostic factor for HCC. The performance of the signature of 6-IS prognostic was verified in a validation set and compared to an external data set. It was revealed that the 6-IS could effectively predict the prognosis of patients with HCC.

This study provides new insights into the role of IMRGs in the pathogenesis of HCC, and presents a novel signature (6-IS) to predict the prognosis of HCC.
This study provides new insights into the role of IMRGs in the pathogenesis of HCC, and presents a novel signature (6-IS) to predict the prognosis of HCC.
Long non-coding RNA (lncRNA) was frequently abnormally expressed in cancers. LINC00641 was reported to play crucial roles in regulating tumor progression. However, its role in prostate cancer (PCa) has not been fully explored.

In this work, proliferation, invasion and apoptosis assays were performed to detect the biological roles of LINC00641 in PCa. Bioinformatic analyses, Luciferase activity reporter assay, and rescue experiments were performed to investigate the potential mechanisms of LINC00641 in PCa. Expression levels of LINC00641, microRNA-365a-3p (miR-365a-3p), and vestigial like family member 4 (VGLL4) in PCa tissues and normal tissues were analyzed at ENCORI.

We found LINC00641 and VGLL4 was reduced, while miR-365a-3p was elevated expression in PCa tissues compared with normal tissues. LINC00641 overexpression inhibited growth and invasion abilities of PCa cells in vitro. Functional assays revealed that miR-365a-3p/VGLL4 pair was the downstream targets of LINC00641.

The findings of our work provided evidence that LINC00641 serves as a tumor suppressive lncRNA in PCa by regulating miR-365a-3p/VGLL4 axis.
The findings of our work provided evidence that LINC00641 serves as a tumor suppressive lncRNA in PCa by regulating miR-365a-3p/VGLL4 axis.
To explore the effect and mechanism of miR-217 in cisplatin resistance, as well as invasion and metastasis of ovarian cancer by inhibiting the expression of Cullin 4B (CUL4B) and the activation of Wnt/β-catenin signaling pathway.

Human ovarian cancer cell lines COC1 (cisplatin sensitive) and COC1/DDP (cisplatin resistant) were cultured and were used to construct the COC1 group and COC1/DDP group, respectively. COC1/DDP cells were divided into blank group, NC group, miR-217 mimic group, miR-217 mimic NC group, miR-217 inhibitor group, miR-217 inhibitor NC group, si-CUL4B group, si-CUL4B NC group, overexpressed (oe) oe-CUL4B group, oe-CUL4B NC group, and miR-217 mimic +oe-CUL4B group, with the identification of cell transfection simultaneously. Bioinformatics prediction and Dual-Luciferase reporter gene assay of the targeting effect of miR-217 on CUL4B were performed, followed by MTT assay for cell proliferation, associated with the measurement of median inhibitory concentration (IC50). Real-time quantitatin, IC50, invasion and migration, and decreased apoptosis (all p<0.05).

CUL4B gene is the target gene of miR-217. MiR-217 can silence the expression of this gene, and inhibit the activation of Wnt/β-catenin signaling pathway to enhance the cisplatin sensitivity and reverse drug resistance, inhibit cell invasion and migration, and promote cell apoptosis.
CUL4B gene is the target gene of miR-217. MiR-217 can silence the expression of this gene, and inhibit the activation of Wnt/β-catenin signaling pathway to enhance the cisplatin sensitivity and reverse drug resistance, inhibit cell invasion and migration, and promote cell apoptosis.
Circular RNAs (circRNAs) could regulate gene expression which may induce tumor occurrence and progression. In the current study, we first investigated the expression of circMTO1 in osteosarcoma, and the underlying mechanism was further elucidated.

Circular RNA microarrays were used to identify the differential expression of circRNAs in osteosarcoma tissues and the corresponding normal tissues. qRT-PCR was used to examine the level of circMTO1 in osteosarcoma tissues and cell lines. In addition, circMTO1 overexpression was constructed using lentiviral transfection in cell lines. Subsequently, the Cell Counting Kit-8 (CCK8), cell migration and invasion, and flow cytometry were used to investigate the effect of circMTO1 on the biological functions of cells. The Western Blot and the recovery experiments were used to explore the potential mechanism.

Here, we measured 20 circRNAs which were downregulated in osteosarcoma tissues using circRNA microarray. Bomedemstat CircMTO1 expression was decreased in osteosarcoma cell lines.
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