Notes

Trigeminal neuropathy: Two case studies of gasserian ganglion stimulation.
eutic potential for advanced PCa.
Taken together, our results show that PVT1 acts as an inducer of PCa metastasis via targeting miRNAs, thereby promoting NOP2. This axis may have diagnostic and therapeutic potential for advanced PCa.
Exosomal microRNAs (miRNAs) play essential roles in the development of hepatocellular carcinoma (HCC). Nevertheless, the role and mechanism of exosomal miR-638 in HCC development remain largely unknown.

Exosomes were isolated and confirmed via transmission electron microscopy and western blot. The abundances of miR-638 and specificity protein 1 (SP1) were measured via quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation was investigated by Cell Counting Kit-8, colony formation assay, apoptosis, cell cycle distribution and related protein expression. Cell migration and invasion were detected via transwell assay and western blot. Co-culture experiment was performed to assess exosome transfer from HCC cells to endothelial cells. The target correlation between miR-638 and SP1 was analyzed via dual-luciferase reporter and RNA immunoprecipitation assays. The subcutaneous xenograft experiment was conducted to test the function of miR-638 in vivo.

The miR-638 level declined in exosomes from serum or HCC cell medium. miR-638 overexpression repressed HCC cell proliferation by decreasing viability and colony formation and inducing apoptosis and cell cycle arrest at G1 phase, and decreased abilities of migration and invasion. Exosomal miR-638 from HCC cells could transfer to human umbilical vein endothelial cells (HUVECs) and suppress HUVEC proliferation, migration and invasion. SP1 was a target of miR-638 and overexpression of SP1 reversed the effect of miR-638 on HCC cells. Overexpression of miR-638 reduced xenograft tumor growth via decreasing SP1.

Exosomal miR-638 inhibited HCC tumorigenesis by targeting SP1. This study indicated the potential clinical implications of miR-638 in HCC.
Exosomal miR-638 inhibited HCC tumorigenesis by targeting SP1. This study indicated the potential clinical implications of miR-638 in HCC.
Ribosome binding protein 1 (RRBP1) is reported to be correlated with tumor formation and progression. However, the role of RRBP1 in bladder cancer is unclear. In this study, we aimed to investigate the expression of RRBP1 and its influence on cell proliferation in bladder cancer.

Quantification real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) were used to detect the expression levels of RRBP1 in 138 bladder cancer and matched adjacent normal bladder tissues. Then, the clinical significance of RRBP1 in bladder cancer was evaluated. The effect of RRBP1 on cell proliferation and its potential mechanism were further explored.

Results show that the mRNA levels of RRBP1 in bladder cancer were significantly higher compared with those in normal tissues (
< 0.001). IHC results show the high-expression rate of RRBP1 in bladder cancer was 68.8%, which was significantly greater than those in normal tissues (40.6%,
< 0.001). RRBP1 high-expression was significantly associated with differentiation, T stage and lymph node metastasis in bladder cancer (
< 0.05). The overall survival time of patients with RRBP1 high-expression was significantly reduced compared to those with RRBP1 low-expression. Moreover, RRBP1 overexpression significantly promoted cell proliferation, which was correlated with Smad1/Smad3/TGF-β1 signal pathway.

RRBP1 high-expression correlates with prognosis and promotes cell proliferation in bladder cancer, which could be a potential biomarker.
RRBP1 high-expression correlates with prognosis and promotes cell proliferation in bladder cancer, which could be a potential biomarker.
Pediatric acute promyelocytic leukemia (APL) accounts for 10% of pediatric acute myelogenous leukemia (AML) case and is accompanied by a tendency to hemorrhage. miR-188-5p plays an important role in adult AML. Therefore, the purpose of this study was to explore the effects of miR-188-5p on cell proliferation and apoptosis and tumor growth, and its mechanism in pediatric APL patients.

Survival-associated miRNAs or mRNAs from TCGA database associated with AML were identified via using the "survival R" package in R language. CCK8, clone formation, flow cytometry, RT-PCR, immunohistochemistry and Western blot assays were used to detect the viability, proliferation, apoptosis, cell cycle, and related gene expression in APL cell lines. The prognostic value of miR-188-5p was evaluated using a ROC curve. The tumorigenic ability of APL cell lines was determined using a nude mouse transplantation tumor experiment. Tumor cell apoptosis was determined by TUNEL assay in vivo. The target genes of miR-188-5p were predicprogression of pediatric APL in vitro and in vivo via targeting CD2AP and activating the PI3K/AKT/mTOR signaling pathway.
Evidence indicates that the actin-binding protein Coronin 3, which is aberrantly expressed in various cancers, is associated with cancer development and progression. However, little is known about the role of Coronin 3 in glioma tumorigenesis. Here, we aimed to explore the biological function and regulatory mechanism of Coronin 3 in glioblastoma (GBM).

Coronin 3 level in human GBM clinical samples and cell lines was investigated. The shRNA knockdown strategy was used to assess the tumor characteristics of GBM cell lines. The role of β-catenin in Coronin 3-mediated oncogenic phenotypes was evaluated.

Coronin 3 was found to be highly upregulated in glioma cell lines. Furthermore, knockdown of Coronin 3 significantly inhibited the growth of glioma cells both in vivo and in vitro and suppressed the expression of Wnt/β-catenin pathway genes, including β-catenin, Cyclin D1, and c-Myc. Moreover, we demonstrated that Coronin 3 regulates the expression of β-catenin in glioma. Our results revealed that Coronin 3-stimulated tumor growth was β-catenin-dependent.

Our study reveals a new molecular mechanism of Coronin 3 in promoting glioma growth and development through regulating the Wnt/β-catenin signaling pathway.
Our study reveals a new molecular mechanism of Coronin 3 in promoting glioma growth and development through regulating the Wnt/β-catenin signaling pathway.
Colorectal cancer is one of the most common cancers and the second leading cause of cancer-related deaths worldwide. Targeting cancer stem cells (CSCs) may be a novel strategy for the treatment of colorectal cancer. Previous studies have shown that bone marrow-derived MSCs (BM-MSCs) promote tumor growth and metastasis. However, the role of rat BM-MSCs in the biological behaviors of colorectal CSCs remains unclear until now.

BM-MSCs were isolated from rats and characterized. CSCs were enriched from HCT116 cells using the microsphere culture method, and the microspheres incubated for at least 10 passages were termed HCT116-CSCs that were characterized. The effects of rat BM-MSCs on migration and invasion of HCT116-CSCs were examined using transwell migration and invasion assays and xenograft tumor growth assay.

Rat BM-MSCs appeared typical stem cell morphology. Flow cytometry revealed positive CD29 and CD44 expression in rat BM-MSCs at passage 3, and rat BM-MSCs were found to differentiate into osteocytes following incubation in osteogenic induction medium. Microscopy, flow cytometric detection of stem cell surface markers, colony-formation assay and transwell migration and invasion assays characterized the successful preparation of HCT116-CSCs, and subcutaneous injection of HCT116-CSCs produced xenograft tumors in nude mice, while HE staining of the xenograft tumors displayed cancer specimen shapes. Transwell migration and invasion assays showed that rat BM-MSCs promoted the migration and invasion of HCT116-CSCs, and injection of rat BM-MSCs was found to promote the growth of the mouse xenograft tumor derived from HCT116-CSCs.

Rat BM-MSCs promote the migration and invasion of colorectal CSCs, and colorectal CSCs may be a potential target for the therapy against colorectal cancer.
Rat BM-MSCs promote the migration and invasion of colorectal CSCs, and colorectal CSCs may be a potential target for the therapy against colorectal cancer.
Although assertion that long non-coding RNA (lncRNA) exerts crucial functions in the progression of multiple myeloma (MM) is well documented, few studies investigate function and underlying mechanism of long intergenic non-protein coding RNA 665 (LINC00665) in MM.

A total of 25 MM patient samples and 15 healthy volunteer samples were collected, and quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the expressions of LINC00665. PSMD10 and ASF1B expressions were determined by qRT-PCR and Western blot assays. U266 cell and H929 cell were used in functional experiments. Besides, CCK-8 assay and flow cytometry analysis were utilized to determine cell proliferation and apoptosis. Bioinformatics analysis and dual-luciferase reporter assays were used to predict and verify the targeting relationships between LINC00665 and miR-214-3p, PSMD10 and miR-214-3p, as well as ASF1B and miR-214-3p. Moreover, the regulatory function of LINC00665 on the expression of PSMD10 and ASF1B was detected by Western blot.

The expression of LINC00665 was up-regulated in MM samples and cell lines. In vitro functional assays indicated that LINC00665 enhanced MM cell proliferation and inhibited its apoptosis. PSMD10 and ASF1B were identified as target genes of miR-214-3p. Additionally, LINC00665 negatively regulated miR-214-3p expression through sponging miR-214-3p and positively regulated PSMD10 and ASF1B.

LINC00665 can promote the expression of PSMD10 and ASF1B by inhibiting the expression of miR-214-3p, thus facilitating the proliferation and inhibiting apoptosis of MM cells.
LINC00665 can promote the expression of PSMD10 and ASF1B by inhibiting the expression of miR-214-3p, thus facilitating the proliferation and inhibiting apoptosis of MM cells.
The aim of this study was to provide a scoping review of the impact of pharmacist-led interventions on medication adherence and clinical outcomes in patients with hypertension and hyperlipidemia.

A scoping review was conducted using pre-defined search terms in three scientific databases, including Google Scholar, ScienceDirect, and PubMed. A multi-stage screening process that considered relevancy, publication year (2009-2019), English language, and article type (original research) was followed. Review articles, meta-analysis studies, and conference proceedings were excluded. Data charting was done in an iterative process using a study-specific extraction form.

Of the initially identified 681 studies, 17 studies with 136,026 patients were included in the review. Of these, 16 were randomized controlled trials, while the remaining study was a retrospective cohort study. The majority of pharmacist-led interventions were face-to-face counseling sessions (n=8), followed by remote- or telephone-based interventtics could increase the effectiveness of these interventions.
Pharmacist-led interventions were associated with improved patients' adherence to their medications but were less likely to be consistently associated with the attainment of clinical outcomes. MDL28170 Face-to-face counseling was the most commonly used intervention; while, the multi-faceted interventions were more likely to be effective in improving the overall outcome measures. The rigorous design of targeted interventions with more frequent follow-ups, careful consideration of the involved medications, and patients' characteristics could increase the effectiveness of these interventions.
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