Role of Exosomes in Cancer and Aptamer-Modified Exosomes as a Promising Platform for Cancer Targeted Therapy.

Exosomes are increasingly recognized as important mediators of intercellular communication in cancer biology. Exosomes can be derived from cancer cells as well as cellular components in tumor microenvironment. After secretion, the exosomes carrying a wide range of bioactive cargos can be ingested by local or distant recipient cells. The released cargos act through a variety of mechanisms to elicit multiple biological effects and impact most if not all hallmarks of cancer. Moreover, owing to their excellent biocompatibility and capability of being easily engineered or modified, exosomes are currently exploited as a promising platform for cancer targeted therapy. In this review, we first summarize the current knowledge of roles of exosomes in risk and etiology, initiation and progression of cancer, as well as their underlying molecular mechanisms. The aptamer-modified exosome as a promising platform for cancer targeted therapy is then briefly introduced. We also discuss the future directions for emerging roles of exosome in tumor biology and perspective of aptamer-modified exosomes in cancer therapy.

Plant long noncoding RNAs: Recent progress in understanding their roles in growth, development, and stress responses.

Long noncoding RNA (lncRNA) transcripts are longer than 200 nt and are not translated into proteins. LncRNAs function in a wide variety of processes in plants and animals, but, perhaps because of their lower expression and conservation levels, plant lncRNAs had attracted less attention than protein-coding mRNAs. Now, recent studies have made remarkable progress in identifying lncRNAs and understanding their functions. In this review, we discuss a number of lncRNAs that have important functions in growth, development, reproduction, responses to abiotic stresses, and regulation of disease and insect resistance in plants. Additionally, we describe the known mechanisms of action of plant lncRNAs according to their origins within the genome. This review thus provides a guide for identifying and functionally characterizing new lncRNAs in plants.

Comprehensive transcriptomic analysis of three varieties with different brown planthopper-resistance identifies leaf sheath lncRNAs in rice.

BACKGROUND: Long non-coding RNAs (lncRNAs) have been brought great attention for their crucial roles in diverse biological processes. However, systematic identification of lncRNAs associated with specialized rice pest, brown planthopper (BPH), defense in rice remains unexplored. RESULTS: In this study, a genome-wide high throughput sequencing analysis was performed using leaf sheaths of susceptible rice Taichung Native 1 (TN1) and resistant rice IR36 and R476 with and without BPH feeding. A total of 2283 lncRNAs were identified, of which 649 lncRNAs were differentially expressed. During BPH infestation, 84 (120 in total), 52 (70 in total) and 63 (94 in total) of differentially expressed lncRNAs were found only in TN1, IR36 and R476, respectively. Through analyzing their cis-, trans-, and target mimic-activities, not only the lncRNAs targeting resistance genes (NBS-LRR and RLKs) and transcription factors, but also the lncRNAs acting as the targets of the well-studied stress-related miRNAs (miR2118, miR528, and miR1320) in each variety were identified. Before the BPH feeding, 238 and 312 lncRNAs were found to be differentially expressed in TN1 vs. IR36 and TN1 vs. R476, respectively. Among their putative targets, the plant-pathogen interaction pathway was significantly enriched. It is speculated that the resistant rice was in a priming state by the regulation of lncRNAs. Furthermore, the lncRNAs extensively involved in response to BPH feeding were identified by Weighted Gene Co-expression Network Analysis (WGCNA), and the possible regulation networks of the key lncRNAs were constructed. These lncRNAs regulate different pathways that contribute to the basal defense and specific resistance of rice to the BPH. CONCLUSION: In summary, we identified the specific lncRNAs targeting the well-studied stress-related miRNAs, resistance genes, and transcription factors in each variety during BPH infestation. Additionally, the possible regulating network of the lncRNAs extensively responding to BPH feeding revealed by WGCNA were constructed. These findings will provide further understanding of the regulatory roles of lncRNAs in BPH defense, and lay a foundation for functional research on the candidate lncRNAs.

Bone marrow mesenchymal stem cells-derived exosomal microRNA-16-5p restrains epithelial-mesenchymal transition in breast cancer cells via EPHA1/NF-κB signaling axis.

OBJECTIVE: This study intends to conquer the mystery of microRNA-16-5p/erythropoietin-producing hepatocellular A1/nuclear factor-κB signaling (miR-16-5p/EPHA1/NF-κB signaling) in breast cancer. METHODS: Expression of miR-16-5p, EPHA1 and NF-κB signaling-related proteins were detected. Gene overexpression or silencing was used to examine the biological roles of bone marrow mesenchymal stem cells (BMSCs)-derived exo-miR-16-5p in breast cancer. The effect of exo-miR-16-5p on tumorigenesis of breast cancer was confirmed by the xenograft nude mouse model. RESULTS: Low miR-16-5p and high EPHA1 expression were examined in breast cancer. BMSCs-derived exosomes, up-regulated miR-16-5p or down-regulated EPHA1 restrained epithelial-mesenchymal transition (EMT) of breast cancer cells and tumor growth in nude mice. Down-regulated miR-16-5p or up-regulated EPHA1 activated NF-κB signaling. Knockdown of EPHA1 or inhibition of NF-κB signaling reversed the effects of down-regulated miR-16-5p on breast cancer cells. CONCLUSION: BMSCs-derived exosomal miR-16-5p hinders breast cancer cells progression via EPHA1/NF-κB signaling axis.

Identification of differentially expressed genes and signaling pathways using bioinformatics in interstitial lung disease due to tyrosine kinase inhibitors targeting the epidermal growth factor receptor.

Interstitial lung disease (ILD) is a rare but lethal adverse effect of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) treatment. The specific mechanism of this disease is not fully understood. To systematically analyze genes associated with EGFR-TKI induced ILD, gene data of EGFR-TKI induced ILD were extracted initially using text mining, and then the intersection between genes from text mining and Gene Expression Omnibus (GEO) dataset was taken for further protein-protein interaction (PPI) analysis using String-bd database. Go ontology (GO) and pathway enrichment analysis was also conducted based on Database of Annotation, Visualization and Integrated Discovery (DAVID) platform. The PPI network generated by STRING was visualized by Cytoscape, and the topology scores, functional regions and gene annotations were analyzed using plugins of CytoNCA, molecular complex detection (MCODE) and ClueGo. 37 genes were identified as EGFR-TKI induced ILD related. Gene enrichment analysis yield 18 enriched GO terms and 12 associated pathways. A PPI network that included 199 interactions for a total of 35 genes was constructed. Ten genes were selected as hub genes using CytoNCA plugin, and four highly connected clusters were identified using MCODE plugin. GO and pathway annotation analysis for the cluster one revealed that five genes were associated with either response to dexamethasone or with lung fibrosis, including CTGF, CCL2, IGF1, EGFR and ICAM1. Our data might be useful to reveal the pathological mechanisms of EGFR-TKI induced ILD and provide evidence for the diagnosis and treatment in the future.

Genetic Deletion of Fbw7 in the mouse intestinal epithelium aggravated dextran sodium sulfate-induced colitis by modulating the inflammatory response of NF-κB pathway.

Fbw7 is a type of E3 ubiquitin ligase that targets various proteins for degradation and has been found to have a high expression level in progenitor cells. Deletion of Fbw7 in the intestine results in the accumulation of progenitor cells. Moreover, Fbw7 loss increases the susceptibility of colorectal cancer. However, the involvement of Fbw7 in the progress and development of inflammatory bowel disease (IBD) is still controversial. To identify the function of Fbw7 on dextran sodium sulfate (DSS)-induced colonic inflammation, we generated Fbw7ΔG mice, lacking Fbw7 specifically in intestinal epithelium. Colitis was induced in male Fbw7 ΔG and wild-type (WT) mice (both age and body weight matched) by treating with 3% DSS in drinking water. We demonstrate that deletion of Fbw7 in the mouse intestinal epithelium aggravates DSS-induced colitis, showing inflammatory response and reduced survival rate. Furthermore, we found that Fbw7 loss caused activation of NF-κB signaling. Thus, FBW7 plays a protective role in acute intestinal inflammation by modulating the inflammatory response of NF-κB pathway.

Targeting of Discoidin Domain Receptor 2 (DDR2) Prevents Myofibroblast Activation and Neovessel Formation During Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a lethal human disease with short survival time and few treatment options. Herein, we demonstrated that discoidin domain receptor 2 (DDR2), a receptor tyrosine kinase that predominantly transduces signals from fibrillar collagens, plays a critical role in the induction of fibrosis and angiogenesis in the lung. In vitro cell studies showed that DDR2 can synergize the actions of both transforming growth factor (TGF)-ß and fibrillar collagen to stimulate lung fibroblasts to undergo myofibroblastic changes and vascular endothelial growth factor (VEGF) expression. In addition, we confirmed that late treatment of the injured mice with specific siRNA against DDR2 or its kinase inhibitor exhibited therapeutic efficacy against lung fibrosis. Thus, this study not only elucidated novel mechanisms by which DDR2 controls the development of pulmonary fibrosis, but also provided candidate target for the intervention of this stubborn disease.

Protective autophagy promotes the resistance of HER2-positive breast cancer cells to lapatinib.

Lapatinib, a tyrosine kinase inhibitor of HER2/EGFR, can inhibit the proliferation of HER2-positive breast cancer cells. Additionally, the combination of lapatinib and chemotherapy can markedly prolong patient survival time. However, the clinical therapeutic effect of lapatinib is severely limited by drug resistance. We previously found that brief treatment with lapatinib induced both apoptosis and autophagy in HER2-positive breast cancer cells. Additionally, the apoptosis induced by lapatinib was dependent on autophagy. In our current study, however, we used extended treatment of HER2-positive breast cancer cells with lapatinib to confirm the presence of protective autophagy in the previously established lapatinib-resistant cells. Specifically, we found that inhibition of autophagy could reduce the proliferation, DNA synthesis, and colony-forming capacity of resistant cells. Thus, autophagy is a potential novel therapeutic target for reversing lapatinib resistance of HER2-positive breast cancer cells. Our data provide clear, novel evidence of both anti-apoptotic and pro-apoptotic functions of autophagy in breast cancer during lapatinib treatment.

Histochemical analysis of testis specific gene 13 in human normal and malignant tissues.

Testis-specific gene 13 (TSGA13) is abundantly expressed in testis. As previous studies of TSGA13 expression pattern have all been based on mRNA analysis, it is imperative to investigate its actual protein expression. Here, we first examined TSGA13 gene tree and protein homology among species, and found that TSGA13 is relatively well conserved. Next, we detected its protein expression in normal human tissues as well as in a limited number of malignant tumors by immunohistochemistry (IHC). It was demonstrated that, in addition to testis, high expression of TSGA13 could also be observed in multiple normal tissues, including stomach, larynx, spleen, bladder, tonsil, liver and thyroid. Notably, most types of human carcinoma tissues displayed reduced expression of TSGA13 rather than their adjacent normal tissues except glioblastoma and lung cancer. Hence, the data from the current study strongly suggest the association between TSGA13 and tumor malignancy.

The effect of Fe2O3 and ZnO nanoparticles on cytotoxicity and glucose metabolism in lung epithelial cells.

Metallic nanoparticles (NPs) have potential applications in industry and medicine, but they also have the potential to cause many chronic pulmonary diseases. Mechanisms for their cytotoxicity, glucose and energy metabolism responses need to be fully explained in lung epithelial cells after treatment with metallic nanoparticles. In our study, two different metallic nanoparticles (Fe2 O3 and ZnO) and two cell-based assays (BEAS-2B and A549 cell lines) were used. Our findings demonstrate that ZnO nanoparticles, but not Fe2 O3 nanoparticles, induce cell cycle arrest, cell apoptosis, reactive oxygen species (ROS) production, mitochondrial dysfunction and glucose metabolism perturbation, which are responsible for cytotoxicity. These results also suggest that the glucose metabolism and bioenergetics had a great potential in evaluating the cytotoxicity and thus were very helpful in understanding their underlying molecular mechanisms.

Hypercholesterolemia increases the production of leukotriene B4 in neutrophils by enhancing the nuclear localization of 5-lipoxygenase.

AIMS: Neutrophils can synthesize leukotriene B4 (LTB4) by activating the 5-lipoxygenase (5-LO)signaling pathway. LTB4 is a pro-inflammatory mediator associated with the etiology and progression of atherosclerosis. It can increase function and number of neutrophils in an autocrine manner. Since hypercholesterolemia is associated with an increase in the number and function of neutrophils, we hypothesized that this effect could be mediated through increased production of LTB4 in neutrophils. METHODS/RESULTS: Hypercholesterolemia was modeled in Wistar rats by feeding them with a high cholesterol diet. The induction of hypercholesterolemia caused an increase in the plasma levels of LTB4, following lipopolysaccharide stimulation. This effect was recapitulated in vitro, both in the presence and absence of stimulation with the activator of 5-LO, A23187. Neutrophils in hypercholesterolemia rats expressed similar total levels of 5-LO as control rats, but displayed increased nuclear localization of 5-LO, as well as elevated levels of phosphorylated 5-LO and ERK1/2. In vitro, MßCD/cholesterol complexes enriched cholesterol in neutrophils, resulted in similar changes in 5-LO/LTB4. In addition, these alterations could be inhibited with the ERK inhibitor PD98059. CONCLUSION: Hypercholesterolemia increases LTB4 production in neutrophils by increasing the nuclear localization of 5-LO, which is the result of its phosphorylation by activated ERK1/2.

Exosomal miR-221/222 enhances tamoxifen resistance in recipient ER-positive breast cancer cells.

Recent studies have demonstrated that specific miRNAs, such as miR-221/222, may be responsible for tamoxifen resistance in breast cancer. Secreted miRNAs enclosed in exosomes can act as intercellular bio-messengers. Our objective is to investigate the role of secreted miR-221/222 in tamoxifen resistance of ER-positive breast cancer cells. Transmission electron microscopy analysis and nanoparticle tracking analysis were performed to determine the exosomes difference between MCF-7(TamR) (tamoxifen resistant) and MCF-7(wt) (tamoxifen sensitive) cells. PKH67 fluorescent labeling assay was used to detect exosomes derived from MCF-7(TamR) cells entering into MCF-7(wt) cells. The potential function of exosomes on tamoxifen resistance transmission was analyzed with cell viability, apoptosis ,and colony formation. MiRNA microarrays and qPCR were used to detect and compare the miRNAs expression levels in the two cells and exosomes. As the targets of miR-221/222, p27 and ERα were analyzed with western blot and qPCR. Compared with the MCF-7(wt) exosomes, there were significant differences in the concentration and size distribution of MCF-7(TamR) exosomes. MCF-7(wt) cells had an increased amount of exosomal RNA and proteins compared with MCF-7(TamR) cells. MCF-7(TamR) exosomes could enter into MCF-7(wt) cells, and then released miR-221/222. And the elevated miR-221/222 effectively reduced the target genes expression of P27 and ERα, which enhanced tamoxifen resistance in recipient cells. Our results are the first to show that secreted miR-221/222 serves as signaling molecules to mediate communication of tamoxifen resistance.

Metformin enhances tamoxifen-mediated tumor growth inhibition in ER-positive breast carcinoma.

BACKGROUND: Tamoxifen, an endocrine therapy drug used to treat breast cancer, is designed to interrupt estrogen signaling by blocking the estrogen receptor (ER). However, many ER-positive patients are low reactive or resistant to tamoxifen. Metformin is a widely used anti-diabetic drug with noteworthy anti-cancer effects. We investigated whether metformin has the additive effects with tamoxifen in ER-positive breast cancer therapy. METHODS: The efficacy of metformin alone and in combination with tamoxifen against ER-positive breast cancer was analyzed by cell survival, DNA replication activity, plate colony formation, soft-agar, flow cytometry, immunohistochemistry, and nude mice model assays. The involved signaling pathways were detected by western blot assay. RESULTS: When metformin was combined with tamoxifen, the concentration of tamoxifen required for growth inhibition was substantially reduced. Moreover, metformin enhanced tamoxifen-mediated inhibition of proliferation, DNA replication activity, colony formation, soft-agar colony formation, and induction of apoptosis in ER-positive breast cancer cells. In addition, these tamoxifen-induced effects that were enhanced by metformin may be involved in the bax/bcl-2 apoptotic pathway and the AMPK/mTOR/p70S6 growth pathway. Finally, two-drug combination therapy significantly inhibited tumor growth in vivo. CONCLUSION: The present work shows that metformin and tamoxifen additively inhibited the growth and augmented the apoptosis of ER-positive breast cancer cells. It provides leads for future research on this drug combination for the treatment of ER-positive breast cancer.

Unilateral bi-portal endoscopy for the treatment of thalassemia with extramedullary hematopoietic compression of the spinal cord: Two case reports.

RATIONALE: Thalassemia combined with extramedullary hematopoietic spinal cord compression is extremely rare; its ideal treatment is still controversial. Herein, we present 2 cases of thalassemia combined with extramedullary hematopoietic compression of the spinal cord wherein satisfactory results were obtained using unilateral bi-portal endoscopy (UBE). PATIENT CONCERNS: Case 1 was of a 43-year-old male who presented with a chief complaint of numbness of the left lower limb since 1-month. Case 2 involved a 23-year-old male who was admitted to the hospital with a chief complaint of numbness in both toes since 3 months and walking instability since 2 weeks. Both cases had a history of being diagnosed with thalassemia. DIAGNOSES: Computed tomography and magnetic resonance imaging showed spinal canal space-occupying lesions causing dural compression and spinal stenosis. Postoperative pathology confirmed the spinal canal lesions to be extramedullary hematopoietic tissue. INTERVENTIONS: For spinal canal decompression, UBE supplemented by blood transfusion was performed for both cases. OUTCOMES: All preoperative symptoms were relieved postoperatively; no recurrence was noted at the 6-month follow-up. LESSONS: Thalassemia combined with extramedullary hematopoiesis can lead to acute spinal cord compression. UBE significantly relieves spinal stenosis symptoms; furthermore, UBE combined with blood transfusion for spinal canal extramedullary hematopoiesis gives satisfactory results, is safe, and has a low risk of spinal cord injury.

Recycling and Recovery of Deactivated CsPbBr3 Perovskite after Photocatalytic CO2 Reduction Reaction.

CsPbBr3 perovskite nanocrystals have emerged as promising candidates for photocatalysis. However, their conversion efficiency is hampered by material instability, and the accumulation of deactivated perovskites produced after photocatalytic reactions raises significant environmental concerns. To address this issue, we developed a mechanochemical grinding approach assisted by oleylamine as an additive to restore the optical properties and photocatalytic activity of deactivated CsPbBr3, which was due to aggregation in the photocatalytic CO2 reduction reaction. Upon regeneration, the CsPbBr3 nanocrystals exhibited an average length of 34.21 nm and an average width of 20.86 nm, demonstrating optical properties comparable to those of the pristine CsPbBr3 nanocrystals. Moreover, they achieved a conversion efficiency of 88.7% compared with pristine CsPbBr3 nanocrystals in the photocatalytic CO2 reduction reaction. This method effectively enhanced the utilization of CsPbBr3, offering a novel approach for the recycling and recovery of perovskite materials and thereby minimizing material waste and environmental pollution.

Integrated metabolomic and transcriptomic analyses of two peanut (Arachis hypogaea L.) cultivars differing in amino acid metabolism of the seeds.

Peanut is an important economic crop worldwide. The content of amino acids, especially essential amino acids, is an important nutritional quality trait of peanut seeds. However, the regulation of amino acid metabolism in peanut seeds is poorly understood. Here, two peanut cultivars, Zhonghuahei 1 and Zhongkaihua 151, with high and low free amino acids in mature seeds, respectively, were selected to investigate the regulatory mechanisms of amino acids during seed development. Zhonghuahei 1 is composed of significantly higher arginine (Arg), asparagine (Asn), and glutamate (Glu) contents than Zhongkaihua 151. However, the metabolomic analyses indicated that the contents of most amino acids were significantly lower in Zhonghuahei 1 at the early developmental stage, while they were reverse at the middle and late stages. Transcriptomic analyses also revealed that the differentially expressed genes between the two cultivars during different stages were enriched in multiple pathways associated with amino acid metabolism. Among them, the Arg biosynthesis pathway showed different regulatory profiles between the two cultivars according to the temporal analysis of gene expression patterns. Subsequent gene co-expression network analysis showed that the gene module darkorange was significantly correlated with Arg content, with an enriched Arg biosynthesis pathway. Accordingly, a gene regulatory network for Arg biosynthesis and metabolism, including key genes (ALDH, ASS1, OTC, and GAD) and transcription factors (GATA, HEX, and ATF), was constructed. These findings provide insights into the regulatory network of amino acid metabolism in peanuts and provide candidate genes that can be applied to facilitate peanut breeding with desirable seeds.

Analysis and Experimental Validation of Rheumatoid Arthritis Innate Immunity Gene CYFIP2 and Pan-Cancer.

Rheumatoid arthritis (RA) is a chronic, heterogeneous autoimmune disease. Its high disability rate has a serious impact on society and individuals, but there is still a lack of effective and reliable diagnostic markers and therapeutic targets for RA. In this study, we integrated RA patient information from three GEO databases for differential gene expression analysis. Additionally, we also obtained pan-cancer-related genes from the TCGA and GTEx databases. For RA-related differential genes, we performed functional enrichment analysis and constructed a weighted gene co-expression network (WGCNA). Then, we obtained 490 key genes by intersecting the significant module genes selected by WGCNA and the differential genes. After using the RanddomForest, SVM-REF, and LASSO three algorithms to analyze these key genes and take the intersection, based on the four core genes (BTN3A2, CYFIP2, ST8SIA1, and TYMS) that we found, we constructed an RA diagnosis. The nomogram model showed good reliability and validity after evaluation, and the ROC curves of the four genes showed that these four genes played an important role in the pathogenesis of RA. After further gene correlation analysis, immune infiltration analysis, and mouse gene expression validation, we finally selected CYFIP2 as the cut-in gene for pan-cancer analysis. The results of the pan-cancer analysis showed that CYFIP2 was closely related to the prognosis of patients with various tumors, the degree of immune cell infiltration, as well as TMB, MSI, and other indicators, suggesting that this gene may be a potential intervention target for human diseases including RA and tumors.

CLP1 is a Prognosis-Related Biomarker and Correlates With Immune Infiltrates in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic, heterogeneous autoimmune disease with a high disability rate that seriously affects society and individuals. However, there is a lack of effective and reliable diagnostic markers and therapeutic targets. In this study, we identified diagnostic markers of RA based on RNA modification and explored its role as well as degree of immune cell infiltration. We used the gene expression profile data of three synovial tissues (GSE55235, GSE55457, GSE77298) from the Gene Expression Omnibus (GEO) database and the gene of 5 RNA modification genes (including m6A, m1A, m5C, APA, A-1), combined with cluster analysis, identified four RNA modifiers closely related to RA (YTHDC1, LRPPRC, NOP2, and CLP1) and five immune cells namely T cell CD8, CD4 memory resting, T cells regulatory (Tregs) Macrophages M0, and Neutrophils. Based on the LASSO regression algorithm, hub genes and immune cell prediction models were established respectively in RA and a nomogram based on the immune cell model was built. Around 4 key RNA modification regulator genes, miRNA-mRNA, mRNA-TF networks have been established, and GSEA-GO, KEGG-GSEA enrichment analysis has been carried out. Finally, CLP1 was established as an effective RA diagnostic marker, and was highly positively correlated with T cells follicular helper (Tfh) infiltration. On the other hand, highly negatively correlated with the expression of mast cells. In short, CLP1 may play a non-negligible role in the onset and development of RA by altering immune cell infiltration, and it is predicted to represent a novel target for RA clinical diagnosis and therapy.

Comparison of clinical and radiological outcomes of full-endoscopic versus microscopic lumbar decompression laminectomy for the treatment of lumbar spinal stenosis: a systematic review and meta-analysis.

BACKGROUND: To determine the clinical and radiological outcomes of full-endoscopic (FE) versus microscopic (MI) lumbar decompression laminectomy in the treatment of lumbar spinal stenosis (LSS), we performed a meta-analysis to explore the best choice for patients with LSS requiring surgical relief. METHODS: Literature searches of the PubMed, the Cochrane Library, Embase, Medline, Embase, and Web of Science databases were performed. The searches covered all indexed studies published between 2008 and 2020, using keywords identifying the patient group (lumbar spine stenosis) and the interventions (full-endoscopic lumbar decompression laminectomy and microscopic lumbar decompression laminectomy). A total of 1,727 patients were included in 10 studies. The primary outcomes of the analysis were visual analogue scale (VAS) scores for leg and back pain, and Oswestry Disability Index (ODI) score. RESULTS: The meta-analysis of the VAS score for low back pain showed that in the first 24 hours postoperatively, participants who underwent FE had better pain control than those who underwent MI [FE: mean difference (MD) =-0.78, 95% confidence interval (CI): -1.11, -0.45; MI: MD =-1.53, 95% CI: -1.94, -1.12]. In all subgroup analyses, the VAS score for back pain was lower in the FE group than in the MI group (MD =-0.71, 95% CI: -0.96, -0.47). Regarding the VAS score for leg pain, the FE group had a significantly lower score than the MI group in the first 24 hours (Total: MD =-1.02, 95% CI: -1.31, -0.73). The meta-analysis demonstrated that the FE group had a significantly lower ODI score than the MI group (MD =-1.03, 9% CI: -1.54, -0.51). At 6 months, the MI group had a significantly lower score than the FE group (MD =1.09, 95% CI: 0.53, 1.64), but at 12 months, the FE group had a significantly lower score than the MI group (MD =-2.40, 95% CI: -3.12, -1.67). DISCUSSION: Compared to MI decompression, the FE decompression method resulted in better pain control in the early postoperative period, both in the lower back and legs, as well as shorter operative and shorter hospitalization times.

MiR-30a-5p frequently downregulated in prostate cancer inhibits cell proliferation via targeting PCLAF.

MicroRNAs (miRNAs) have vastly expanded our view of RNA world in intracellular signal regulating networks. Here, we functionally characterized a normally highly expressed miRNA, miR-30a-5p (MIMAT0000087), which exhibits downregulated expression profiles in prostate cancer samples. MiR-30a-5p knockdown and overexpression in PC-3 cell line alters cell proliferation supporting a tumour suppressor role. We also discovered that PCLAF is the direct target of miR-30a-5p. Notably, PC-3 cell proliferation is inhibited by miR-30a-5p/PCLAF axis. miR-30a-5p represents a novel molecule of functionally important miRNAs which may shed light on the novel therapeutic targets for prostate cancer.