Transcutaneous electrical cranial-auricular acupoint stimulation versus escitalopram for mild-to-moderate depression: An assessor-blinded, randomized, non-inferiority trial.

AIM: Transcutaneous electrical cranial-auricular acupoint stimulation (TECAS) is a novel non-invasive therapy that stimulates acupoints innervated by the trigeminal and auricular vagus nerves. An assessor-blinded, randomized, non-inferiority trial was designed to compare the efficacy of TECAS and escitalopram in mild-to-moderate major depressive disorder. METHODS: 468 participants received two TECAS sessions per day at home (n = 233) or approximately 10-13 mg/day escitalopram (n = 235) for 8 weeks plus 4-week follow-up. The primary outcome was clinical response, defined as a baseline-to-endpoint ≥50% reduction in Montgomery-Åsberg Depression Rating Scale (MADRS) score. Secondary outcomes included remission rate, changes in the severity of depression, anxiety, sleep and life quality. RESULTS: The response rate was 66.4% on TECAS and 63.2% on escitalopram with a 3.2% difference (95% confidence interval [CI], -5.9% to 12.9%) in intention-to-treat analysis, and 68.5% versus 66.2% with a 2.3% difference (95% CI, -6.9% to 11.4%) in per-protocol analysis. The lower limit of 95% CI of the differences fell within the prespecified non-inferiority margin of -10% (P ≤ 0.004 for non-inferiority). Most secondary outcomes did not differ between the two groups. TECAS-treated participants who experienced psychological trauma displayed a markedly greater response than those without traumatic experience (81.3% vs 62.1%, P = 0.013). TECAS caused much fewer adverse events than escitalopram. CONCLUSIONS: TECAS was comparable to escitalopram in improving depression and related symptoms, with high acceptability, better safety profile, and particular efficacy in reducing trauma-associated depression. It could serve an effective portable therapy for mild-to-moderate depression.

Integrated analysis of the functions of RNA binding proteins in clear cell renal cell carcinoma.

RNA binding proteins (RBPs) dysregulation is involved in the processes of various tumors. However, the roles of RBPs in clear cell renal cell carcinoma (ccRCC) remain poorly understand. In present study, we first performed consensus clustering and identified two clusters, of which cluster 2 was closely correlated with the malignancy of ccRCC. Differentially expressed RBPs between normal and tumor tissues were obtained, comprising 71 up-regulated and 44 down-regulated ones. Then, ten hub genes were selected and validated using The Human Protein Atlas database and receiver operating characteristic curves, showing good diagnostic value for cancers. Besides, we identified ten RBPs with the most useful prognostic values, and were used to construct a risk score model. The model could be used to stratify patients with different prognosis and phenotype distributions. The model showed good performance and can be used as a complementation for clinical factors to guide clinical practice in the future.

Optical Fiber Probe Microcantilever Sensor Based on Fabry-Perot Interferometer.

Optical fiber Fabry-Perot sensors have long been the focus of researchers in sensing applications because of their unique advantages, including highly effective, simple light path, low cost, compact size, and easy fabrication. Microcantilever-based devices have been extensively explored in chemical and biological fields while the interrogation methods are still a challenge. The optical fiber probe microcantilever sensor is constructed with a microcantilever beam on an optical fiber, which opens the door for highly sensitive, as well as convenient readout. In this review, we summarize a wide variety of optical fiber probe microcantilever sensors based on Fabry-Perot interferometer. The operation principle of the optical fiber probe microcantilever sensor is introduced. The fabrication methods, materials, and sensing applications of an optical fiber probe microcantilever sensor with different structures are discussed in detail. The performances of different kinds of fiber probe microcantilever sensors are compared. We also prospect the possible development direction of optical fiber microcantilever sensors.

How do soil microbes exert impact on soil respiration and its temperature sensitivity?

Understanding how soil microorganisms influence the direction and magnitude of soil carbon feedback to global warming is vital to predict future climate change. Although microbial activities are major contributors to soil respiration (RS ) and its temperature sensitivity (Q10 ), the mechanisms underpinning microbial influence on RS and Q10 remain unclear. Coupling variation partitioning analysis (VPA), correlation analysis and multiple stepwise linear regression analysis, we illustrate that bacteria mainly affect RS and its temperature sensitivity (Q10 ) by shifting bacterial community composition (denoted by principal coordinates analysis). We also found that soil water content (SWC) and available nutrient (AN) were the factor key to changing bacterial community composition (P < 0.05). Co-occurrence network demonstrated that Mod 0 ecological cluster composed of copiotrophic taxa groups was significantly associated with RS and Q10 (P < 0.01, R > 0.5), including Proteobacteria, Actinobacteria, and Bacteroidetes. Illuminating the mechanisms underpinning the influence of soil microbes on RS and Q10 values is fundamental to understanding mechanistic soil-climate carbon cycles.

Systematic analyses of the role of prognostic and immunological EIF3A, a reader protein, in clear cell renal cell carcinoma.

BACKGROUND: Eukaryotic initiation factor 3a (EIF3A), a "reader" protein for RNA methylation, has been found to be involved in promoting tumorigenesis in a variety of cancers. The impact of EIF3A in clear cell renal cell carcinoma (ccRCC) has yet to be reported. This study aimed to identify the prognostic value of EIF3A in ccRCC and investigate the relationship between EIF3A expression and immune infiltration. METHODS: We collected 29 m6A-related mRNA data and clinicopathological parameters from The Cancer Genome Atlas (TCGA) database. Logistic regression analyses were used to analyse the correlation between EIF3A expression and clinical characteristics. Immunohistochemistry (IHC) was applied to examine EIF3A levels in normal and ccRCC tissues. Univariate and multivariate analyses were conducted to recognize independent factors associated with overall survival (OS) and disease-free survival (DFS). The nomogram aimed to predict the 1-, 3- and 5-year survival probabilities. Gene set enrichment analysis (GSEA) was carried out to determine the potential functions and related signalling pathways of EIF3A expression. To investigate EIF3A of coexpressed genes, we used LinkedOmics, and the results were subjected to enrichment analysis. Simultaneously, LinkedOmics and STRING datasets were used to identify EIF3A coexpressed genes that were visualized via Cytoscape. Finally, we evaluated whether EIF3A expression correlated with the infiltration of immune cells and the expression of marker genes in ccRCC by Tumour Immune Estimation Resource (TIMER) and Gene Expression Profiling Interactive Analysis (GEPIA). RESULT: EIF3A expression was significantly different between ccRCC tissues and normal tissues. EIF3A expression was correlated with poor prognostic clinicopathological factors, and K-M analyses revealed that low EIF3A expression was correlated with a poor prognosis. The results of univariate and multivariate analyses proved that EIF3A was a prognostic factor in ccRCC patients. GSEA results indicated that EIF3A high expression was enriched in the renal cell carcinoma pathway. EIF3A expression was significantly positively correlated with B cells, CD8 + T cells, CD4 + T cells, neutrophils, macrophages, and dendritic cells. Furthermore, EIF3A expression was associated with most marker genes of immune cells. CONCLUSIONS: EIF3A could serve as a potential biomarker for prognostic and diagnostic stratification of ccRCC and is related to immune cell infiltrates.

IMPDH1/YB-1 Positive Feedback Loop Assembles Cytoophidia and Represents a Therapeutic Target in Metastatic Tumors.

Recently, cytoophidium, a nonmembrane-bound intracellular polymeric structure, has been shown to exist in various organisms, including tumor tissues, but its function and mechanism have not yet been examined. Examination of cytoophidia-assembled gene inosine monophosphate dehydrogenase (IMPDH) and cytidine triphosphate synthetase (CTPS) mRNA levels showed that only IMPDH1 levels were significantly higher in the clear cell renal cell carcinoma (ccRCC). IMPDH1 was positively correlated with the metastasis-related gene Y-box binding protein 1 (YB-1) and served as an independent prognostic factor in ccRCC. Kaplan-Meier analysis indicated that patients with tumors that expressed high IMPDH1 levels had a shorter overall survival (OS) and disease-free survival (DFS). Furthermore, detection of cytoophidia by immunofluorescence staining in ccRCC tissues showed that IMPDH1-assembled cytoophidia are positively associated with tumor metastasis. Mechanistically, IMPDH1 and YB-1 formed an autoregulatory positive feedback loop: IMPDH1 maintained YB-1 protein stabilization; YB-1 induced IMPDH1 expression by binding to the IMPDH1 promoter motif. Functionally, IMPDH1-assembled cytoophidia physically interacted with YB-1 and translocated YB-1 into the cell nucleus, thus correlating with ccRCC metastasis. Our findings provide the first solid theoretical rationale for targeting the IMPDH1/YB-1 axis to improve metastatic renal cancer treatment.

Effects of land use and land cover on soil erosion control in southern China: Implications from a systematic quantitative review.

The degradation of soil resources is accelerating owing to water erosion induced by detrimental land use/land cover (LULC) practices. Although the relationship between affecting factors associated with LULC and soil erosion has been well-documented, a systematic review of LULC for erosion control is lacking. A quantitative synthesis of 1270 runoff and 1302 sediment observations from 79 references covering 57 sites was conducted to assess the effects of LULC on erosion control in the red soil hilly region (RSHR) of southern China. The results indicated that the maximum runoff and soil loss were found in bare land (BL), but the minimum runoff and soil loss were detected in cropland and grassland, respectively. Among the 16 land use subtypes, BL left for natural succession had the highest runoff, but the lowest runoff was found in orchard with contact cover; the soil loss was largest for cropland without conservation measures, while the minimum value was detected in natural shrubland. When the vegetation coverage exceeded 60%, runoff and soil loss both tended to reach a stable rate. Land use with a multi-layer vegetation structure or ground/contact cover or broadleaf plant had less runoff and lower sediment values. In addition, soil loss decreased sharply during the initial 3 y of vegetation restoration, and then slowly declined until reaching a relatively stable rate after 15 y of succession. Our results confirmed that land use (except for BL) has a limited influence on soil erosion provided that suitable land cover is established. This study revealed that sustainable land management measures should be adopted based on local conditions to reduce soil erosion induced by irrational LULC. These findings can serve as a scientific basis for policy makers and land managers with respect to water erosion control in the RSHR.

Long noncoding RNA SNHG12 indicates the prognosis of prostate cancer and accelerates tumorigenesis via sponging miR-133b.

Prostate cancer (PCa) is the second leading cause of death among American men. Increasing evidence has shown that long noncoding RNAs (lncRNAs) play important roles in tumorigenesis of PCa. In this study, we explored the biological functions of small nucleolar RNA host gene 12 (SNHG12) and investigated the interaction between miR-133b and SNHG12 in the progression of PCa. Data was downloaded from The Cancer Genome Atlas and Human Cancer Metastasis Database, and clinicopathological characteristics were analyzed with relapse-free survival rate. We detected SNHG12 expression level in PCa cells and tissues, and then analyzed its clinical significance, which revealed that SNHG12 has the potent to predict prognosis of PCa. Bioinformatic analysis revealed that SNHG12 was closely related to the progression of PCa and could target candidate microRNA (miR-133b). After transfecting SNHG12 silencing plasmid and miR-133b mimic/sponge, biological function assays were conducted and results illustrated that SNHG12 associated with miR-133b exerted biological effects on cancer cell growth, migration, and invasion. Direct interactions between miR-133b and SNHG12 have been found and SNHG12 acts as an oncogene to promote tumorigenesis of PCa by sponging tumor suppressor gene miR-133b.

LncRNA SNHG3 promotes clear cell renal cell carcinoma proliferation and migration by upregulating TOP2A.

LncRNA plays a vital role in many diseases, and abnormal expression of LncRNA has been reported in many types of tumors. In this study, we analyzed the available public TCGA and GEO databases, and found that the expression of SNHG3 was increased in clear cell renal cell carcinoma (ccRCC), which was positively correlated with many clinicopathological parameters, and the higher expression of SNHG3 predicted worse clinical prognosis. Functional experiments indicated that knockdown of SNHG3 could significantly inhibit the proliferation and metastasis of ccRCC in vitro and in vivo. Subsequently, through luciferase reporter assays, qPCR and rescue experiments, it was found that SNHG3 could bind to miR-139-5p, thereby up-regulating the expression of its target gene TOP2A, and play a role in promoting tumor progression in ccRCC. The correlation analysis showed that there was a significant positive correlation between the expression of SNHG3 and TOP2A, and both of them were significantly negative correlated with the expression of miR-139-5p. Our work suggested that the SNHG3/miR-139-5p/TOP2A axis plays an important role in the proliferation and metastasis of ccRCC, and was expected to be a new biomarker for diagnosis, prognosis and a target for treatment of ccRCC.

Melatonin/PGC1A/UCP1 promotes tumor slimming and represses tumor progression by initiating autophagy and lipid browning.

Metabolic adaptations are emerging hallmarks of cancer progression and cellular transformation. Clear cell renal cell carcinoma (ccRCC) is a metabolic disease defined histologically by lipid accumulation and lipid storage, which promote tumor cell survival; however, the significance of eliminating the lipid remains unclear. Here, we demonstrate that melatonin activates transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1A (PGC1A) and uncoupling protein 1 (UCP1)-dependent lipid autophagy and a lipid browning program to elicit a catabolic state called "tumor slimming," thus suppressing tumor progression. Metabolic coregulator data analysis revealed that PGC1A expression was decreased in ccRCC tissues versus normal tissues, and poor patient outcome was associated with lower expression of PGC1A in The Cancer Genome Atlas (TCGA-KIRC). PGC1A was downregulated in ccRCC and associated with disease progression. Restoration of PGC1A expression by melatonin in ccRCC cells significantly repressed tumor progression and eliminated the abnormal lipid deposits. Furthermore, a phenomenon called "tumor slimming" was observed, in which tumor cell volume was reduced and lipid droplets transformed into tiny pieces. Additional studies indicated that melatonin promoted "tumor slimming" and suppressed ccRCC progression through PGC1A/UCP1-mediated autophagy and lipid browning. During this process, autophagy and lipid browning eliminate lipid deposits without providing energy. These studies demonstrate that the novel "tumor slimming" pathway mediated by melatonin/PGC1A/UCP1 exhibits prognostic potential in ccRCC, thus revealing the significance of monitoring and manipulating this pathway for cancer therapy.

RCAN1.4 acts as a suppressor of cancer progression and sunitinib resistance in clear cell renal cell carcinoma.

Clear cell renal cell carcinoma (ccRCC) is one of the most common malignant tumors in the urinary system, and its incidence continues to increase. Regulator of calcineurin 1 (RCAN1), one of the genes on chromosome 21, is a crucial mediator of tumor inhibition. RCAN1.4 is best characterized as an endogenous inhibitor of the phosphatase calcineurin, and it has been observed to be downregulated in numerous types of cancer. However, its essential function remains unclear in ccRCC. In the present study, we found that RCAN1.4 expression was frequently downregulated in renal cell carcinoma tissues and cells and was inversely correlated with various clinicopathological parameters. Low RCAN1.4 expression was associated with poor overall survival and disease-free survival and could act as a diagnostic indicator in ccRCC patients. Furthermore, the overexpression of RCAN1.4 inhibited cell proliferation, migration and invasion, whereas RCAN1.4 knockdown promoted these functions in ccRCC cell lines. In addition, RCAN1.4 expression was downregulated in sunitinib-resistant renal cancer cell lines, and inhibition of RCAN1.4 promoted sunitinib resistance. We also found that RCAN1.4 could regulate epithelial-mesenchymal transition (EMT) and the expression of HIF2α in sunitinib-resistant cell lines. Taken together, these findings indicate that downregulation of RCAN1.4 may be crucial for the metastasis of ccRCC and may induce sunitinib resistance. RCAN1.4 may act as a prognostic indicator and potential therapeutic target for ccRCC.

Regulation of glucose metabolism by p62/SQSTM1 through HIF1α.

The signaling adaptor sequestosome 1 (SQSTM1)/p62 is frequently overexpressed in tumors and plays an important role in the regulation of tumorigenesis. Although great progress has been made, biological roles of p62 and relevant molecular mechanisms responsible for its pro-tumor activity remain largely unknown. Here, we show that p62 knockdown reduces cell growth and the expression of glycolytic genes in a manner that depends on HIF1α activity in renal cancer cells. Knockdown of p62 decreases HIF1α levels and transcriptional activity by regulating mTORC1 activity and NF-κB nuclear translocation. Furthermore, p62 interacts directly with the von Hippel-Lindau (VHL) E3 ligase complex to modulate the stability of HIF1α. Mechanistically, p62 binds to the VHL complex and competes with HIF1α. Expression of p62 inhibits the interaction of DCNL1 (also known as DCUN1D1) with CUL2 and attenuates the neddylation of CUL2, and thus downregulates the VHL E3 ligase complex activity. Functionally, HIF1α expression is required for p62-induced glucose uptake, lactate production and soft agar colony growth. Taken together, our findings demonstrate that p62 is a crucial positive regulator of HIF1α, which is a facilitating factor in p62-enhanced tumorigenesis.

Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma.

BACKGROUND/AIMS: MIAT is a long noncoding RNA (lncRNA) involved in cell proliferation and the development of tumor. However, the exact effects and molecular mechanisms of MIAT in clear cell renal cell carcinoma (ccRCC) progression are still unknown. METHODS: We screened the lncRNAs' profile of ccRCC in The Cancer Genome Atlas database, and then examined the expression levels of lncRNA MIAT in 45 paired ccRCC tissue specimens and in cell lines by q-RT-PCR. MTS, colony formation, EdU, and Transwell assays were performed to examine the effect of MIAT on proliferation and metastasis of ccRCC. Western blot and luciferase assays were performed to determine whether MIAT can regulate Loxl2 expression by competitively binding miR-29c in ccRCC. RESULTS: MIAT was up-regulated in ccRCC tissues and cell lines. High MIAT expression correlated with worse clinicopathological features and shorter survival rate. Functional assays showed that knockdown of MIAT inhibited renal cancer cell proliferation and metastasis in vitro and in vivo. Luciferase and western blot assays further confirmed that miR-29c binds with MIAT. Additionally, the correlation of miR-29c with MIAT and Loxl2 was further verified in patients' samples. CONCLUSION: Our data indicated that MIAT might be an oncogenic lncRNA that promoted proliferation and metastasis of ccRCC, and could be a potential therapeutic target in human ccRCC.

Up-regulation of SR-BI promotes progression and serves as a prognostic biomarker in clear cell renal cell carcinoma.

BACKGROUND: Scavenger receptor class B type I (SR-BI) has been reported to be involved in carcinogenesis of several human cancers. However, it is currently unknown whether SR-BI plays a role in clear cell renal cell carcinoma (ccRCC). Here, we aimed to evaluate a tumor promotive mechanism for SR-BI in ccRCC. METHODS: The expression of SR-BI was evaluated by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot and immunohistochemistry (IHC) in ccRCC tissues and cell lines. Lipid droplets in ccRCC tissues and normal kidney tissues were examined by Oil Red O (ORO) and hematoxylin-eosin (HE) staining. The correlation between SR-BI mRNA levels and clinicopathological features was analyzed by Pearson's chi-square test or Fisher's exact test. Kaplan-Meier analysis and Cox model were used to evaluate the difference in progression-free survival (PFS) associated with expression of SR-BI. Inhibition of SR-BI was conducted by using small interfering RNA (siRNA). In vitro assays were performed to assess the impact of SR-BI knockdown on cell biological behaviors. High density lipoprotein (HDL)-cholesterol content in ccRCC cells and extracellular media was also measured after transfection with siRNA. RESULTS: The expression of SR-BI was markedly up-regulated in ccRCC tissues and tumor cell lines. ORO and HE staining revealed huge amounts of lipid droplets accumulation in ccRCC. Clinical analysis showed that over-expression of SR-BI was positively associated with tumor size, grade, distant metastasis and inversely correlated with PFS. Furthermore, SR-BI was proved to be an independent prognostic marker in ccRCC patients. The inhibition of SR-BI attenuated the tumorous behaviors of ccRCC cells, expression of metastasis and AKT pathway related proteins. The content of HDL-cholesterol was reduced in cells while increased in extracellular media after transfection with si-SR-BI. CONCLUSIONS: Our results demonstrate that SR-BI functions as an oncogene and promotes progression of ccRCC. SR-BI may serve as a potential prognostic biomarker and therapeutic target for ccRCC.

Mir-144-3p Promotes Cell Proliferation, Metastasis, Sunitinib Resistance in Clear Cell Renal Cell Carcinoma by Downregulating ARID1A.

BACKGROUND/AIMS: We previously performed microRNA (miRNA) microarray to identify effective indicators of clear cell renal cell carcinoma (ccRCC) tissue samples and preoperative/postoperative plasma in which we identified miR-144-3p as an oncomiRNA. However, the molecular mechanism of miR-144-3p remains unclear. This study aims to explore the roles of miR-144-3p in the invasion, migration and Sunitinib-resistance in ccRCC and to elucidate the underlying mechanisms. METHODS: Gain and loss of function approaches were used to investigate the cell proliferation, cycle distribution, clonogenicity, migration, invasion, chemosensitivity of miR-144-3p in vitro. The xenograft model was used to assess the effects of miR-144-3p overexpression on tumorigenesis. Bioinformatics analysis and dual-luciferase reporter assay were used to indentify AT-rich interactive domain 1A (ARID1A) as a direct target gene of miR-144-3p. Quantitative RT-PCR, Western blotting, and immunohistochemical (IHC) staining were used to explore ARID1A expression level of the mRNA and protein. RESULTS: We found that miR-144-3p overexpression enhanced cell proliferation, clonogenicity, migration, invasion, and chemoresistance in ccRCC cells. Notably, the oncotumor activities of miR-144-3p were mediated by repressing the expression of ARID1A. The downregulation of ARIDIA could promote the function of miR-144-3p in cell proliferation, metastasis and chemoresistance. Consistently, ARID1A mRNA and protein levels were decreased in ccRCC and in nude mice, and they negatively correlated with miR-144-3p. CONCLUSION: Higher miR-144-3p may enhance malignancy and resistance to Sunitinib in ccRCC by targeting ARID1A, the observations may uncover novel strategies of ccRCC treatment.

Diagnostic and prognostic value of scavenger receptor class B type 1 in clear cell renal cell carcinoma.

Aberrant expression of scavenger receptor class B type 1 has been reported in several human cancers. Nevertheless, the roles of scavenger receptor class B type 1 in clear cell renal cell carcinoma remain unclear. The aim of this study was to evaluate the diagnostic and prognostic value of scavenger receptor class B type 1 in clear cell renal cell carcinoma. The messenger RNA level of scavenger receptor class B type 1 in clear cell renal cell carcinoma tissues was detected by quantitative reverse transcription polymerase chain reaction, while protein level was determined by western blot and immunohistochemistry. The lipid content between clear cell renal cell carcinoma tissues and normal kidney tissues was differentiated by Oil Red O and hematoxylin-eosin staining. The diagnostic value of scavenger receptor class B type 1 was determined by receiver operating characteristic curve. The prognostic significance of scavenger receptor class B type 1 was assessed by Kaplan-Meier analysis and Cox regression analysis. Our results showed that the expression of scavenger receptor class B type 1 in clear cell renal cell carcinoma tissues at both messenger RNA and protein level was much higher than that in normal kidney tissues. Receiver operating characteristic curve analysis exhibited a significant value of area under the curve (0.8486, 95% confidence interval: 0.7926-0.9045) with strong sensitivity (0.75, 95% confidence interval: 0.6535-0.8312) and specificity (0.90, 95% confidence interval: 0.8238-0.9510). Kaplan-Meier analysis revealed that patients with higher scavenger receptor class B type 1 expression had shorter progression-free survival time. Cox analysis indicated that scavenger receptor class B type 1 was an independent prognostic biomarker. In conclusion, our findings implied that scavenger receptor class B type 1 might serve as a diagnostic and independent prognostic biomarker in clear cell renal cell carcinoma.

miR-490-5p suppresses tumour growth in renal cell carcinoma through targeting PIK3CA.

BACKGROUND INFORMATION: Dysregulated micro-RNAs have been reported in many human cancers, including renal cell carcinoma. Recent studies indicated that miR-490 is involved in tumour development and progression. However, the expression profile and function in renal cell carcinoma remains unknown. RESULTS: Herein, we showed that miR-490-5p was down-regulated in renal cell carcinoma tissues and cells compared with the adjacent normal tissues and normal cells. We also provided evidence that miR-490-5p acts as a tumour suppressor in renal carcinoma in a variety of in vitro and in vivo assays. Mechanistically, miR-490-5p was verified to directly bind to 3' UTR of the PIK3CA mRNA and reduce the expression of PIK3CA at both mRNA and protein levels, which further inhibits phosphatidylinositol 3-kinase/Akt signalling pathway. We further showed that knockdown of PIK3CA can block the growth inhibitory effect of miR-490-5p, and over-expression of PIK3CA can reverse the inhibitory effect of miR-490-5p on renal cancer cell tumourigenicity. CONCLUSIONS: Taken together, our results indicated for the first time that miR-490-5p functions as a tumour suppressor in renal carcinoma by targeting PIK3CA. SIGNIFICANCE: Our findings suggest that miR-490-5p may be a potential gene therapy target for the treatment of renal cell carcinoma.

Soil Organic Carbon Fractions and Stocks Respond to Restoration Measures in Degraded Lands by Water Erosion.

Assessing the degree to which degraded soils can be recovered is essential for evaluating the effects of adopted restoration measures. The objective of this study was to determine the restoration of soil organic carbon under the impact of terracing and reforestation. A small watershed with four typical restored plots (terracing and reforestation (four different local plants)) and two reference plots (slope land with natural forest (carbon-depleted) and abandoned depositional land (carbon-enriched)) in subtropical China was studied. The results showed that soil organic carbon, dissolved organic carbon and microbial biomass carbon concentrations in the surface soil (10 cm) of restored lands were close to that in abandoned depositional land and higher than that in natural forest land. There was no significant difference in soil organic carbon content among different topographic positions of the restored lands. Furthermore, the soil organic carbon stocks in the upper 60 cm soils of restored lands, which were varied between 50.08 and 62.21 Mg C ha-1, were higher than 45.90 Mg C ha-1 in natural forest land. Our results indicated that the terracing and reforestation could greatly increase carbon sequestration and accumulation and decrease carbon loss induced by water erosion. And the combination measures can accelerate the restoration of degraded soils when compared to natural forest only. Forest species almost have no impact on the total amount of soil organic carbon during restoration processes, but can significantly influence the activity and stability of soil organic carbon. Combination measures which can provide suitable topography and continuous soil organic carbon supply could be considered in treating degraded soils caused by water erosion.