Search

We carried out a cyanopolyyne line survey towards a large sample of HMSFRs using the Shanghai Tian Ma 65m Radio Telescope (TMRT). Our sample consisted of 123 targets taken from the TMRT C band line survey. It included three kinds of sources, namely those with detection of the 6.7 GHz CH3OH maser alone, with detection of the radio recombination line (RRL) alone, and with detection of both (hereafter referred to as Maser-only, RRL-only, and Maser-RRL sources, respectively). We detected HC3N in 38 sources, HC5N in 11 sources, and HC7N in G24.790+0.084, with the highest detection rate being found for Maser-RRL sources and a very low detection rate found for RRL-only sources. Their column densities were derived using the rotational temperature measured from the NH3 lines. And we constructed and fitted the far-infrared (FIR) spectral energy distributions. Based on these, we derive their dust temperatures, H2 column densities, and abundances of cyanopolyynes relative to H2. The detection rate, the column density, and the relative abundance of HC3N increase from Maser-only to Maser-RRL sources and decrease from Maser-RRL to RRL-only sources. This trend is consistent with the proposed evolutionary trend of HC3N under the assumption that our Maser-only, Maser-RRL, and RRL-only sources correspond to massive young stellar objects, ultra-compact HII regions, and normal classical HII regions, respectively. Furthermore, a statistical analysis of the integrated line intensity and column density of HC3N and shock-tracing molecules (SiO, H2CO) enabled us to find positive correlations between them. This suggests that HC3N may be another tracer of shocks, and should therefore be the subject of further observations and corresponding chemical simulations. Our results indirectly support the idea that the neutral--neutral reaction between C2H2 and CN is the dominant formation pathway of HC3N., 23 pages, 5 figures, 4 tables, Accepted to A&A

Renal cell carcinoma (RCC) is the most common kidney malignancy that frequently leads to metastasis. Increasing evidence has shown that long non-coding RNAs (lncRNAs) play crucial roles affecting the progression of RCC. The role of lncRNA DUXAP10 in the evolution of RCC has not been defined yet. This project was designed to clarify the effects of DUXAP10 on the proliferation and tumorigenesis of RCC.We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR) to evaluate DUXAP10 expression in human RCC tissues and cell lines. The correlation between the expression of DUXAP10 and clinical characteristics of RCC patients was analyzed by univariate and Kaplan-Meier analyses. To unveil the biological function of DUXAP10 in cell cycle progression, cell growth, and invasion of RCC, we conducted knockdown experiments in vitro. qRT- PCR and western blotting assays were performed to further investigate the function of DUXAP10 in cancer biology.The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues. Moreover, ONCOMINE database analysis indicated that high DUXAP10 levels were correlated with high clinical stages, inferior TNM classification, and poor overall survival. Furthermore, the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP10 may serve as a novel predictive biomarker and therapeutic target for RCC.

The aim of this study was to explore the expression of long non-coding RNA (lncRNA) FAM83H-AS1 and its clinical significance in ovarian cancer (OC).Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression level of lncRNA FAM83H-AS1 in 100 pairs of OC tissues and para-cancerous specimens. Meanwhile, the relationship between lncRNA FAM83H-AS1 expression and clinical features of OC patients was analyzed. According to the mean expression level of lncRNA FAM83H-AS1 (3.693), OC patients were divided into two groups, including the high-expression group (n=48) and low-expression group (n=52). After that, the association between lncRNA FAM83H-AS1 expression and clinicopathological features of OC patients was analyzed. Moreover, the correlation between the expression level of lncRNA FAM83H-AS1 and the survival time of patients was estimated using the Kaplan-Meier method. After OVCAR-3 cells were transfected with Si-FAM83H-AS1 or si-NC, the expression of FAM83H-AS1 in OVCAR-3 cells was detected by qRT-PCR.First, qRT-PCR was used to detect the expression of lncRNA FAM83H-AS1 in OC tissues and cell lines. The results showed that lncRNA FAM83H-AS1 was significantly up-regulated in both OC tissues and OC cells when compared with normal controls. Meanwhile, lncRNA FAM83H-AS1 expression was correlated with tumor pathological grade, FIGO stage and distant metastasis of OC patients. Survival analysis was performed by the Kaplan-Meier method. The results indicated that the overall survival time of patients with higher lncRNA FAM83H-AS1 expression was markedly shorter than those with lower lncRNA FAM83H-AS1 expression. In addition, down-regulation of lncRNA FAM83H-AS1 by si-FAM83H-AS1 transfection could remarkably inhibit proliferation and invasion of OC cells in vitro.LncRNA FAM83H-AS1 was a novel factor involved in OC progression. Our findings suggested that FAM83H-AS1 could serve as a potential biomarker and therapeutic target for OC.

Long non-coding RNA DUXAP10 plays a significant role in the tumorigenesis and development of human cancer. The present study was performed to investigate the role of DUXAP10 in biological functions and underlying molecular mechanisms of prostate cancer cells.First, the quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the expression of DUXAP10 in human prostate cancer cell lines 22RV1, PC3, and DU145. Subsequently, small interfering RNAs (siRNAs) targeting at DUXAP10 mRNA were used to downregulate DUXAP10 expression. Then, the biological functions of DUXAP10 in prostate cancer cells, proliferation, migration, and apoptosis were studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony-formation assay, cell cycle analysis, transwell migration assay, wound healing assay, and cell apoptosis assay, respectively. Finally, qRT-PCR analysis and Western blot assay were used to investigate the molecular mechanisms of DUXAP10 underlying the progression of prostate cancer.Results showed that the expression of DUXAP10 was higher in PC3 and DU145 cell lines than that in the 22RV1 cell line. Additionally, the knockdown of DUXAP10 could remarkably inhibit the proliferation, migration, and induce apoptosis of prostate cancer cells, and significantly increase the number of G0/G1 cells in PC3 and DU145 cell lines. Moreover, DUXAP10 could promote the development of prostate cancer by regulating the process of epithelial-mesenchymal transition (EMT).The findings of this study suggested that the down-regulation of DUXAP10 expression suppressed the progression of prostate cancer by inhibiting cell proliferation, migration and promote cell apoptosis.

The aim of this study was to investigate the effect of microRNA-539-3p (miR-539-3p) on the development of epithelial ovarian cancer (EOC), and to explore the possible underlying mechanism.A total of 40 paired EOC tissues and adjacent normal ovarian tissues were surgically resected in Hanchuan People's Hospital. Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of miR-539-3p in EOC tissues and cell lines. Targeted regulatory mechanism of miR-539-3p on SPARC-like protein 1 (SPARCL1) was identified by luciferase reporter and Western blot assays. Furthermore, the effects of miR-539-3p/SPARCL1 axis on the malignant behaviors of EOC cells, including proliferation, invasion and migration abilities, were confirmed by cell counting kit-8 (CCK-8), transwell and scratch wound assays.QRT-PCR showed that the expression of miR-539-3p was significantly up-regulated in EOC tissues and cell lines. SPARCL1 was a direct target of miR-539-3p in EOC cells. Overexpression of miR-539-3p significantly promoted the proliferation, migration and invasion of SKOV3 cells. Furthermore, co-transfection of miR-539-3p inhibitor and si-SPARCL1 could remarkably restore the migration and invasion abilities of SKOV3 cells.MiR-539-3p acted as an oncogene in EOC by targeting SPARCL1. MiR-539-3p/SPARCL1 axis, as a target for the treatment of EOC, might become a feasible and new method of tumor treatment.

The aim of this study was to investigate the role of long non-coding RNA (lncRNA) TCL6 in early abortion and to explore its underlying mechanism.The expression levels of lncRNA-TCL6 and epidermal growth factor receptor (EGFR) in placental tissues of normal pregnancy, threatened abortion pregnancy, spontaneous abortion pregnancy, and induced abortion pregnancy were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), respectively. Trophoblast cells were transfected with siRNA to knock-down lncRNA-TCL6. Cell viability of trophoblast cells was detected by cell counting kit-8 (CCK-8) assay. The protein expression levels of EGFR, extracellular regulated protein kinases (ERK) and protein kinase B (AKT) in trophoblast cells after lncRNA-TCL6 knockdown were detected by Western blot. Rescue experiments were performed to investigate the relationship between EGFR and lncRNA-TCL6.The expression of lncRNA-TCL6 in placenta tissues of threatened abortion pregnancy was significantly higher than that of normal pregnancy. Meanwhile, the expression of lncRNA-TCL6 in placenta tissues of spontaneous abortion pregnancy was also markedly higher than induced abortion pregnancy. However, the expression of EGFR showed an opposite trend. After knockdown of lncRNA-TCL6 in trophoblast cells, the protein expression levels of EGFR, ERK, and AKT were significantly increased when compared with those of the control group. CCK-8 assay indicated that cell viability was remarkably increased after knockdown of lncRNA-TCL6, which could be reversed by EGFR knockdown.Compared with normal pregnancy, lncRNA-TCL6 was highly expressed in placental tissues of threatened abortion pregnancy. Moreover, the expression of lncRNA-TCL6 in placenta tissues of spontaneous abortion pregnancy was significantly higher than induced abortion pregnancy. Knockdown of lncRNA-TCL6 promoted the proliferation of trophoblast cells and inhibited the abortion via the EGFR signaling pathway.

Miyun reservoir, the only surface water source for Beijing city, has experienced water supply decline in recent decades. Previous studies suggest that both land use change and climate contributes the changes of water supply in this critical watershed. However, the specific causes of the decline in Miyun reservoir are debatable in a non-stationary climate in the past four decades. The central objective of this study was to quantify the separate and collective contributions of land use change and climate variability to the decreasing inflow into Miyun reservoir during 1961–2008. Different from previous studies, this work objectively identified breakpoints by analyzing the long-term historical hydrometeorology and land cover records. To effectively study the different impacts of the climate variation and land cover change during different sub-periods, annual water balance model (AWB), climate elasticity model (CEM), and rainfall–runoff model (RRM) were employed to conduct attribution analysis synthetically. We found a significant decrease in annual streamflow (p < 0.01), a significant positive trend in annual potential evapotranspiration (p < 0.01), and an insignificant negative trend in annual precipitation (p > 0.1) during 1961–2008. Combined with historical records, we identified two breakpoints as in 1983 and 1999 for the period 1961–2008 by the sequential Mann–Kendall Test and Double Mass Curve. Climate variability alone did not explain the decrease in inflow to Miyun reservoir. Reduction of water yield was closely related to increase in evapotranspiration rates due to the expansion of forestlands and reduction in cropland and grassland, and was likely exacerbated by increased water consumption for domestic and industrial uses in the basin. Our study found that the contribution to the observed streamflow decline from land use change fell from 64–92 % during 1984–1999 to 36–58 % during 2000–2008, whereas the contribution from climate variation climbed from 8–36 % during the 1984–1999 to 42–64 % during 2000–2008. Model uncertainty analysis further demonstrated that climate warming played a dominant role in streamflow reduction in the 2000s. We conclude that future climate change and variability will further challenge the goal of water supply of Miyun reservoir to meet water demand. A comprehensive watershed management strategy needs to consider the climate variations besides vegetation management.