It is well recognized that hypoxia-inducible factor 1 alpha (HIF-1α) is involved in cancer metastasis, chemotherapy and poor prognosis. We previously found that deferoxamine, a hypoxia-mimetic agent, induces epithelial-mesenchymal transition (EMT) in colorectal cancer. Therefore, here we explored a new molecular mechanism for HIF-1α contributing to EMT and cancer metastasis through binding to ZEB1. In this study, we showed that overexpression of HIF-1α with adenovirus infection promoted EMT, cell invasion and migration in vitro and in vivo. On a molecular level, HIF-1α directly binding to the proximal promoter of ZEB1 via hypoxia response element (HRE) sites thus increasing the transactivity and expression of ZEB1. In addition, inhibition of ZEB1 was able to abrogate the HIF-1α-induced EMT and cell invasion. HIF-1α expression was highly correlated with the expression of ZEB1 in normal colorectal epithelium, primary and metastatic CRC tissues. Interestingly, both HIF-1α and ZEB1 were positively associated with Vimentin, an important mesenchymal marker of EMT, whereas negatively associated with E-cadherin expression. These findings suggest that HIF-1α enhances EMT and cancer metastasis by binding to ZEB1 promoter in CRC. HIF-1α and ZEB1 are both widely considered as tumor-initiating factors, but our results demonstrate that ZEB1 is a direct downstream of HIF-1α, suggesting a novel molecular mechanism for HIF-1α-inducing EMT and cancer metastasis.

Yersinia pestis, a Gram-negative bacterium that causes bubonic and pneumonic plague, is able to rapidly disseminate to other parts of its mammalian hosts. Y. pestis expresses plasminogen activator (PLA) on its surface, which has been suggested to play a role in bacterial dissemination. It has been speculated that

Summary Objective To determine if antagonizing miR 29 enhances elastin (ELN) levels in cells and tissues lacking ELN. Methods and Results miR-29 mimics reduced ELN levels in fibroblasts and smooth muscle cells, whereas miR-29 inhibition increased ELN levels. Antagonism of miR-29 also increased ELN levels in cells from patients haploinsufficient for ELN and in bioengineered human vessels. Conclusion miR-29 antagonism may promote increased ELN levels during conditions of ELN deficiencies.

Clinical studies indicate that Neisseria gonorrhoeae (gonococci (GC)) has the capacity to enhance HIV type 1 (HIV-1) infection. We studied whether GC enhances HIV infection of activated dendritic cells (DCs). The results show that GC can dramatically enhance HIV replication in human DCs during coinfection. The GC component responsible for HIV infection enhancement may be peptidoglycan, which activates TLR2. TLR2 involvement is suggested by bacterial lipoprotein, a TLR2-specific inducer, which stimulates a strong enhancement of HIV infection by human DCs. Moreover, participation of TLR2 is further implicated because GC is unable to stimulate expression of HIV in DCs of TLR2-deficient HIV-1-transgenic mice. These results provide one potential mechanism through which GC infection increases HIV replication in patients infected with both GC and HIV.

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / a g r f o r m e t Energy and water exchanges over a riparian Tamarix spp. stand in the lower Tarim River basin under a hyper-arid climate a b s t r a c t Determining the maintenance and control mechanisms of the energy and water exchanges over the desert riparian forest zone in the lower Tarim River of China could improve our understanding of land surface processes of the groundwater-dependent ecosystems in the hinterland area of the Eurasian continent under hyper-arid climate. Nearly three years of continuous measurements of meteorological factors, surface water and energy fluxes, soil water content, and groundwater table were carried out over a riparian Tamarix spp. stand in the lower Tarim River basin. Because of scarce precipitation and low air humidity, the diurnal and seasonal variations of most meteorological factors exhibited simple unimodal dynamics. However, the seasonal variation of latent heat exchange (LE) was distinctly related to plant phenology. The sensible heat exchange (H) exhibited reverse course with the LE seasonal course, which suggested seasonal variation of the H was controlled by the LE course. In the daytime, a good linear relationship existed between evapotranspiration (ET) and reference evapotranspiration. The yearly ET over the tamarisk stand was approximately 500 mm year −1 , and the mean daily ET is about 3.85 mm d −1 in a vibrant growing season. The groundwater table and the soil water content (SWC) near the groundwater table exhibited obvious seasonal and diurnal variations in the growing seasons but SWC in the shallow soil layer did not, suggesting the groundwater was the water source of the tamarisk. Our analysis indicated that under a hyper-arid climate, the energy and water exchanges over riparian tamarisk stands in the lower Tarim River basin showed certain features: (1) plant transpiration accounted for most of the surface ET, with soil evaporation weak and negligible; (2) the seasonal processes of surface energy and water exchanges were highly related with plant phenology; (3) the diurnal processes of ET resulted from the comprehensive effects of all atmospheric factors; and (4) ET depends on groundwater, rather than precipitation.

Long non-coding RNA colon cancer-associated transcript 2 (CCAT2) is commonly investigated in a number of cancers. However, little is known of its expression and biological function in glioma biology. In the current study, we used quantitative real-time PCR (qRT-PCR) to determine the expression of CCAT2 in glioma tissues. We found that expression of CCAT2 was up-regulated in glioma tissues and significantly correlated with the advanced tumor stage (III/IV). Functional assays in vitro and in vivo demonstrated that knockdown of CCAT2 could inhibit proliferation, cell cycle progression and migration of glioma cells. Further analysis indicated the effect of CCAT2 knockdown on glioma cell phenotype through inhibiting Wnt/β-catenin signal pathway activity. Thus, our study provides evidence that CCAT2 may function as a potential biomarker for glioma.

Abstract. The Tibetan Plateau observatory (Tibet-Obs) of plateau scale soil moisture and soil temperature was established 10 years ago and has been widely used to calibrate/validate satellite- and model-based soil moisture (SM) products for their applications to the Tibetan Plateau (TP). This paper reports on the status of the Tibet-Obs and presents a 10-year (2009–2019) surface SM dataset produced based on in situ measurements taken at a depth of 5 cm collected from the Tibet-Obs that consists of three regional-scale SM monitoring networks, i.e. the Maqu, Naqu, and Ngari (including Ali and Shiquanhe) networks. This surface SM dataset includes the original 15 min in situ measurements collected by multiple SM monitoring sites of the three networks and the spatially upscaled SM records produced for the Maqu and Shiquanhe networks. Comparisons between four spatial upscaling methods – i.e. arithmetic averaging, Voronoi diagrams, time stability, and apparent thermal inertia – show that the arithmetic average of the monitoring sites with long-term (i.e. ≥ 6-year) continuous measurements is found to be most suitable to produce the upscaled SM records. Trend analysis of the 10-year upscaled SM records indicates that the Shiquanhe network in the western part of the TP is getting wet, while there is no significant trend found for the Maqu network in the east. To further demonstrate the uniqueness of the upscaled SM records in validating existing SM products for a long-term period (∼10 years), the reliability of three reanalysis datasets is evaluated for the Maqu and Shiquanhe networks. It is found that current model-based SM products still show deficiencies in representing the measured SM dynamics in the Tibetan grassland (i.e. Maqu) and desert ecosystems (i.e. Shiquanhe). The dataset would also be valuable for calibrating/validating long-term satellite-based SM products, evaluation of SM upscaling methods, development of data fusion methods, and quantifying the coupling of SM and precipitation at a 10-year scale. The dataset is available in the 4TU.ResearchData repository at https://doi.org/10.4121/12763700.v7 (Zhang et al., 2020).

Transcriptional factor FOXK1 is a member of the FOX family, involved in the cell growth and metabolism. The higher expression of FOXK1 leads to a variety of diseases and may play an important role in the development of various tumors. However, the role of FOXK1 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that FOXK1 was overexpressed in 16 types of solid tumor tissues via tissue multi-array (TMA). We found that FOXK1 induced elevated expressions and transactivities of five major oncogenes in CRC. Moreover, the elevated expression of FOXK1 was showed to be correlated with tumor progression and was a significant predictor of overall survival in CRC patients. Furthermore, it was showed that the depletion of FOXK1 expression could inhibit the migratory and invasive abilities of CRC cells. In contrast, ectopic expression of FOXK1 elicited the opposite effects on these phenotypes in vitro. FOXK1 promoted tumor metastasis through EMT program induction. In addition, TGF-β1 induced FOXK1 expression in a time-dependent pattern and the knockdown of FOXK1 inhibited TGF-β1-induced EMT. In vivo, higher expression of FOXK1 promotes CRC cell invasion and metastasis, and induces EMT in CRC as well. Alltogether, it was concluded that the higher expression of FOXK1 could indicate a poor prognosis in CRC patients since that FOXK1 induces EMT and promotes CRC cell invasion in vitro and in vivo.