Long-term effects of rewetting and drought on GPP in a temperate peatland based on satellite remote sensing data.

Rewetting previously drained peatlands restores the critical function of peatlands as long-term carbon storages and sinks currently threatened by climate change and additional human-induced disturbances. Understanding and projecting the restoration process by rewetting, however, currently face a pressing challenge, the lack of consistent and gap-free records of important carbon cycling indicators of peatlands such as the gross primary production (GPP) over long term. In this study, we reconstructed the GPP in a rewetted peatland called Zarnekow (Fluxnet-ID: DE-Zrk) in Germany from 2000 to 2020 by combining long-term satellite observations and limited-term tower-based eddy covariance (EC) measurements based on Random Forest regression models. The R2 between the reconstructed data and EC data was 0.6. The reasonable reconstruction of long-term GPP enabled trend analysis that identified two distinct periods of decreasing/increasing in GPP due to rewetting and droughts. Rewetting in the winter of 2004 and 2005 stabilized GPP after a decreasing period. A drought in 2018 significantly increased GPP, and GPP remained high over the following two years. Furthermore, the month-specific trends show significant seasonality at this site, specifically, an increasing trend over the 21 years in the growing-season months of June to August and a decreasing trend in the other months. The most important variables for satellite-based estimates of GPP at this site include total evapotranspiration, land surface temperature, enhanced vegetation index and near-infrared reflectance vegetation index. Long-term analyses of carbon fluxes through the combination of satellite observations and EC measurements provide crucial insights into the restoration of carbon sequestration functions in rewetted peatlands.

Epigenetically upregulated GEFT-derived invasion and metastasis of rhabdomyosarcoma via epithelial mesenchymal transition promoted by the Rac1/Cdc42-PAK signalling pathway.

BACKGROUND: Metastasis of rhabdomyosarcoma (RMS) is the primary cause of tumour-related deaths. Previous studies have shown that overexpression of the guanine nucleotide exchange factor T (GEFT) is correlated with a poorer RMS prognosis, but the mechanism remains largely unexplored. METHODS: We focused on determining the influence of the GEFT-Rho-GTPase signalling pathway and the epithelial-mesenchymal transition (EMT) or mesenchymal-epithelial transition (MET) on RMS progression and metastasis by using RMS cell lines, BALB/c nude mice and cells and molecular biology techniques. FINDINGS: GEFT promotes RMS cell viability, migration, and invasion; GEFT also inhibits the apoptosis of RMS cells and accelerates the growth and lung metastasis of RMS by activating the Rac1/Cdc42 pathways. Interestingly, GEFT upregulates the expression levels of N-cadherin, Snail, Slug, Twist, Zeb1, and Zeb2 and reduces expression level of E-cadherin. Thus, GEFT influences the expression of markers for EMT and MET in RMS cells via the Rac1/Cdc42-PAK1 pathways. We also found that the level of GEFT gene promoter methylation in RMS is lower than that in normal striated muscle tissue. Significant differences were observed in the level of GEFT gene methylation in different histological subtypes of RMS. INTERPRETATION: These findings suggest that GEFT accelerates the tumourigenicity and metastasis of RMS by activating Rac1/Cdc42-PAK signalling pathway-induced EMT; thus, it may serve as a novel therapeutic target. FUND: This work was supported by grants from the National Natural Science Foundation of China (81660441, 81460404, and 81160322) and Shihezi University Initiative Research Projects for Senior Fellows (RCZX201447). Funders had no role in the design of the study, data collection, data analysis, interpretation, or the writing of this report.

MicroRNA-410-3p upregulation suppresses proliferation, invasion and migration, and promotes apoptosis in rhabdomyosarcoma cells.

Rhabdomyosarcoma (RMS) is one of the most common types of soft tissue sarcoma in children; however, the pathogenesis of RMS is unclear. MicroRNAs (miRs) are involved in the development and progression of RMS. The role of miR-410-3p in RMS cell invasion, migration, proliferation and apoptosis, and its possible mechanism were investigated in the current study. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were performed to detect the expression of miR-410-3p in RMS tissues and cells. In addition, the present study investigated the expression levels of molecules associated with the epithelial-mesenchymal transition (EMT), including E-cadherin, N-cadherin, Slug and Snail, and apoptotic factors, including Bcl-2-associated X protein (bax), cleaved-caspase 3, cleaved poly (ADP-ribose) polymerase (PARP), p53 and Bcl-2. Cell Counting Kit-8, terminal deoxynucleotidyl transferase dUTP nick end labeling and Transwell assays were conducted to determine the functional roles of miR-410-3p. Exogenous expression of miR-410-3p inhibited RMS cell invasion, migration and proliferation, induced apoptosis, suppressed the expression of Snail, Slug, N-cadherin and Bcl-2, and increased the expression of E-cadherin, bax, cleaved-caspase 3, cleaved PARP and p53. In summary, it was proposed that miR-410-3p overexpression suppressed invasion, migration and proliferation, downregulated the expression of EMT-associated molecules, and promoted apoptosis and the expression of apoptotic factors in RMS cells. Therefore, miR-410-3p may serve as a novel tumor suppressor gene in RMS, and could possess diagnostic and therapeutic potentials for the treatment of RMS.

MicroRNA-874 functions as a tumor suppressor in rhabdomyosarcoma by directly targeting GEFT.

MicroRNA-874 (miR-874) is downregulated and acts as a tumor suppressor gene in several human cancers. Its biological function and underlying molecular mechanism in rhabdomyosarcoma (RMS), however, remain unclear. In this study, we found that miR-874 expression was downregulated in human RMS tissue samples and cell lines through quantitative real-time polymerase chain reaction (qRT-PCR). Functional studies revealed that miR-874 overexpression in RMS cells remarkably inhibited proliferation, invasion, migration, and induced apoptosis. The results of luciferase activity assay, qRT-PCR and western blot analyses showed that miR-874 inhibited GEFT translation and suppressed GEFT expression by directly targeting the 3'-untranslated region (3'-UTR) of GEFT mRNA. GEFT expression was upregulated in RMS tissue samples and cell lines and was inversely correlated with miR-874 expression. Downregulation of GEFT has similar effects to miR-874 overexpression in RMS cells. Notably, GEFT restoration partially reversed the tumor-suppressive effects of miR-874. Our results indicated that miR-874 functions as a tumor suppressor in RMS and may suppress the growth and metastasis of RMS cells partially by targeting GEFT.

GEFT aberrant expression in soft tissue sarcomas.

BACKGROUND: Guanine nucleotide exchange factor T (GEFT) exhibits high amplification level using high-resolution array comparative genomic hybridization in rhabdomyosarcoma. The overexpression rate of GEFT protein is higher in rhabdomyosarcoma than in normal striated muscle tissues. This study evaluated the aberrant expression of GEFT in multiple subtypes of soft tissue sarcoma (STS) and compared the differences in clinical pathology, histological feature and expression levels of GEFT protein and mRNA between chromosomal translocation-associated sarcomas (CTAS) and non-chromosomal translocation-associated sarcomas (NCTAS). METHODS: GEFT protein expression was detected using immunohistochemistry (IHC) and tissue microarrays. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to detect the expression of GEFT mRNA. RESULTS: The rates of GEFT positive expression (196/219, 89.50%) and overexpression (113/219, 51.60%) were higher in multiple subtypes of STS than in normal striated muscle tissues. The rates of GEFT positive expression and overexpression in all subtypes of STS detected were significantly higher than that in the controls. No difference of GEFT expression was detected between CTAS and NCTAS. CONCLUSIONS: The abnormal expression of GEFT exists in various subtypes of STS, which may play an important role in tumorigenesis of STS.

Ectopic hamartomatous thymoma (biphenotypic branchioma): A case report and review of the literature.

RATIONALE: Ectopic hamartomatous thymoma is a very rare soft tissue neoplasm that commonly occurs in the lower neck of adult men. PATIENT CONCERNS: A 32-year-old male presented 1-year history of the tumor lying in left supraclavicular fossa. DIAGNOSES: Initial consideration of ultrasound and computed tomography was lipoma. After the operation, the pathologist diagnosed it as Ectopic Hamartomatous Thymoma. INTERVENTIONS: A complete resection was performed. OUTCOMES: To date, the patient had no evidence of metastasis or recurrence for 26 months after the operation. LESSONS: Ectopic hamartomatous thymoma is rare. The mastery of the clinical and pathological features of the disease will contribute to the rapid diagnosis and treatment of the disease. In addition, it can be considered to update the name to "biphenotypic branchioma" in order to avoid conceptual confusion.

c-MET expression potentially contributes to the poor prognosis of rhabdomyosarcoma.

Rhabdomyosarcoma (RMS) is one of the most common soft-tissue sarcomas with a poor prognosis. c-MET is a prognostic biomarker associated with growth, proliferation, invasion, and metastasis in various carcinomas. In this study, we aim to investigate the expression of c-MET in RMS and its effect on the prognosis of patients with rhabdomyosarcoma. We performed immunohistochemistry and a quantitative real-time polymerase chain reaction (qRT-PCR) to determine the expression levels of c-MET proteins and mRNAs. Results indicated that the c-MET protein and mRNA expression levels in the RMS samples were significantly higher than those in normal controls (P<0.01 and P=0.0492). However, the correlation between c-MET expression and any other clinicopathological parameter and survival was not significant (P=0.837). Nevertheless, c-MET expression had a significant influence on the overall survival rates of patients with ERMS (χ2=9.673, P=0.002) and fusion gene-negative patients (χ2=5.400, P=0.020). These findings suggest that c-MET may serve as a promising biomarker capable of predicting poor prognosis in patients with RMS.