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Cotton is an important cash crop with an indeterminate growth characteristic. The labor costs of multiple management practices, including repeated foliar applications of mepiquat chloride (MC) and topdressing with potassium (K) fertilizers, restrict its planting area and benefits. To help address this problem, a field experiment was performed to evaluate the effects of controlled-release potassium chloride containing mepiquat chloride (CRKMC) on soil K forms and cotton yield. CRKMC, 70%CRKMC (30% reduced K dosage), CRK (coated potassium chloride), KCl and no K fertilizer used treatments were carried out. Results showed that MC and K from CRKMC exhibited a trend of slow release, followed by fast release and eventually stabilization. Soils maintained more non-exchangeable K than available K. The contents of all soil K forms for the CRKMC treatment were significantly higher than these for KCl. Plant heights, SPAD values and stem diameters in CRKMC and 70%CRKMC were larger than those in KCl. Cotton yield, K use efficiency and net profit in the CRKMC treatment were increased than KCl. The successive release pattern of MC and K from CRKMC corresponded well to the demands of cotton, sufficiently manipulated the plant canopy and provided adequate K nutrition. [ABSTRACT FROM AUTHOR]

Choriocarcinoma is a rare gestational trophoblastic tumour. Propofol is one of the commonly used intravenous anaesthetic agents and exerts an anti-tumour role in multiple cancers. However, the effect of propofol on choriocarcinoma has not been well explored. We investigated the effect of propofol on JEG-3 cells. The effects of propofol on cell proliferation and metastasis were determined. The expression of miR-495 was suppressed while Twist1 overexpressed. Cell viability, migration and invasion were respectively measured using CCK-8 assay and transwell migration/invasion assay. The expression of miR-495, AKT1 and Twist1 was detected using qRT-PCR. Western blot analysis was performed to assess the expression levels of EMT- and proliferation-related factors, and TGF-β pathway proteins. Propofol treatment significantly inhibited cell proliferation, migration and invasion, and reduced the releasing of EMT. miR-495 was up-regulated by profocol, and miR-495 inhibition reversed the effect of propofol on cell proliferation and metastasis in JEG-3 cells. Furthermore, propofol decreased the expression of AKT1 and Twist1 through up-regulating miR-495, and Twist1 participated in the regulation of propofol on TGF-β signalling inactivation in JEG-3 cells. This study demonstrates that propofol suppresses cell proliferation and metastasis through up-regulation of miR-495 and down-regulation of Twist1 in JEG3 cells. Propofol inhibits proliferation and metastasis in JEG-3 cells; miR-495 is up-regulated by propofol in JEG-3 cells; miR-495 suppression blocks the effect of propofol in JEG-3 cells; Propofol decreases Twist1 expression through up-regulating miR-495; Propofol inhibits TGF-β signalling via regulation of Twist1. [ABSTRACT FROM AUTHOR]

This study was aimed to explore the effects of miR-29a-5p expression and its target gene TPX2 (target protein for Xenopus kinesin-like protein 2) on endometrial cancer (EC) devel on EC development and to assess the prognostic impacts of TPX2. Microarray-based GEO and TCGA (the Cancer Genome Atlas) EC expression data were used to identify differentially expressed miRNAs and mRNAs. The observed potential target relationship between miR-29a-5p and TPX2 was verified using TargetScan and luciferase reporter assays. The mRNA and protein expression levels of miR-29a-5p and TPX2 were confirmed by qRT-PCR and western blot, respectively. Associations between TPX2 expression and patient prognosis were assessed using Kaplan-Meier and log-rank assays. Changes in EC-derived cell proliferation, invasion and apoptosis after exogenous miR-29a-5p and TPX2 over-expression and/or silencing were assessed using CCK-8 (cell counting kit-8), colony formation, Transwell and flow cytometry assays, respectively. We found that in primary EC tissues the expression of miR-29a-5p was down-regulated and the expression of TPX2 was up-regulated. We also found that low expression of TPX2 were associated with a better prognosis, and vice versa. Subsequent exogenous miR-29a-5p over-expression and TPX2 silencing could inhibit EC-derived cell proliferation and invasion, and to induce apoptosis. We also found that miR-29a-5p might target and repress TPX2, thereby inhibiting EC-derived cell proliferation and invasion and enhancing apoptosis. We conclude that miR-29a-5p could inhibit the proliferation and invasion of EC-derived cells and enhance the apoptosis of EC-derived cells via TPX2 down-regulation. A high TPX2 expression in primary EC tissues was found to be associated with a poor prognosis. As such, these biomarkers may serve as promising prognostic indicators. ABBREVIATIONS: EC: Endometrial cancer; 3ʹ-UTR: 3ʹ-untranslated regions; TPX2: target protein for Xenopus kinesin-like protein 2; TCGA: the Cancer Genome Atlas; UCEC: uterine corpus endometrial carcinoma; CCK-8: cell counting kit-8; OD: optical density; FCM: flow cytometry; EMT: epithelial-mesenchymal transition [ABSTRACT FROM AUTHOR]