[Retracted] Arnebin­1 promotes angiogenesis by inducing eNOS, VEGF and HIF­1α expression through the PI3K­dependent pathway.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the α­tubulin protein bands shown in Fig. 2A on p. 689 were strikingly similar to data appearing in different form in the following paper: Tian R, Li Y and Gao M: Shikonin causes cell­cycle arrest and induces apoptosis by regulating the EGFR­NF­κB signalling pathway in human epidermoid carcinoma A431 cells. Biosci Rep 35: e00189, 2015. Moreover, there were a pair of overlapping data panels shown in the cell invasion and migration assay data in Fig. 5B on p. 692, one identified instance of western blot data being shared between Figs. 3D and 4F, and a pair of overlapping data panels in Fig. 5D, such that all these data, which were intended to have shown the results from differently performed experiments, may have been derived from a smaller number of original sources. Owing to the fact that the contentious data in the above article were already under consideration for publication prior to its submission to International Journal of Molecular Medicine and an overall lack of confidence in the presented data, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 36: 685­697, 2015; DOI: 10.3892/ijmm.2015.2292].

Analysis of Drought Tolerance and Associated Traits in Upland Cotton at the Seedling Stage.

(1) Background: Upland cotton (Gossypium hirsutum L.) is the most important natural fiber worldwide, and it is extensively planted and plentifully used in the textile industry. Major cotton planting regions are frequently affected by abiotic stress, especially drought stress. Drought resistance is a complex, quantitative trait. A genome-wide association study (GWAS) constitutes an efficient method for dissecting the genetic architecture of complex traits. In this study, the drought resistance of a population of 316 upland cotton accessions was studied via GWAS. (2) Methods: GWAS methodology was employed to identify relationships between molecular markers or candidate genes and phenotypes of interest. (3) Results: A total of 8, 3, and 6 SNPs were associated with the euphylla wilting score (EWS), cotyledon wilting score (CWS), and leaf temperature (LT), respectively, based on a general linear model and a factored spectrally transformed linear mixed model. For these traits, 7 QTLs were found, of which 2 each were located on chromosomes A05, A11, and D03, and of which 1 was located on chromosome A01. Importantly, in the candidate regions WRKY70, GhCIPK6, SnRK2.6, and NET1A, which are involved in the response to abscisic acid (ABA), the mitogen-activated protein kinase (MAPK) signaling pathway and the calcium transduction pathway were identified in upland cotton at the seedling stage under drought stress according to annotation information and linkage disequilibrium (LD) block analysis. Moreover, RNA sequencing analysis showed that WRKY70, GhCIPK6, SnRK2.6, and NET1A were induced by drought stress, and the expression of these genes was significantly different between normal and drought stress conditions. (4) Conclusions: The present study should provide some genomic resources for drought resistance in upland cotton. Moreover, the germplasm of the different phenotypes, the detected SNPs and, the potential candidate genes will be helpful for molecular marker-assisted breeding studies about increased drought resistance in upland cotton.

Prognostic value of glypican-1 for patients with advanced pancreatic cancer following regional intra-arterial chemotherapy.

Regional intra-arterial chemotherapy (RIAC) is a potential alternative treatment for advanced pancreatic cancer (APC) with fewer adverse effects than other treatment options. However, specific biomarkers to determine the prognosis of patients with APC have thus far, been unsatisfactory. Glypican-1 (GPC1) in exosomes has been identified as an early diagnostic biomarker for pancreatic adenocarcinoma. The aim of the present study was to investigate whether the presence of GPC1 in extracellular vesicles (EVs) could serve as a predictor of RIAC outcome for patients with APC. EVs in circulation were isolated and the percentage of GPC1+ EVs was measured using flow cytometry. Compared with healthy individuals, the levels of GPC1+ EVs were significantly increased in patients with APC (P<0.01). Following RIAC treatment, the percentage of GPC1+ EVs was decreased (P=0.023). Furthermore, patients with APC exhibiting a greater decrease of GPC1+ EVs experienced improved overall survival (OS) rates. In summary, the present study provides insights into identifying GPC1 as a novel prognostic biomarker for patients with APC following RIAC treatment.

Arnebin-1 promotes angiogenesis by inducing eNOS, VEGF and HIF-1α expression through the PI3K-dependent pathway.

Arnebin-1, a naphthoquinone derivative, plays a crucial role in the wound healing properties of Zicao (a traditional wound healing herbal medicine). It has been noted that Arnebin-1, in conjunction with vascular endothelial growth factor (VEGF), exerts a synergistic pro-angiogenic effect on human umbilical vein endothelial cells (HUVECs) and accelerates the healing process of diabetic wounds. However, the mechanisms responsible for the pro-angiogenic effect of arnebin­1 on HUVECs and its healing effect on diabetic wounds have not yet been fully elucidated. In this study, in an aim to elucidate these mechanisms of action of arnebin­1, we investigated the effects of arnebin­1 on the VEGF receptor 2 (VEGFR2) and the phosphoinositide 3-kinase (PI3K)­dependent signaling pathways in HUVECs treated with VEGF by western blot analysis. The pro­angiogenic effects of arnebin­1 on HUVECs, including its effects on proliferation and migration, were evaluated by MTT assay, Transwell assay and tube formation assay in vitro. The expression levels of hypoxia-inducible factor (HIF)­1α, endothelial nitric oxide synthase (eNOS) and VEGF were determined by western blot analysis in the HUVECs and wound tissues obtained from non­diabetic and diabetic rats. CD31 expression in the rat wounds was evaluated by immunofluorescence staining. We found that the activation of the VEGFR2 signaling pathway induced by VEGF was enhanced by arnebin­1. Arnebin­1 promoted endothelial cell proliferation, migration and tube formation through the PI3K­dependent pathway. Moreover, Arnebin­1 significantly increased the eNOS, VEGF and HIF­1α expression levels in the HUVECs and accelerated the healing of diabetic wounds through the PI3K­dependent signaling pathway. CD31 expression was markedly enhanced in the wounds of diabetic rats treated with arnebin­1 compared to the wounds of untreated diabetic rats. Therefore, the findings of the present study indicate that arnebin-1 promotes the wound healing process in diabetic rats by eliciting a pro-angiogenic response.

Drosophila miR-5 suppresses Hedgehog signaling by directly targeting Smoothened.

Hedgehog (Hh) signaling plays many important roles in developmental processes and cancers. Smoothened (Smo) is an important signal transducer in the Hh pathway, and its expression is tightly regulated by several different post-transcriptional mechanisms. However, whether microRNAs (miRNAs) are involved in Smo regulation is still unclear. Here, we found that miR-5 acts as a suppressor of the Hh pathway by targeting Smo. Through in vivo sensor assay and in vitro luciferase assay, we found that miR-5 downregulates Smo through directly binding to its 3'UTR. Moreover, our data indicated Costal-2 (Cos2) and Fused (Fu) do not play a role in the reduction of Smo mediated by miR-5. Furthermore, we determined that miR-5 not involved in Notch or Dpp signaling pathways by detecting target gene expression. Together, our results indicate that miR-5 can specifically suppress Hh signaling by directly targeting Smo in Drosophila.