Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the Transwell assay data shown in Fig. 2C and 4D, two pairs of overlapping sections of data were identified comparing the panels in these figures, where the results from differently performed experiments were intended to have been portrayed. An Expression of Concern statement was published to account for these concerns (doi: 10.3892/or.2025.9001), after which the authors have responded to the Editorial Office to offer an explanation for this apparent duplication of data within the two figures. To address the issue of the scientific rigor and integrity of this paper, the affected experiments in Figs. 2C and 4D have been performed again in triplicate by the authors. The results obtained were broadly similar to those obtained in the original experiments, and the revised versions of Figs. 2 and 4 are shown on the next page. Also note that the following changes are required to the text in the paper describing the results of these experiments: In the Results section, the corrected data values and text for these experiments should now read as follows: For Fig. 2: 'The cells that invaded through the pores to the lower surface of the filter were 29±16 and 95±36 (P<0.05), respectively (Fig. 2C and D)'; and for Fig. 4: 'Smad2 RNAi abrogated the TGF‑β1‑induced suppression of E‑cadherin expression (Fig. 4C) and suppressed the invasion capacity of Tu686 cells (P<0.05, 70±22 vs. 23±8; Fig. 4D and E)'. The data values have also been amended in the respective figure legends for Figs. 2 and 4, as shown on the next page. Note that these errors did not have a significant impact on the conclusions reached in this study. The authors regret the errors that were made during the compilation of the original figures, and are grateful to the editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership for any incon-venience caused. [Oncology Reports 25: 1581‑1587, 2011; DOI: 10.3892/or.2011.1251].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the Transwell assay data shown in Fig. 2C and 4D, two pairs of overlapping sections of data were identified comparing the panels in these figures, where the results from differently performed experiments were intended to have been portrayed. The authors were contacted by the Editorial Office to offer an explanation for this apparent duplication of data within the two figures; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 25: 1581‑1587, 2011; DOI: 10.3892/or.2011.1251].

In wheat ( Triticum aestivum L.), yield component traits (YCTs) are the most important yield traits. Only several genes for YCTs have been originally cloned. The efficient cloning of genes for YCTs directly from wheat remains a challenge. Here, we proposed a strategy for cloning genes from quantitative trait loci (QTLs) by sequencing of recombinant inbred lines (RILs) (QTL-Seq-RIL). Using the ‘TN18 × LM6’ RIL population as an example, we identified 138 candidate unigenes (CUGs) for YCTs from 77 stable QTLs. The average of CUGs per QTL was 1.8, which enabled us to confirm the CUGs directly. We have confirmed seven CUGs, TaIFABPL, TaDdRp, TaRLK, TaTD, TaTFC3, TaKMT and TaSPL17 , via the CRISPR/Cas9 system. Of these, six genes were found firstly to regulate YCTs in crops except for TaSPL17 . Five CUGs (include TaSPL17 ) for which orthologous genes have been cloned previously with the same or similar agronomic functions. It is to say, 11 CUGs were preliminarily validated using a single RIL population. QTL-Seq-RIL provides an efficient method for rapid gene cloning using existing RIL populations.### Competing Interest StatementThe authors have declared no competing interest.

Nanozymes are nanomaterials with enzyme-like properties that have attracted significant interest owing to their high stability, easy preparation, and tunable catalytic properties, especially in the field of cancer therapy. However, the unfavorable catalytic effects of nanozymes in the acidic tumor microenvironment have limited their applications. Herein, we developed a biomimetic erythrocyte membrane-camouflaged ultrasmall black phosphorus quantum dots (BPQDs) nanozymes that simultaneously exhibited an exceptional near-infrared (NIR) photothermal property and dramatically photothermal-enhanced glucose oxidase (GOx)-like activity in the acidic tumor microenvironment. We demonstrated the engineered BPQDs gave a photothermal conversion efficiency of 28.9% that could rapidly heat the tumor up to 50 °C while effectively localized into tumors via homing peptide iRGD leading after intravenously injection. Meanwhile, the significantly enhanced GOx-like activity of BPQDs under NIR irradiation was capable of catalytical generating massive toxic reactive oxygen species via using cellular glucose. By combining the intrinsic photothermal property and the unique photothermal-enhanced GOx-like catalytic activity, the developed BPQDs were demonstrated to be an effective therapeutic strategy for inhibiting tumor growth in vivo. We believe that this work will provide a novel perspective for the development of nanozymes in tumor catalytic therapy.

Head and neck squamous cell carcinoma (HNSCC) is the sixth most frequent malignancy with a 5-year survival rate of 54%. Therefore, disease management improvement is required. The present study aimed to assess the role of caveolin-1 (Cav-1) in the metastasis of head and neck tumor cells. Short hairpin RNA was used to silence Cav-1 expression in Tu686 cells. Proliferation, migration, invasion, morphology and the levels of effector proteins were assessed in cells. Upon Cav-1 silencing, E-cadherin levels were decreased, while vimentin levels were significantly increased. Cell migration, quantified by wound healing and Transwell assays, was significantly increased. Meanwhile, Cav-1 and transforming growth factor β1 (TGF-β1) receptor were identified to be co-localized. In addition, Cav-1-knockdown resulted in increased phosphorylation of SMAD family member 2 (P<0.05), a downstream effector of TGF-β signaling. In addition, there was a mutual regulation, with increasing TGF-β1 levels leading to a dose-dependent decrease of Cav-1 expression levels (P<0.05). These findings indicate that Cav-1 inhibits cell metastasis in HNSCC, suggesting the involvement of the TGF-β signaling pathway.

The deregulation of Bcl2L12 expression in cancer has been recognized, but the causative factors are unknown. Histone acetyltransferases (HAT) play critical roles in the regulation gene transcription. This study tests a hypothesis that the aberrant activities of HAT induce deregulation of Bcl2L12 in nasopharyngeal cancer (NPC). In this study, human NPC tissues were collected from the clinic. The expression of Bcl2L12 and HATs in NPC cells was analyzed by real time RT-PCR and Western blotting. NPC cell apoptosis was analyzed by flow cytometry. The results showed that by screening the subtypes of HAT, the levels of HAT1 were uniquely higher in NPC as compared with non-cancer nasopharyngeal tissue. The levels of Bcl2L12 in NPC cells were positively correlated with HAT1. HAT1 involved in the STAT5 binding to the Bcl2L12 promoter. HAT1 increased the expression of Bcl2L12. Bcl2L12 mediated the effects of HAT1 on suppressing NPC cell apoptosis. Absorption of the HAT1 shRNA plasmid-carrying liposomes induced NPC cell apoptosis. In conclusion, inhibition of HAT1 can induce NPC cell apoptosis via increasing Bcl2L12 expression, which can be a potential therapy for NPC treatment.

The uptake and utilization of nitrogen (N) by plants are affected by the different forms of N in the soil. In this study, eight morphological traits at the seedling stage were investigated using a set of recombinant inbred lines (RILs). Three hydroponic culture experiments were conducted using three different NO3 −/NH4 + ratios (T1 at 50/50 %, T2 at 100/0 % and T3 at 0/100 %). The investigated traits in T2 and T1 were significantly higher than T3 in all three experiments, indicating that NO3 − promoted or NH4 + suppressed the production of biomass. Comparing T1 with T2, NO3 − significantly increased the values of root fresh weight (RFW), total fresh weight (TFW) and root dry weight (RDW) and significantly decreased shoot dry weight (SDW). A total of 147 quantitative trait loci (QTLs) for the eight traits were detected on 18 chromosomes (except 2A, 3D and 4D). Among them, 16 QTLs (QRfw-1A, QRfw-1D, QSfw-1D, QSfw-2B.1, QTfw-1A, QTfw-1D, QRsfw-2B, QRsfw-3B.1, QRdw-1A.1, QRdw-1A.2, QSdw-6B.1, QSdw-7A.1, QTdw-1A.1, QRsdw-1A.1, QRsdw-5A.1 and QRsdw-7A.1) were detected in more than three of the nine treatment–experiments, and most of the 16 QTLs made large contributions of approximately 15 %. Surprisingly, QRsfw-4A.1 and QRsfw-4A.2 explained as much as 47.9 and 55.5 % of the phenotypic variation, respectively. Thirteen important QTL clusters (C1-C13) with more than four QTLs and involving 66 QTLs (44.9 %) were mapped on chromosomes 1A, 1D, 2B, 2D, 4A, 4B, 5B, 5D, 6B, 7A and 7B.

为了获得与小麦产量性状关联的分子标记,筛选相关标记的等位变异,以128份黄淮麦区小麦品种(系)为材料,在4个环境下鉴定产量性状,并选用在小麦全基因组21条染色体上的64个SSR、27个EST-SSR和47个功能标记检测所有材料的基因型.91个SSR和EST-SSR标记共检测到315个等位变异,单个引物检测到2～7个等位变异,平均3.5个;47个功能标记共检测到107个等位变异,单个引物检测到2～5个等位变异,平均2.3个.关联分析表明,49个位点与4个环境的产量性状及其均值显著关联(P≤0.005),其中38个位点在2个或以上环境或均值下被重复验证,16个位点与2个或以上性状相关联.对相对稳定的等位变异作进一步分析,发掘了一批与产量性状相关的优异等位变异,如降低株高的等位变异Ax2 *-null和UMN19*-A362,增加穗长的等位变异barc21-A220,增加可育小穗数的等位变异gpw2111-A156,增加总小穗数的等位变异swes65-A120,增加穗数的等位变异VRN-A1*-A 1068,增加穗粒数的等位变异cfdS-A215和增加千粒重的等位变异wmc626-A 170.研究结果对利用分子标记辅助选择进行小麦产量性状的遗传改良具有一定的指导意义.

Glutamine synthetase (GS) is a key enzyme in the formation of the amino acid glutamine during N assimilation. The characterization of GS genes and the development of functional markers are important for marker-assisted selection (MAS) in wheat breeding programs. In the present study, the full-length genomic DNA (gDNA) sequence of TaGS1a was obtained from 60 wheat varieties. TaGS1a comprises 3415 bp and has eleven exons and ten introns. Nine single nucleotide polymorphisms (SNPs) and two insertions and deletions of DNA segments (InDels) were detected in introns, resulting two haplotypes: Hap 1 and Hap 2. A cleaved amplified polymorphic sequence (CAPS) marker was developed to distinguish the two haplotypes. The TaGS1a-CAPS marker was located on chromosome 6D using Chinese Spring nullisomic-tetrasomic lines, and mapped at 2.5 cM from the SSR marker barc1121b in a RIL population. The completely corresponding results between quantitative trait locus (QTL) analysis and association analysis suggested that the TaGS1a gene had functions for grain size traits, including thousand grain weight (TGW), grain width (GW), grain height (GH), GL/GW ratio (GLW), factor form density (FFD), grain area (GA) and grain volume (GV) during maturity stage, and for the ratio of root/shoot for dry weight and nitrogen, phosphorus, potassium contents (RSDW, RSNC, RSPC and RSKC) during seedling stage. (C) 2013 Elsevier B.V. All rights reserved.

Development of metastasis is a major cause of death for squamous cell carcinoma of the head and neck (SCCHN) patients. Epithelial to mesenchymal transition (EMT) is now regarded as a correlate of tumor metastasis. Given that transforming growth factor-β1 (TGF-β1) is an important inducer of EMT, we examined the effects of TGF-β1 on the human SCCHN cell line Tu686. We found that TGF-β1 mediated cell morphological changes. Phase-contrast microscopy revealed a loss of the adherent phenotype with cellular elongation, decrease in cell-to-cell contact, and the induction of a fibroblast-like state. Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis demonstrated that TGF-β1 could induce down-regulation of the epithelial marker E-cadherin and up-regulation of the mesenchymal marker vimentin in Tu686 cells in a concentration- and time-dependent manner. Wound- healing and transwell invasion assay indicated that TGF-β1 promoted Tu686 cell migration and invasion dramatically. In addition, these changes were mediated via canonical TGF-β/Smad signaling with concomitant up-regulation of phosphorylated Smad2. Smad2 RNAi abrogated both expression and functional effects of TGF-β1 on Tu686 cells. In conclusion, the present study demonstrates that TGF-β1 could induce EMT in the SCCHN cell line via the TGF-β/Smad signaling pathway. More importantly, a cell model for EMT was established, which is valuable for future studies on the metastasis of SCCHN.

Background and Aims. Bone morphogenetic proteins (BMPs) have recently been shown to be involved in the genesis and progression of a wide variety of carcinomas. The present study was undertaken to estimate the effect of BMP-4 on squamous cell carcinoma of the head and neck (SCCHN) in tissue and cell levels.Methods. In this study, immunohistochemistry, Western blotting and RT-PCR were utilized to detect the expression of BMP-4, Smad1 and phosphorylated Smad1 in SCCHN tissues or SCCHN cell lines. Those three proteins in tissues were further correlated with prognosis of SCCHN by Kaplan-Meier analysis. The epithelial-mesenchymal transition (EMT)-associated changes in SCCHN cells were detected after stimulation by human BMP-4 recombinant protein and knockdown of Smad1 gene. Meanwhile, the effect on invasiveness and migration was evaluated by invasion and scratch assays, respectively.Results. BMP-4 and p-Smad1 protein were overexpressed in SCCHN tissues with cervical lymph node metastasis, which was significantly higher than those without metastasis. The expression of BMP-4 and p-Smad1 protein was negatively correlated with the prognosis of SCCHN. BMP-4 promoted the invasiveness and migration through EMT, which was demonstrated by morphological alterations, loss of E-cadherin, increase of vimentin and activation of the Smad1 signal pathway. Knockdown of Smad 1 expression suppressed BMP-4 induced EMT in both cell lines and weakened the invasiveness and migration of Tu686 and Tu212 in vitro.Conclusions. Our results demonstrate that BMP-4 protein may contribute to the malignant metastasis of SCCHN, which presents as a novel prognostic marker and a potential therapeutic target for patients with SCCHN. (C) 2011 IMSS. Published by Elsevier Inc.

OBJECTIVE To investigate the effect of epigallocatechin-3-gallate(EGCG)on the induction of apoptosis and its possible molecular mechanism in head and neck cancer cells. METHODS Head and neck cancer cells Tu177 and Tu212 were treated with EGCG at different concentration for 72 hours. Flow cytometry analysis was employed for apoptosis, and Western blot was used to detect the expression of apoptosis-related proteins. Meanwhile, Tu177 and Tu212 were treated with EGCG, AKT activity was detected at different time points. RESULTS EGCG induced apoptosis of head and neck cancer cells in a dose dependent manner, the expression levels of cleaved-caspase 9, -caspase 3, and PARP were obviously up-regulated in EGCG treated cells. At the same time, the expression of p-AKT was down-regulated in a time-dependent manner by EGCG. CONCLUSION EGCG could induce apoptosis in head and neck cancer cells possibly through AKT and mitochondrial mediated pathways.