[Corrigendum] miR­27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker.

Following the publication of this article, an interested reader drew to the authors' attention that the western blots in Fig. 4B on p. 3560 and Fig. 6B on p. 3562 shared remarkably similar data (including both the GAPDH and the FAM172A blots in Fig. 4B), such that these data were likely to have been derived from the same original source. Upon asking the authors to provide an explanation, the authors realized that these errors inadvertently arose during the process of assembling these figures. Due to a mislabelling of the files, representative blots for FAM172A and GAPDH were chosen incorrectly for Fig. 4B. The authors had retained their original data, however, and were also able to present to the Editorial Office for our perusal the uncropped versions of their western blots, which resolved any other potential issues of anomalies associated with the data. The revised version of Fig. 4, now showing alternative data for Fig. 4B, is shown on the next page (note that, in the repeated experiment, relative to the original version of this figure the miR­27a, miR27a­inhibitor and negative control experiments were run on different lanes of the gel). Also note that the errors made in terms of assembling the data in Fig. 4 did not greatly affect either the results or the conclusions reported in this paper, and all the authors agree to the publication of this corrigendum. The authors regret that these errors went unnoticed prior to the publication of their article, are grateful to the Editor of Oncology Reports for granting them this opportunity to publish a corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 37: 3554­3564, 2017; DOI: 10.3892/or.2017.5592].

[Retracted] AdipoR1­mediated miR­3908 inhibits glioblastoma tumorigenicity through downregulation of STAT2 associated with the AMPK/SIRT1 pathway.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blotting data shown in Figs. 3B and 9, and the migration assay data shown in Fig. 6C, were strikingly similar to data that had already appeared in other publications written by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 37: 3387­3396, 2017; DOI: 10.3892/or.2017.5589].

[Retracted] MicroRNA­520a attenuates proliferation of Raji cells through inhibition of AKT1/NF­κB and PERK/eIF2α signaling pathway.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that a pair of the lanes featured in the western blot gel for Fig. 3B on p. 1705 were strikingly similar, suggesting that the same data may have been imported into the figure to represent data that were intended to show the results from differently performed experiments. In addition, the western data shown in Fig. 6 on p. 1706 for the GRP78 and the p­PERK proteins also appeared to be strikingly similar, such that the same data may have also been inserted into this figure to show the results from different experiments. Finally, certain of the data in this paper were shown to have appeared in a previous publication that featured some of the same authors, albeit in different form [Zhang L, Huang D, Wang Q, Shen D, Wang Y, Chen B, Zhang J and Gai L: MiR­132 inhibits expression of SIRT1 and induces pro­inflammatory processes of vascular endothelial inflammation through blockade of the SREBP­1c metabolic pathway. Cardiovasc Drugs Ther 8: 303­311, 2014]. Owing to the fact that some of the contentious data in the above article had already been published elsewhere prior to its submission to Oncology Reports, and because of 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 36: 1702­1708, 2016; DOI: 10.3892/or.2016.4975].

[Retracted] Resveratrol reduces acute lung injury in a LPS­induced sepsis mouse model via activation of Sirt1.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the ß­actin control western blotting data shown in Fig. 3D on p. 1893 were very similar to the contol data shown in Fig. 4A on p. 1894; furthermore, the data shown for the MMP­9 and the INOS protein bands in Fig. 4C were remarkably similar to the data shown for the IL­1ß and IL­6 proteins, respectively, albeit the backgrounds surrounding the bands were different. Moreover, various of the western blotting data shown in these figures were strikingly similar to data that had already been published in different form in other articles written by (largely) different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, and due to the number of apparent duplications of strikingly similar data between Figs. 3 and 4, 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. [Molecular Medicine Reports 7: 1889­1895, 2013; DOI: 10.3892/mmr.2013.1444].

[Retracted] MicroRNA­449 suppresses proliferation of hepatoma cell lines through blockade lipid metabolic pathway related to SIRT1.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that several of the protein bands featured in the western blot assay data shown in Fig. 3A­D on p. 2147 were strikingly similar to other protein bands, both comparing the data within the same gel slices and comparing the data across the four different parts of the figure. In addition, the control blots featured in Fig. 3A, B and D had already appeared in a different form written by (largely) different authors at different research institutes. After having conducted an independent review of the data in this Figure in the Editorial Office, the concerns of the reader were found to be validated. Therefore, since contentious data in the above article had already been published prior to its submission to International Journal of Oncology, and owing to 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 reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 45: 2143­2152, 2014; DOI: 10.3892/ijo.2014.2596].

[Retracted] Consecutive stimulation of HBsAg promotes the viability of the human B lymphoblastoid cell line IM­9 through regulating the SIRT1­NF­κB pathway.

[This retracts the article DOI: 10.3892/ol.2017.6114.].

Erratum: [Corrigendum] Expression of family with sequence similarity 172 member A and nucleotide­binding protein 1 is associated with the poor prognosis of colorectal carcinoma.

[This corrects the article DOI: 10.3892/ol.2017.6585.].

[Retracted] FAM172A induces S phase arrest of HepG2 cells via Notch 3.

Following the publication of the above article, a concerned reader drew to the Editor's attention that the western blots featured in Figs. 1G, 2B, 3B and 4E contained groupings of bands that were markedly similar in appearance, both within the same gel slices and comparing across different gel slices between the figures in the case of Figs. 3 and 4. After having conducted an internal investigation of this matter, the Editor of Oncology Reports has judged that the anomalous groupings of data were too extensive that their apperance could have been attributed to pure coincidence. Therefore, the Editor has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the data. After having been in contact with the authors of this study, they accepted the Editor's decision to retract this article. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for bringing this matter to our attention. [Oncology Reports 29: 1154­1160, 2013; DOI: 10.3892/or.2013.2235].

[Retracted] FAM172A modulates apoptosis and proliferation of colon cancer cells via STAT1 binding to its promoter.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that lanes 1­3 of the EMSA results shown in Fig. 6 on p. 1278 were strikingly similar to data that had already appeared in a different form in the following publication by different authors at different research institutes: Qiu K, Li Z, Chen J, Wu S, Zhu X, Gao S, Gao J, Ren G and Zhou X: EIN3 and ORE1 accelerate degreening during ethylene­mediated leaf senescence by directly activating chlorophyll catabolic genes in Arabidopsis. PLoS Genet 11: e1005399, 2015. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 1273­1280, 2016; DOI: 10.3892/or.2015.4485.

[Retracted] SIRT3 regulates cell proliferation and apoptosis related to energy metabolism in non­small cell lung cancer cells through deacetylation of NMNAT2.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control ß­actin western blots shown in Fig. 4C were strikingly similar to data appearing in different form in Fig. 9B in a previously published paper featuring one author in common; moreover, the immunoblotting experiments shown in Figs. 1B and D and 2B appeared to have been derived, either wholesale or in part, from data that had already appeared in the following publication: Lei Y, Liu H, Yang Y, Wang X, Ren N, Li B, Liu S, Cheng J, Fu X and Zhang J: Interaction of LHBs with C53 promotes hepatocyte mitotic entry: A novel mechanism for HBV­induced hepatocellular carcinoma. Oncol Rep 29: 151­159, 2012. Owing to the fact that the contentious data in the above article had already been published prior to its submission to International Journal of Oncology, and due to a lack of overall 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 reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 43: 1420­1430, 2013; DOI: 10.3892/ijo.2013.2103].

[Retracted] SIRT1 promotes tumorigenesis of hepatocellular carcinoma through PI3K/PTEN/AKT signaling.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control ß­actin western blots shown in Figs. 1B and 6 were strikingly similar to data that had already appeared in a different form in the following publication: Lei Y, Liu H, Yang Y, Wang X, Ren N, Li B, Liu S, Cheng J, Fu X and Zhang J: Interaction of LHBs with C53 promotes hepatocyte mitotic entry: A novel mechanism for HBV­induced hepatocellular carcinoma. Oncol Rep 29: 151­159, 2012. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 28: 311­318, 2012; DOI: 10.3892/or.2012.1788].

Olfactory impairment in COVID-19: Two methods for the assessment of olfactory function.

Background: Olfactory impairment is a major symptom of COVID-19. Is it necessary for COVID-19 patients to perform the detection of olfactory function, even how to select the olfactory psychophysical assessment tool. Methods: Patients infected with SARS-CoV-2 Delta variant were firstly taken into three categories (mild, moderate, and severe) according to the clinical classification. The Odor Stick Identification Test for the Japanese (OSIT-J) and the Simple Olfactory Test were used to assess olfactory function. Moreover, these patients were divided into three groups based on the results of the olfactory degree (euosmia, hyposmia, and dysosmia), too. The statistical analysis of the correlations between olfaction and clinical characteristics of patients were performed. Results: Our study demonstrated that the elderly men of Han were more susceptible to infected SARS-CoV-2, the clinical symptoms of the COVID-19 patients showed a clear correspondence with the disease type and the degree of olfactory disturbance. Whether or not to vaccinate and whether to complete the whole course of vaccination was closely related to the patient's condition. OSIT-J Test and Simple Test were consistent in our work, indicating that olfactory grading would worsen with the aggravation of symptoms. Furthermore, the OSIT-J method maybe better than Simple Olfactory Test. Conclusion: The vaccination has an important protective effect on the general population, and vaccination should be vigorously promoted. Moreover, it is necessary for COVID-19 patients to perform the detection of olfactory function, and the easier, faster and less expensive method for determination of olfactory function should be utilized to COVID-19 patients as the vital physical examination.

Application of Biomechanics Based on Intelligent Technology and Big Data in Physical Fitness Training of Athletes.

Physical training has a high degree of participation all over the world. With the opening of the era of national fitness, physical training has become more popular from the original specialization, and the complex training methods and contents have gradually become simplified. The development and change of physical training has also brought many problems to the professional training of athletes, such as high training intensity but poor effect, insufficient training posture, and long-term physical injury. In order to help athletes achieve better results in physical training and reduce the probability of injury, taking sprint training as an example, this article adopted the sports and body data of elite athletes through intelligent technology and big data analysis, established a human motion model from the perspective of biomechanics, and then conducted a corresponding test run experiment for athletes. The experimental results suggested that drag resistance running could improve the specific strength quality of sprinting. At the same time, when using resistance load for training, the maximum speed should not exceed 90% of the maximum speed without resistance. The average horizontal maximum velocity decreased by approximately 9% when training under a resistance load, and the best training results were obtained by training athletes within this range.

Influence of Sports Biomechanics on Martial Arts Sports and Comprehensive Neuromuscular Control under the Background of Artificial Intelligence.

Neuromuscular control refers to the reflexes of nerves that affect muscle balance and function. In addition, there are interactions between joint structure, muscle function, and the central nervous system. In the integration with other intelligent control methods and optimization algorithms, such as fuzzy control/expert verification and genetic algorithm, it provides nonparametric object models, optimization parameters, reasoning models, and fault diagnosis. The central nervous system is the main research object of neuromuscular control. Martial arts often cause injuries or affect the progress of martial arts because of some irregular movements. Chinese traditional martial arts is another name for "martial arts" in the late Qing Dynasty in China. It is mainly reflected in the individual's application and attainments in martial arts traditional teaching methods and personal cultivation. Therefore, this paper proposes an analysis of the influence of sports biomechanics on martial arts sports and comprehensive neuromuscular control in the context of artificial intelligence. In this paper, the specific research of Wushu sports is carried out mainly in two aspects: sports biomechanics and neuromuscular control. It uses a variety of algorithms, successively using particle swarm algorithm, neural network structure, fitness function, and so on. This paper compares and analyzes their accuracy and then selects the optimal algorithm. It then conducts experimental research on the martial arts movements of professional martial arts Sanda players. The final experimental conclusion shows that, regarding lower limb selective response time and the middle left lower limb prereaction time (L-PMT) of the elite athlete group and the ordinary athlete group, the average movement value of the elite group of 2.336 is significantly greater than that of the ordinary group of 1.938. This shows that, within a certain range, the larger the knee angle and the smaller the hip angle, the stronger the ability to buffer the impact of the ground, without causing greater damage to the muscles and joints.

Biomechanics and Neuromuscular Control Training in Table Tennis Training Based on Big Data.

Thinking of big data as a collection of huge and sophisticated data sets, it is hard to process it effectively with current data management tools and processing methods. Big data is reflected in that the scale of data exceeds the scope of traditional volume measurement, and it is difficult to collect, store, manage, and analyze through traditional methods. Analyzing the biomechanics of table tennis training through big data is conducive to improving the training effect of table tennis, so as to formulate corresponding neuromuscular control training. This paper mainly analyzes various indicators in biomechanics and kinematics in table tennis training under big data. Under these metrics, an improved decision tree method was then used to analyze the differences between athletes trained for neuromuscular control and those who did not. It analyzed the effect of neuromuscular control training on the human body through different experimental control groups. Experiments showed that after nonathletes undergo neuromuscular control training, the standard rate of table tennis hitting action increases by 10% to 20%, reaching 80%. The improvement of athletes is not very obvious.

miR-452 Reverses Abnormal Glycosylation Modification of ERα and Estrogen Resistance in TNBC (Triple-Negative Breast Cancer) Through Targeting UGT1A1.

Background: The breast epithelial cells in patients with triple-negative breast cancer (TNBC) actually have specific estrogen receptor (ER) expression, and the abnormal glycosylation of UGT1A1 in TNBC cells resulted in abnormal expression and function of ERα through regulating the modification of ERα. Therefore, our study targets the role of UGT1A1 expression, then glycosylation modification of ERα (estrogen receptor α) and estrogen resistance in development of TNBC. Methods: The differential expression of mRNA and miRNA in TNBC tissues was tested. Luciferase activity was analyzed in TNBC cells treated with miR-452. Moreover, the human mammary gland and TNBC cell lines were dealt with estrogen and miR-452 or its inhibitors, then proliferation ability was further determined. Moreover, the role of interaction between UGT1A1 and ERα in the glycosylation modification of ERα and UGT activity, and metabolism of estrogen were assessed. The effects of miR-452 on TNBC by improving abnormal glycosylation modification of ERα by targeting UGT1A1 and estrogen resistance were studied in vitro and in vivo. Results: The expression level of UGT1A1 in TNBC tumor tissues was higher than its matched para-tumorous tissues, but the miR-452 expression was opposite. The glycosylation modification site of ERα expressed in TNBC cells was different from that of normal mammary epithelial cells. The estrogen 17ß-estradiol (E2) significantly promoted mitotic entry of TNBC cells. The interaction between UGT1A1 and ERα affected the expression level of each other, as well as the UGT enzyme activity and proliferation of TNBC cells. UGT1A1 induced production of intracellular estrogens and TNBC proliferation, but it could be reversed by overexpression of ERα. Upregulation of ERα caused the downregulation of UGT1A1 and marked decrease of intracellular estrogen products, and then suppressed TNBC proliferation. Moreover, UGT1A1 was the target gene of miR-452; miR-452 antagomir restrained TNBC xenograft. Conclusion: Our results demonstrated that estrogen was a positive factor in the proliferation of TNBC cells at onset of mitosis through accentuating the expression and enzyme activity of UGT1A1. However, miR-452 targeted to UGT1A1, then regulated glycosylation modification of ERα, estrogen metabolism, and TNBC development associated with estrogen resistance.

miR-494 induces EndMT and promotes the development of HCC (Hepatocellular Carcinoma) by targeting SIRT3/TGF-ß/SMAD signaling pathway.

EndMT has an important effect on metastasis and progression of tumor. This work will elucidate the effect of miR-494 on EndMT and development of HCC. Therefore, the differential miRNA expression among non-tumorous, para-tumorous and tumorous tissues was analyzed. Moreover, luciferase activities of SIRT3 3'UTR treated with miR-494 were determined. Then human hepatoma cell lines were dealt with mimics or inhibitors of miR-494, migration and proliferation ability were assessed. The expression of SIRT3 and markers of mesenchymal cell were analyzed. The influences of miR-494 on development of HCC through inducing EndMT by targeting SIRT3 and TGF-ß/SMAD signaling pathways in hepatoma cell lines were investigated. Xenograft mice were used to explore the potential roles of miR-494 on EndMT and development of HCC in vivo. Our results showed that, compared with non-tumorous tissues, 17 miRNAs were upregulated and 3 miRNAs were down-regulated in tumor tissues. In tumor tissues, the miR-494 expression level was much more than the expression of para-tumorous and non-tumorous tissues. MiR-494 suppressed SIRT3 expression, additionally enhanced expression of mesenchymal cell markers, while exerted effects on cell proliferation and migration of hepatoma cell lines. Moreover, the antagomir of miR-494 could protect against development process in xenogarft murine model. In conclusions, our work demonstrated that miR-494 targeted to SIRT3, and was a crucial mediator of EndMT and development of HCC through regulating SIRT3/TGF-ß/SMAD signaling pathway. It suggested that aim at SIRT3/TGF-ß/SMAD signaling pathway through suppressing the miR-494 expression level, was a feasible therapy strategy for HCC.

miR-449a induces EndMT, promotes the development of atherosclerosis by targeting the interaction between AdipoR2 and E-cadherin in Lipid Rafts.

EndMT plays an important role in the relationship between endothelial dysfunction and atherosclerosis. This work will elucidate the biofunction induced by miR-449a and lipid rafts in EndMT and development of atherosclerosis. The differential miRNA expression between atherosclerotic plaques and normal arteries were analyzed. The luciferase activities of AdipoR2 3' UTR treated with miR-449a were determined. ECs were dealt with miR-449a mimics or inhibitors, then cell proliferation and migration were assessed. Moreover, the expression of AdipoR2 and mesenchymal cell markers were analyzed. The influences of lipid rafts related to reciprocity between E-cadherin and AdipoR2 on TNF-α-induced damage in ECs were investigated. ApoE KO diabetic mice were used to explore the potential roles of miR-449a on atherosclerosis. Our results indicated that compared with normal arteries, 17 miRNAs were upregulated and 3 miRNAs were down-regulated in atherosclerotic plaques. The relative expression of miR-449a in plaques was significantly higher than that in normal arteries. MiR-449a suppressed AdipoR2 expression, additionally its interaction protein E-cadherin in ECs. MiR-449a enhanced expression of mesenchymal cell markers, induced cell proliferation and migration of ECs, regulated the interaction between E-cadherin and AdipoR2 interceded by lipid rafts. The miR-449a antagomir could protect against the development process of atherosclerosis in ApoE KO diabetic mice. In conclusion, miR-449a targeted to AdipoR2, and was a crucial mediator of EndMT and atherosclerosis in ECs through regulating E-cadherin bindability with AdipoR2 in lipid rafts. These results suggested that aim to lipid rafts and miR-449a in chronic EC inflammation response, was a feasible therapy strategy for atherosclerosis.