SWNHs (Single-Wall Carbon Nanohorns) Supervises Endoplasmic Reticulum (ER) Stress in Hepatocellular Carcinoma.

SWNHs can act as a good biocompatible nanomaterials and show potential application in the field of drug carriers or therapy to influence biological function on cell. HCC (Hepatocellular carcinoma) is a most common type of malignant neoplasms in the digestive system. SWNHs have been reported to be able to induce HepG2 cell apoptosis. In the study, we implant HepG2 cell into nude mice and observe the effect of SWNHs on these tumor model mice. And then 38 apoptosis proteins were determined using Human Apoptosis Antibody Array kit. The proteins related to ER stress were examined through immunohistochemical staining and western blotting assay. Our results indicated that SWNHs did not influence on tumor in model mice. There were no significant difference expression of the 38 apoptosis proteins in xenograft between the treatment group and control. However, the proteins related to ER stress were increased. In summary, we identified that SWNHs was as a stimulator of ER stress to influence the biological function of hepatoma cells, and may be used as a potential anti-cancer agent in HCC.

SSRP1 Contributes to the Malignancy of Hepatocellular Carcinoma and Is Negatively Regulated by miR-497.

The aim of this study is to clarify the clinical implication and functional role of structure specific recognition protein 1 (SSRP1) in hepatocellular carcinoma (HCC) and explore the underlying mechanism of aberrant high expression of SSRP1 in cancers. In the present investigation, we validated that SSRP1 was upregulated in HCC samples. We also demonstrated that its upregulation was associated with several clinicopathologic features such as higher serum AFP level, larger tumor size, and higher T stage of HCC patients; and its high expression indicated shorter overall survival and faster recurrence. To investigate the role of SSRP1 in HCC progression, both loss- and gain-function models were established. We demonstrated that SSPR1 modulated both proliferation and metastasis of HCC cells in vitro and vivo. Furthermore, we demonstrated that SSRP1-modulated apoptosis process and its knockdown increased the sensitivity of HCC cells to doxorubicin, 5-Fluorouracil, and cisplatin. We also identified microRNA-497 (miR-497) as a posttranscriptional regulator of SSRP1. Ectopic expression of miR-497 inhibited 3'-untranslated-region-coupled luciferase activity and suppressed endogenous SSRP1 expression at both messenger RNA and protein levels. For the first time, we proved that SSRP1 upregulation contributed to HCC development and the tumor-suppressive miR-497 served as its negative regulator.

HCBP6 Modulates Triglyceride Homeostasis in Hepatocytes Via the SREBP1c/FASN Pathway.

Hypertriglyceridemia leads to liver steatosis, cardiovascular disease, and type 2 diabetes. Although HCBP6 (hepatitis C virus core-binding protein 6) was previously shown to be an HCV (hepatitis C virus) core-binding protein, its biological function remains unclear. Here, we demonstrate that HCBP6 negatively regulates intracellular triglyceride (TG) levels in hepatocytes. We found that bidirectional manipulation of hepatocyte HCBP6 expression by knockdown or overexpression results in increased or decreased TG accumulation, respectively. In addition, HCBP6 mRNA and protein levels exhibited significant time- and dose-dependent increases in a cellular model of lipid-overload hepatic steatosis. Furthermore, TG levels are regulated by HCBP6-sterol regulatory element binding protein 1c (SREBP1c)-mediated fatty acid synthase (FASN) expression. We also demonstrate that HCBP6 mRNA and protein expression is inhibited by microRNA-122 (miR-122), and miR-122 overexpression elicited more robust translational repression of luciferase activity driven by the full 3'-UTR of HCBP6. Taken together, our results provide new evidence that miR-122-regulated HCBP6 functions as a sensor protein to maintain intrahepatocyte TG levels.

Regulation of HepG2 cell apoptosis by hepatitis C virus (HCV) core protein via the sirt1-p53-bax pathway.

Hepatitis C virus (HCV) core protein stimulates many signaling pathways related to apoptosis inhibition resulting in hepatocellular carcinoma (HCC). It has been reported that sirt1 is involved in regulating apoptosis; therefore, we investigated the influence of HCV core protein on sirt1 expression and apoptosis in human HepG2 cells. Our study showed that HCV core protein inhibited apoptosis of HepG2 cells as well as caspase-3 expression and activity (P < 0.05). At the same time, sirt1 expression was increased at both the mRNA (P < 0.05) and protein (P < 0.05) levels. Furthermore, apoptosis inhibition was reversed when sirt1 was knocked down (P < 0.05). Our study provides further evidence that the sirt1-p53-Bax signaling pathway plays an important role in regulating the suppression of cell apoptosis induced by HCV core protein.

MiR-132 inhibits expression of SIRT1 and induces pro-inflammatory processes of vascular endothelial inflammation through blockade of the SREBP-1c metabolic pathway.

PURPOSE: Inflammation participates centrally in all stages of atherosclerosis (AS), which begins with pro-inflammatory processes and inflammatory changes in the endothelium, related to lipid metabolism. MicroRNA (miRNA) inhibition of inflammation related to SIRT1 has been shown to be a promising therapeutic approach for AS. However, the mechanism of action is unknown. METHODS: We investigated whether miRNAs regulate the SIRT1 and its downstream SREBP-lipogenesis-cholesterogenesis metabolic pathway in human umbilical vein endothelial cells (HUVECs). HUVECs were transfected with miR-132 mimics and inhibitors, and then treated with or without tumor necrosis factor α (TNFα). The effects of miR-132 on pro-inflammatory processes, proliferation and apoptosis were assessed. RESULTS: We identified that the relative 3' UTR luciferase activities of SIRT1 were significantly decreased in miR-132 transfected HUVECs (0.338 ± 0.036) compared to control (P = 0.000). miR-132 inhibited SIRT1 expression of mRNA level in HUVECs (0.53 ± 0.06) (P < 0.01) as well as proteins of SIRT1. mRNA expression and protein levels of SREBP (0.45 ± 0.07), fatty acid synthase (FASN) (0.55 ± 0.09) and 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR) (0.62 ± 0.08) (P < 0.01), which are downstream regulated genes, were reduced in HUVECs by miR-132. MiR-132 promoted pro-inflammatory processes and apoptosis of HUVECs induced by TNF-α, and inhibited its proliferation, viability and migration. CONCLUSIONS: SIRT1 mRNAs are direct targets of miR-132. miR-132 controls lipogenesis and cholesterogenesis in HUVECs by inhibiting SIRT1 and SREBP-1c expression and their downstream regulated genes, including FASN and HMGCR. Inhibition of SIRT1 by miR-132 was associated with lipid metabolism-dependent pro-inflammatory processes in HUVECs. The newly identified miRNA, miR-132 represents a novel targeting mechanism for AS therapy.

[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].

[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] 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] 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] 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] 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].

[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.

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.

Adiponectin and its receptors in chronic hepatitis B patients with metabolic syndrome in China.

BACKGROUND/AIMS: Adiponectin can initiate a broad range of metabolic and immunological effects. Little is known about the role of adiponectin in hepatitis B related liver disease and metabolic syndrome (MS). METHODOLOGY: We studied 138 patients with untreated chronic hepatitis B (CHB), who were from Beijing Ditan hospital in 2005 to 2009. According to MS, two groups (65 with MS vs. 73 without MS) were established. They were compared with characteristics and stained immunohistochemically for adiponectin and adiponectin receptor2 (adipoR2). RESULTS: In the group of CHB patients with MS, the levels of LDH, γ-GT, FPG, FINS, HOMA-IR, HOMA-ß, TG and HBeAg positive were significantly higher than those in the group without MS (p<0.05). Liver steatosis in the group with MS is significantly more severe than that in the group without MS (p<0.001). With binary logistic regression analyses, BMI and HOMA-IR showed independent predictors to MS in patients with CHB. In patients with chronic HBV, the insulin sensitizing adipokine adiponectin and its receptor AdipoR2 was associated with diabetes in patients with CHB and MS. CONCLUSIONS: Our findings showed the CHB patients with MS may be presence of more severe steatosis. MS in CHB patients may be closely correlated with insulin resistance and less effect of viruses. Reduced hepatic expression of adiponectin and adipoR2 might be of pathophysiological relevance in CHB patients with MS.

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.