HCV-Specific Interleukin-21+CD4+ T Cells Responses Associated with Viral Control through the Modulation of HCV-Specific CD8+ T Cells Function in Chronic Hepatitis C Patients

Guo-Hua Feng,Fu-Sheng Wang,Ji-Yuan Zhang,Qing-Lei Zeng,Lei Jin,Junliang Fu,Bin Yang,Ying Sun,Tianjun Jiang,Xiangsheng Xu,Zheng Zhang,Jinhong Yuan,Liyuan Wu 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.4

Interleukin-21 (IL-21)+CD4+ T cells are involved in the immune response against hepatitis B virus (HBV) by secreting IL-21. However, the role of IL-21+CD4+ T cells in the immune response against chronic hepatitis C (CHC) virus infection is poorly understood. This study aimed to investigate the role of IL-21+CD4+ T cells in CHC patients and the potential mechanisms. The study subjects in-cluded nineteen CHC patients who were grouped by viral load (low, < 106 RNA copies/ml, n = 8; high, > 106 RNA copies/ml, n = 11). The peripheral frequency of HCV-specific IL-21+CD4+ T cells was higher in the low viral load group and was negatively correlated with the serum HCV RNA viral load in all CHC patients. Meanwhile, IL-21+ cells accumulated in the liver in the low viral load group. In vitro, IL-21 treatment increased the expression of proliferation markers and cytolytic molecules on HCV-specific CD8+ T cells. In summary, these findings suggest that HCV-specific IL-21+CD4+ T cells might contribute to HCV control by rescuing HCV-specific CD8+ T cells in CHC patients.

Fibulin-5 is a Prognostic Marker that Contributes to Proliferation and Invasion of Human Glioma Cells

Sheng, Xu-Dong,Chen, Hu,Wang, Hui,Ding, Zhi-Bin,Xu, Gang-Zhu,Zhang, Jun-Feng,Lu, Wen-Chao,Wu, Tao,Zhao, Ling Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.2

Fibulin-5 has recently been considered as a potential tumor suppressor in human cancers. Several studies have shown that it is down-regulated in a variety of tumor types and inhibits tumor growth and metastasis. This study was aimed to investigate the clinical significance of fibulin-5 in glioma and its role in cell proliferation and invasion. We found that the expression of fibulin-5 in glioma tissues was significantly lower than those in normal brain (NB) tissues. Negative expression was significantly correlated with advanced clinical stage (grade III+IV). Furthermore, Fibulin-5 negative expression was correlated with a shorter overall survival of glioma patients. Multivariate Cox repression analysis indicated that fibulin-5 was an independent factor for predicting overall survival of glioma patients. Overexpression obviously inhibited cell proliferation in U251 and U87 cells. Furthermore, it significantly reduced the number of migrating and invading glioma cells. In conclusion, impaired expression of fibulin-5 is correlated with the advanced tumor stage in glioma. Otherwise, Fibulin-5 is an independent prognostic marker for predicting overall survival of glioma patients. Mechanistically, it may function as a tumor suppressor via inhibiting cell proliferation and invasion in gliomas.

MSP58 Knockdown Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma in Vitro and in Vivo

Xu, Chun-Sheng,Zheng, Jian-Yong,Zhang, Hai-Long,Zhao, Hua-Dong,Zhang, Jing,Wu, Guo-Qiang,Wu, Lin,Wang, Qing,Wang, Wei-Zhong,Zhang, Jian Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.7

Esophageal carcinoma (EC) is one of the most aggressive cancers with a poor prognosis. Understanding the molecular mechanisms underlying esophageal cancer progression is a high priority for improved EC diagnosis and prognosis. Recently, MSP58 was shown to behave as an oncogene in colorectal carcinomas and gliomas. However, little is known about its function in esophageal carcinomas. We therefore examined the effects of MSP58 knockdown on the growth of esophageal squamous cell carcinoma (ESCC) cells in vitro and in vivo in order to gain a better understanding of its potential as a tumor therapeutic target. We employed lentiviral-mediated small hairpin RNA (shRNA) to knock down the expression of MSP58 in the ESCC cell lines Eca-109 and EC9706 and demonstrated inhibition of ESCC cell proliferation and colony formation in vitro. Furthermore, flow cytometry and western blot analyses revealed that MSP58 depletion induced cell cycle arrest by regulating the expression of P21, CDK4 and cyclin D1. Notably, the downregulation of MSP58 significantly inhibited the growth of ESCC xenografts in nude mice. Our results suggest that MSP58 may play an important role in ESCC progression.

A liquid phase deposited porous flower-like HNaV6O16⋅4H2O film developed for a novel adsorbent to remove Pb2+, Cu2+, Mn2+ and Cd2+

Xu Hai-Yan,Yang Yi Cai,Li Dong-Cai,Wu Ran Ran,Wang Ai-Guo,Sun Dao-Sheng,Zhang Feng-Jun,오원춘 한국세라믹학회 2023 한국세라믹학회지 Vol.60 No.3

Heavy metal ion pollution of water resources is becoming increasingly serious, and adsorption is one of the most effective strategies for removing heavy metal ions. In the paper, hydrated hydrogen sodium vanadium oxide (HNaV 6O164H2O) fi lm developed for heavy metal ion adsorption was prepared directly via a low-temperature liquid-phase deposition approach. The prepared film shows an interesting porous flower-like morphology and has large spacing ( d = 10.87 Å). The highest adsorption capacity of the obtained HNaV 6O164H2O fi lm for Pb 2+, Cu 2+, Cd 2+ and Mn 2+ is 513 mg/g (2565 mg/m 2), 430 mg/g (2150 mg/m 2), 134 mg/g (875 mg/m 2) and 175 mg/g (670 mg/m 2), respectively. The adsorption percentage of the sample decreased from 92.2 to 86.3% after 4 cycles. The adsorption process follows the Langmuir adsorption isotherm and the pseudo second-order dynamic model, indicating that heavy metal ion adsorption by the fi lm is a single molecular layer chemical adsorption. In combination with various characterizations and comparison tests of samples after adsorption, the adsorption mechanisms include surface electrostatic attraction, complexation, and cation exchange. The results indicate that the fi lm is a potential material to remove heavy metal ions from the aqueous solution.

CHMP1A suppresses the growth of renal cell carcinoma cells via regulation of the PI3K/mTOR/p53 signaling pathway

Wu Youping,Wu Yueguo,Xu Cong,Sun Wei,You Zhenqiang,Wang Yin,Zhang Sheng 한국유전학회 2022 Genes & Genomics Vol.44 No.7

Background: CHMP1A, a member of the ESCRT-III complex family, has been indicated as a brand-new inhibitor gene of tumors. Our previous research has revealed that CHMP1A plays a vital role in the development and progression of renal cell carcinoma (RCC). Objective: To investigate the potential target pathway of the regulation of the tumor cell growth by CHMP1A. Methods: The effect of CHMP1A on mTOR pathway was elucidated by western blotting. The effect of CHMP1A on the expression of p53 was evaluated, and A498 cell growth was assessed by colony formation and MTT assays. The expression of p53 was knocked down by shRNA-p53, and the effect of CHMP1A on mTOR after knockdown of p53 was evaluated. The effect of CHMP1A on apoptosis and its relationship with MDM2 pathway were detected by western blotting and FCM. Finally, the relationship between the regulation of p53 by CHMP1A and the PI3K/mTOR pathway was detected. Results: This study showed that the mTOR pathway was suppressed significantly in CHMP1A-overexpressing A498 and 786-0 cells; moreover, the enhanced expression of p53 and the reduced proliferation were shown in CHMP1A-overexpressing A498 cells. Furthermore, CHMP1A was able to regulate the PI3K/PTEN/mTOR and MDM2/p53 pathways in order to suppress RCC. In addition, CHMP1A regulated Bax and Bcl-2 via MDM2/p53 to induce the apoptosis of tumor cells and upregulated the expression of p53 via the PI3K/mTOR pathway. Conclusions: The results convey that CHMP1A-related suppression of RCC is closely related to the PI3K/mTOR/p53 pathway.

Stabilization Control Strategy for Shore Power System with Surge Loads Based on Virtual Synchronous Generator

Wu Cao,Kangli Liu,Sheng Xu,Haotian Kang,Jianfeng Zhao 대한전기학회 2019 Journal of Electrical Engineering & Technology Vol.14 No.3

The frequent starting of large capacity lifting machines and other surge ship electrical loads will result in severe impacts on a shipboard power network, such as voltage and frequency fl uctuations. Therefore, a novel stabilization control strategy for shore power systems based on virtual synchronous generator is proposed in this paper, so as to improve the power quality and enhance the stability and reliability of shipboard power networks. In this strategy, a reactive power inertia component is embedded into the virtual synchronous generator aiming at shipboard surge reactive powers. On this basis, a voltage and frequency stability control method is presented to improve the static performances of shore power systems. In addition, a d-q decoupling control scheme in synchronous reference frame for the voltage and current double closed-loop control system is designed, and moreover, the infl uence of diff erent feedback voltages on the output characteristics of shore power supplies is studied. The theoretical analysis, simulation and experiment results show that, the proposed control strategy can eff ectively attenuate the frequency and voltage fl uctuations, eliminate the frequency and voltage steady-state errors, as well as realize the power distribution evenly for modular shore power supplies.

Mortality Characteristic and Prediction of Nasopharyngeal Carcinoma in China from 1991 to 2013

Xu, Zhen-Xi,Lin, Zhi-Xiong,Fang, Jia-Ying,Wu, Ku-Sheng,Du, Pei-Ling,Zeng, Yang,Tang, Wen-Rui,Xu, Xiao-Ling,Lin, Kun Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15

Background: To analyze the mortality distribution of nasopharyngeal carcinoma in China from 1991 to 2013, to predict the mortality in the ensuing five years, and to provide evidence for prevention and treatment of nasopharyngeal carcinoma. Materials and Methods: Mortality data for Nasopharyngeal Carcinoma in China from 1991 to 2013 were used to describe its epidemiological characteristics, such as the change of the standardized mortality rate, sex and age differences, urban-rural differences. Trend-surface analysis was used to study the geographical distribution of the mortality. Curve estimation, time series, gray modeling, and joinpoint regression were used to predict the mortality for the ensuing five years in the future. Results: In China, the standardized mortality rate of Nasopharyngeal Carcinoma increased with time from 1996, reaching the peak values of $1.45/10^5$ at the year of 2002, and decreased gradually afterwards. With males being 1.51 times higher than females, and the city had a higher rate than the rural during the past two decades. The mortality rate increased from age 40. Geographical analysis showed the mortality rate increased from middle to southern China. Conclusions: The standardized mortality rate of Nasopharyngeal Carcinoma is falling. The regional disease control for Nasopharyngeal Carcinoma should be focused on Guangdong province of China, and the key targets for prevention and treatment are rural men, especially after the age of 40. The mortality of Nasopharyngeal Carcinoma will decrease in the next five years.

Genomic Sequence Analysis and Organization of BmKαTx11 and BmKαTx15 from Buthus martensii Karsch: Molecular Evolution of α-toxin genes

Xu, Xiuling,Cao, Zhijian,Sheng, Jiqun,Wu, Wenlan,Luo, Feng,Sha, Yonggang,Mao, Xin,Liu, Hui,Jiang, Dahe,Li, Wenxin Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.4

Based on the reported cDNA sequences of $BmK{\alpha}Txs$, the genes encoding toxin $BmK{\alpha}Tx11$ and $BmK{\alpha}Tx15$ were amplified by PCR from the Chinese scorpion Buthus martensii Karsch genomic DNA employing synthetic oligonucleotides. Sequences analysis of nucleotide showed that an intron about 500 bp length interrupts signal peptide coding regions of $BmK{\alpha}Tx11$ and $BmK{\alpha}Tx15$. Using cDNA sequence of $BmK{\alpha}Tx11$ as probe, southern hybridization of BmK genome total DNA was performed. The result indicates that $BmK{\alpha}Tx11$ is multicopy genes or belongs to multiple gene family with high homology genes. The similarity of $BmK{\alpha}$-toxin gene sequences and southern hybridization revealed the evolution trace of $BmK{\alpha}$-toxins: $BmK{\alpha}$-toxin genes evolve from a common progenitor, and the genes diversity is associated with a process of locus duplication and gene divergence.

Effect of Insulin-like Growth Factor-1 on Bone Morphogenetic Protein-2 Expression in Hepatic Carcinoma SMMC7721 Cells through the p38 MAPK Signaling Pathway

Xu, Guan-Jun,Cai, Sheng,Wu, Jian-Bing Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.4

Objective: To observe the effect of insulin-like growth factor-1 (IGF-1) on bone morphogenetic protein (BMP)-2 expression in hepatocellular carcinoma SMMC7721 cells. Methods: Cells were divided into blank control, IGF-1, IGF-1 + SB203580, and SB203580 groups. SB203580 was used to block the p38 MAPK signaling pathway. Changes in the expression of BMP-2, p38 MAPK, and phosphorylated p38, MERK, ERK and JNK were determined using reverse transcription polymerase chain reactions (RT-PCR) and Western blot analysis. Results: Protein expression of phosphorylated BMP-2, MERK, ERK, and JNK was significantly up-regulated by IGF-1 compared with the control group ($1.138{\pm}0.065$ vs. $0.606{\pm}0.013$, $0.292{\pm}0.005$ vs. $0.150{\pm}0.081$, $0.378{\pm}0.006$ vs. $0.606{\pm}0.013$, and $0.299{\pm}0.015$ vs. $0.196{\pm}0.017$, respectively; P<0.05). Levels of BMP-2 and phosphorylated MERK and JNK were significantly reduced after blocking of the p38MAPK signaling pathway ($0.494{\pm}0.052$ vs. $0.165{\pm}0.017$, $0.073{\pm}0.07$ vs. $0.150{\pm}0.081$, and $0.018{\pm}0.008$ vs. $0.196{\pm}0.017$, respectively; P<0.05), but such a significant difference was not observed for phosphorylated ERK protein expression ($0.173{\pm}0.07$ vs. $0.150{\pm}0.081$, P>0.05). Conclusion: IGF-1 can up-regulate BMP-2 expression, and p38 MAPK signaling pathway blockage can noticeably reduce the up-regulated expression. We can conclude that the up-regulatory effect of IGF-1 on BMP-2 expression is realized through the p38 MAPK signaling pathway.

Involvement of FoxM1 in Non-Small Cell Lung Cancer Recurrence

Xu, Nuo,Wu, Sheng-Di,Wang, Hao,Wang, Qun,Bai, Chun-Xue Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.9

Background: Predictive biomarkers for lung cancer recurrence after curative tumor resection remain unclear. This study set out to assess the role of FoxM1 in the recurrence of non-small cell lung cancer. Methods: Immunohistochemistry for FoxM1 expression was performed on paraffin-embedded tumor tissues from 165 NSCLC patients. Association of FoxM1 expression with clinicopathological parameters and disease free survival were evaluated. Results: Our results indicated FoxM1 expression to be significantly associated with poorer tissue differentiation (P =0.03), higher TNM stage (P <0.01), lymph node metastasis (P <0.01), advanced tumor stage (P <0.01), and poorer disease free survival (P <0.01). Multivariable analysis showed that FoxM1 expression increased the hazard of recurrence (hazard ratio= 1.96, 95% CI, 1.04-3.17, P <0.05), indicating that FoxM1 is an independent and significant predictor of lung cancer recurrence. Conclusion: Therefore, FoxM1 is an independent risk factor for recurrence of NSCLC. Elevated FoxM1 expression could be used as an indicator of poor disease free survival.