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132 results on '"Sheng, Jiyao"'

30. Targeting autophagy in chemotherapy-resistant of hepatocellular carcinoma

Author

Sheng, Jiyao, Qin, Hanjiao, Zhang, Kun, Li, Bingjin, and Zhang, Xuewen

Subjects
Review Article, digestive system diseases
Abstract

Hepatocellular carcinoma (HCC) is a malignant tumor with poor prognosis. Surgical resection is recommended for very early-stage and early-stage HCC, but HCC is still prone to recurrence and metastasis after surgery. Furthermore, treatment options for intermediate- and advanced-stage HCC are relatively limited. Systemic therapy is the preferred method to kill residual cancer cells after surgery and prolong survival time of inoperable patients, but most cases are insensitive to chemotherapeutic agents, restricting widespread clinical application of systemic therapy. Many studies have found that various chemotherapeutic drugs for HCC treatment can increase autophagic flux of HCC cells, and it may be related with enhancing drug resistance and promoting cell survival. However, enhancement of autophagic flux may also induce tumor cell death in some cases, leading to marked inconsistency across studies. Here we reviewed the mechanisms underlying the increase in autophagic flux in HCC cells induced by chemotherapeutic drugs and examined the contributions of autophagy and related pathways to chemotherapy drug resistance. Our aim was to identify potential autophagy-related targets for improving the sensitivity of HCC to chemotherapeutic drugs.

Published
2018

34. Bioinspired spike-like double yolk–shell structured TiO2@ZnIn2S4for efficient photocatalytic CO2reductionElectronic supplementary information (ESI) available. See DOI: 10.1039/d1cy02079j

Author

She, Ping, Guan, Buyuan, Sheng, Jiyao, Qi, Yuanyuan, Qiao, Guanyu, Rui, Hongbang, Lu, Geyu, Qin, Jun-Sheng, and Rao, Heng

Abstract

Photocatalytic carbon dioxide (CO2) reduction (PCR) into syngas is one of the sustainable approaches for recycling CO2into value-added chemical feedstocks. However, the PCR efficiency is often limited by the insufficient light-harvesting and poor charge separation. Herein, we design a spike-like double yolk–shell structured TiO2@ZnIn2S4(D-Y-TiO2@ZnIn2S4) photocatalyst with superior PCR efficiency. The unique design not only integrates advantages of increasing active sites, surface areas and light-harvesting capacity induced by the hierarchical morphology, but also facilitates photo-induced charge separation based on the heterojunction of TiO2and ZnIn2S4. Owing to the combination of structural and compositional merits, the optimized D-Y-TiO2@ZnIn2S4photocatalyst shows superior PCR performance (325.29 μmol CO per g; 227.18 μmol H2per g) under visible light. In addition, the ratio of CO/H2can be tuned from 0.03 to 1.43 by changing the sacrificial hole capture condition. This work provides a prospective way to obtain efficient PCR photocatalysts.

Published
2022
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35. Immunotherapy for Hepatocellular Carcinoma: Current Advances and Future Expectations

Author

Xie, Yingjun, Xiang, Yien, Sheng, Jiyao, Zhang, Dan, Yao, Xiaoxiao, Yang, Yongsheng, and Zhang, Xuewen

Subjects
Article Subject
Abstract

Primary liver cancer is a common kind of digestive cancers with high malignancy, causing 745,500 deaths each year. Hepatocellular carcinoma is the major pathological type of primary liver cancer. Traditional treatment methods for patients with hepatocellular carcinoma have shown poor efficacy in killing residual cancer cells for a long time. In recent years, tumor immunotherapy has emerged as a promising method owing to its safety and efficacy with respect to delaying the progression of advanced tumors and protecting postoperative patients against tumor relapse and metastasis. Immune tolerance and suppression in tumor microenvironments are the theoretical basis of immunotherapy. Adoptive cell therapy functions by stimulating and cultivating autologous lymphocytes ex vivo and then reinfusing them into the patient to kill cancer cells. Cancer vaccination is performed using antigenic substances to activate tumor-specific immune responses. Immune checkpoint inhibitors can reactivate tumor-specific T cells and develop an antitumor effect by suppressing checkpoint-mediated signaling. Oncolytic viruses may selectively replicate in tumor cells and cause lysis without harming normal tissues. Here, we briefly introduce the mechanism of immunosuppression in hepatocellular carcinoma and summarize the rationale of the four major immunotherapeutic approaches with their current advances.

Published
2018
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41. The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain

Author

Sheng, Jiyao, Liu, Shui, Wang, Yicun, Cui, Ranji, and Zhang, Xuewen

Subjects
Article Subject
Abstract

Chronic pain, as a stress state, is one of the critical factors for determining depression, and their coexistence tends to further aggravate the severity of both disorders. Unfortunately, their association remains unclear, which creates a bottleneck problem for managing chronic pain-induced depression. In recent years, studies have found considerable overlaps between pain- and depression-induced neuroplasticity changes and neurobiological mechanism changes. Such overlaps are vital to facilitating the occurrence and development of chronic pain and chronic pain-induced depression. In this review, we summarized the role of neuroplasticity in the occurrence and development of the two disorders in question and explored individualized application strategies of analgesic drugs and antidepressants that have different pharmacological effects in the treatment of chronic pain-induced depression. Therefore, this review may provide new insights into the understanding of association between chronic pain and depression.

Published
2017
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47. Drug-Resistant Epilepsy and Surgery

Author

Sheng, Jiyao, Liu, Shui, Qin, Hanjiao, Li, Bingjin, and Zhang, Xuewen

Abstract

Background: Epilepsy is a chronic brain disease that is caused by various factors and characterized by recurrent, episodic and temporary central nervous system dysfunction which results due to excessive discharge of brain neurons. In the past decades, despite the continuous development of antiepileptic drugs, there are still many patients with epilepsy progressing to drugresistant epilepsy. Currently, surgical treatment is one of important way to cure drug-resistant epilepsy. Methods: Data were collected from Web of Science, Medline, Pubmed, through searching of these keywords: “surgery” and “drug-resistant epilepsy”. Results: An increasing number of studies have shown that surgery plays an important role in the treatment of drug-resistant epilepsy. Moreover, the comprehensive treatment mainly based on surgery can achieve the remission and even cure of drug-resistant epilepsy. Conclusion: In this review, we discuss the pathogenesis of drug-resistant epilepsy and the comprehensive treatment mainly based on surgery; this review may provide a reference for the clinical treatment of drug-resistant epilepsy.

Published
2018
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48. FGA influences invasion and metastasis of hepatocellular carcinoma through the PI3K/AKT pathway.

Author

Han X, Liu Z, Cui M, Lin J, Li Y, Qin H, Sheng J, and Zhang X

Subjects
Humans, Animals, Mice, Cell Movement genetics, Male, Cell Line, Tumor, Epithelial-Mesenchymal Transition genetics, Neoplasm Metastasis, Female, Middle Aged, Gene Expression Regulation, Neoplastic, Carcinoma, Hepatocellular pathology, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular metabolism, Liver Neoplasms pathology, Liver Neoplasms metabolism, Liver Neoplasms genetics, Proto-Oncogene Proteins c-akt metabolism, Phosphatidylinositol 3-Kinases metabolism, Phosphatidylinositol 3-Kinases genetics, Fibrinogen metabolism, Fibrinogen genetics, Neoplasm Invasiveness, Signal Transduction
Abstract

Fibrinogen is an important plasma protein composed of three polypeptide chains, fibrinogen alpha (FGA), beta, and gamma. Apart from being an inflammation regulator, fibrinogen also plays a role in tumor progression. Liver cancer usually has a poor prognosis, with chronic hepatitis being the main cause of liver cirrhosis and hepatocellular carcinoma (HCC). FGA serves as a serological marker for chronic hepatitis, but its relationship with liver cancer remains unclear. Through bioinformatics analysis and agarose gel electrophoresis, we found that FGA was downregulated in HCC and correlated with tumor stage and grade. By constructing both FGA gene knockout and overexpression cell models, we demonstrated that overexpressing FGA inhibited migration and invasion of liver cancer cells through Transwell migration/invasion and wound healing assays. Western blotting experiments showed that FGA overexpression increased the expression of the epithelial-mesenchymal transition marker protein E-cadherin while decreasing N-cadherin and slug protein expression. In addition, FGA knockout activated the PI3K/AKT pathway. In a mouse model of metastatic tumors, overexpression of FGA restricted the spread of tumor cells. In conclusion, FGA exhibits an inhibitory effect on tumor metastasis, providing new insights for the treatment of advanced HCC metastatic tumors.

Published
2024
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49. Screening and Validation of Independent Predictors of Poor Survival in Pancreatic Cancer.

Author

Liu S, Cai Y, Changyong E, Sheng J, and Zhang X

Subjects
Gene Expression Profiling, Humans, Pancreatic Neoplasms genetics, Pancreatic Neoplasms pathology, Prognosis, Protein Interaction Maps, Survival Rate, Biomarkers, Tumor genetics, Computational Biology methods, Early Detection of Cancer methods, Gene Regulatory Networks, Pancreatic Neoplasms mortality, Transcriptome
Abstract

Pancreatic cancer is a digestive system malignant tumor with high mortality and poor prognosis, but the mechanisms of progression remain unclear in pancreatic cancer. It's necessary to identify the hub genes in pancreatic cancer and explore the novel potential predictors in the prognosis of pancreatic cancer. We downloaded two mRNA expression profiles from Gene Expression Omnibus and The Cancer Genome Atlas Pancreatic Cancer (TCGA-PAAD) datasets to screen the commonly differentially expressed genes in pancreatic cancer by limma package in R. Subsequently, measurement of the functional similarity among the 38 DEGs in common was performed to identify the hub genes using GOSemSim package. Then, survival analysis and Cox regression were applied to explore prognosis-related hub genes using the survival package. Statistics analysis by two-tailed Student's t-test or one-way based on TCGA-PAAD datasets and qPCR detection in clinical samples were performed to explore the correlations between expression of hub genes in pancreatic cancer tissues and clinical parameters. Based on integrated analysis of TCGA and GEO datasets, we screened 38 DEGs in common, which were all up-regulated. The functional similarity results showed that 10 DEGs including TSPAN1, MSLN, C1orf116, PKP3, CEACAM6, BAIAP2L1, PPL, RAB25, ERBB3, and AP1M2 in the DEGs in common, which had the higher average functional similarity, were considered as the hub genes. Survival analysis results and Cox regression analysis showed that TSPAN1, CEACAM6, as well as ERBB3 were all associated with poor overall survival of PC. qPCR results showed that the expression levels of TSPAN1 and ERBB3 were significantly upregulated in the PC tissues. The statistical analysis results revealed that TSPAN1 expression correlated significantly with histologic grade, T stage, clinical stage, and vital status by two-tailed Student's t-test or one-way ANOVA; ERBB3 expression correlated significantly with T stage, clinical stage, and vital status by two-tailed Student's t-test or one-way ANOVA. We found that TSPAN1 and ERBB3 could be independent predictors of poor survival in pancreatic cancer., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Liu, Cai, Changyong, Sheng and Zhang.)

Published
2021
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50. PI3Kgamma Inhibitor Attenuates Immunosuppressive Effect of Poly(l-Glutamic Acid)-Combretastatin A4 Conjugate in Metastatic Breast Cancer.

Author

Qin H, Yu H, Sheng J, Zhang D, Shen N, Liu L, Tang Z, and Chen X

Abstract

Vascular disrupting agents (VDAs) have great potential for cancer treatment. Poly(l-glutamic acid)-combretastatin A4 conjugate (PLG-CA4) is a novel class of VDAs. Though it has notable antitumor activity, it can induce host immune responses that promote tumor growth. Here, PLG-CA4 induces the polarization of tumor-associated macrophages (TAMs) toward the M2-like phenotype in 4T1 metastatic breast cancer (Control 30% vs PLG-CA4 53%; p < 0.05). Compared to the monotherapy of PLG-CA4, inhibition of phosphoinositide 3-kinase gamma (PI3Kγ) attenuates the immunosuppressive effect of PLG-CA4 treatment by decreasing the number of M2-like TAMs (2.0 × 10 4 to 1.5 × 10 4 per tumor) and potential enhancement of cytotoxic T lymphocyte (3.0 × 10 4 to 5.7 × 10 4 per tumor). Importantly, PI3Kγ inhibitor synergizing with PLG-CA4 significantly extends the mean survival time from 52 days in monotherapy-treated mice to 61.8 days. Additionally, the combination of PLG-CA4 and PI3Kγ inhibitor improves the tumor therapeutic effect of NLG919, an inhibitor of immune checkpoint indoleamine 2,3-dioxygenase (IDO). As far as it is known, this is the first demonstrated study that VDAs induce the reshaping of macrophages to the M2-like phenotype. The findings also indicate a potential therapeutic strategy of the combination VDAs with an accurate immune modifier in the tumor to reverse the immune resistance., Competing Interests: The authors declare no conflict of interest.

Published
2019
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