Xiang Li

Guangzhou University of Chinese Medicine

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Xin Sun

Tianjin Medical University

Guodong Xiao

Anhui Agricultural University

Sida Qin

Kunming Medical University

Boxiang Zhang

First Affiliated Hospital of Xi'an Jiaotong University

Hong Ren

First Affiliated Hospital of Xi'an Jiaotong University

Shou‐Ching Tang

Affiliated Hospital of Shaanxi University of Chinese Medicine

Chongwen Xu

First Affiliated Hospital of Xi'an Jiaotong University

Oluwole Fadare

University of California, San Diego

Feng Guan

Ministry of Education of the People's Republic of China

Ning Du

Zhejiang University

Cooperative Institutions

Huazhong University of Science and Technology

111

Shanghai Jiao Tong University

104

American Association For Cancer Research

Peking University

Sichuan University

First Affiliated Hospital of Xi'an Jiaotong University

Chinese Academy of Medical Sciences & Peking Union Medical College

Chinese Academy of Sciences

Sun Yat-sen University

Memorial Sloan Kettering Cancer Center

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Fecal microbiota transplantation attenuates Alzheimer’s disease symptoms in APP/PS1 transgenic mice via inhibition of the TLR4-MyD88-NF-κB signaling pathway-mediated inflammation

Research Square (Research Square) (2024)

Xiang Li Qingyong Ding Xinxin Wan Qilong Wu Shiqing Ye

Abstract Alzheimer’s disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest thatFMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice.

Dysbiosis

Pathogenesis

Fecal bacteriotherapy

10.21203/rs.3.rs-3828373/v1

Cite

Citations (0)

Luteolin-Zinc Modulates PRR11 Methylation and Ferroptosis in Lung Cancer Cells Under Hypoxia

Pharmacognosy Magazine (2025)

Jiayong Huang Binbo Fang Ting Guo Yiyang Li Yilin Yang

Background Activation of PRR11 contributes to the progression of lung cancer and is related to its methylation status. However, the regulatory mechanism of luteolin-zinc (Lu-Zn) on PRR11 methylation-mediated lung cancer progression under hypoxic conditions remains to be explored.. Purpose This study aims to investigate the inhibitory effect of Lu-Zn on lung cancer cells, its regulation of ferroptosis, and the role of PRR11 in lung cancer progression under hypoxia. Methods In vitro experiments were conducted to evaluate the effect of Lu-Zn on lung cancer cells, focusing on its impact on invasion, migration, and ferroptosis. The expression levels of PRR11, its methylation status, and microRNA-6769b-3p (miR-6769b-3p) were also analyzed. Results Under hypoxic conditions, Lu-Zn significantly inhibited the invasion and migration abilities of lung cancer cells and promoted ferroptosis. Additionally, Lu-Zn reversed the pro-cancer effects induced by PRR11. At the molecular level, Lu-Zn promoted the methylation of PRR11 and regulated miR-6769b-3p. Conclusion Our study demonstrates that Lu-Zn enhances the methylation of PRR11 and reduces its expression under hypoxic conditions through miR-6769b-3p. This leads to inhibition of the downstream PI3K/AKT/mTOR signaling pathway, promoting ferroptosis and exerting anti-lung cancer effects.

Hypoxia

10.1177/09731296241311343

Cite

Citations (0)

Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway

Experimental and Therapeutic Medicine (2023)

Yali Li Jun Long Libo Li Ziyao Yu Yanjing Liang

To the best of our knowledge, the role of peroxisome proliferator-activated receptor γ (PPARγ) in oxidative stress-induced PC12 cell damage is unknown. Using a PC12 cell model with H2O2 treatment, the present study investigated the expression levels of apoptosis-related genes and neuronal apoptosis after oxidative stress injury. The present study further investigated the protective effect and mechanism of pioglitazone, a PPARγ agonist. PC12 cells treated with H2O2 were used as a model of oxidative stress injury. An MTT assay and flow cytometry were used to detect the effect of H2O2 on PC12 cell viability and the protective effect of pioglitazone. A TUNEL assay was used to detect neuronal apoptosis. The expression levels of PPARγ, Bax, Bcl-2 and caspase-3 were examined by reverse transcription-quantitative PCR and western blotting. H2O2 reduced PC12 cell viability in a dose- and time-dependent manner. H2O2 significantly upregulated the protein expression levels of Bax and the cleaved caspase-3/caspase-3 ratio (P<0.01), decreased the protein expression levels of Bcl-2 (P<0.01), and increased the apoptosis rate of PC12 cells. Pioglitazone significantly reduced the protein expression levels of Bax and the cleaved caspase-3/caspase-3 ratio (P<0.01), increased the expression levels of Bcl-2 (P<0.01), decreased the Bax/Bcl-2 expression ratio (P<0.01) and increased the viability of H2O2-damaged PC12 cells in a dose-dependent manner. Treatment with the PPARγ antagonist GW9662 or PPARγ small interfering RNA counteracted the protective effect of pioglitazone on PC12 cells to different extents (P<0.01). Therefore, the present study reported the role of PPARγ in protecting PC12 cells against oxidative stress injury, which may lead to novel therapeutic approaches for neurodegenerative diseases.

Pioglitazone

Viability assay

MTT assay

Bcl-2-associated X protein

10.3892/etm.2023.12221

Cite

Citations (0)

Additional file 3 of ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway

Figshare (2022)

Lin Cai Qiuyuan Gong Lin Qi Tongtong Xu Qian Suo

Additional file 2: Table S2. The detailed criteria of neurobehavioral function assessments.

10.6084/m9.figshare.19643454

Cite

Citations (0)

FBXW7 suppresses epithelial‐mesenchymal transition and chemo‐resistance of non‐small‐cell lung cancer cells by targeting snai1 for ubiquitin‐dependent degradation

Cell Proliferation (2018)

Guodong Xiao Yuan Li Meng Wang Xiang Li Sida Qin

Abstract Objectives FBXW 7 acts as a tumour suppressor by targeting at various oncoproteins for ubiquitin‐mediated degradation. However, the clinical significance and the involving regulatory mechanisms of FBXW 7 manipulation of NSCLC regeneration and therapy response are not clear. Materials and Methods Immunohistochemical staining and qRT ‐ PCR were applied to detect FBXW 7 and Snai1 expression in 100 samples of NSCLC and matched tumour‐adjacent tissues. FBXW 7 manipulation of cancer biological functions were studied by using MTT assay, immunoblotting, flow cytometry, transwells, wound healing assay, and sphere‐formation assays. Immunofluorescence and co‐immunoprecipitation were used to analyse the possible interaction between Snai1 and FBXW 7. Results We detected the decreased FBXW 7 expression in majority of the NSCLC tissues, and lower FBXW 7 level was correlated with advanced TNM stage. Furthermore, those patients with decreased FBXW 7 expression tend to have both poorer 5‐year survival outcomes, and shorter disease‐free survival, comparing to those with higher FBXW 7 levels. Functionally, we found that FBXW 7 enforcement suppressed NSCLC progression by inducing cell growth arrest, increasing chemo‐sensitivity and inhibiting Epithelial‐mesenchymal Transition ( EMT ) progress. Results further showed that FBXW 7 could interact with Snai1 directly to degrade its expression through ubiquitylating alternation in NSCLC , which could be partially abrogated by restoring Snai1 expression. Conclusions FBXW 7 conduction of tumour suppression was partly through degrading Snai1 directly for ubiquitylating regulation in NSCLC

SNAI1

MTT assay

10.1111/cpr.12473

Cite

Citations (47)

Reactive oxygen species reprogram macrophages to suppress antitumor immune response through the exosomal miR-155-5p/PD-L1 pathway

Journal of Experimental & Clinical Cancer Research (2022)

Xiang Li Shaomin Wang Wei Mu Jennifer Barry Anna Han

Cancer cells have an imbalance in oxidation-reduction (redox) homeostasis. Understanding the precise mechanisms and the impact of the altered redox microenvironment on the immunologic reaction to tumors is limited.We isolated exosomes from ovarian cancer cells through ultracentrifuge and characterized by Western-blots and Nanoparticle Tracking Analysis. 2D, 3D-coculture tumor model, and 3D live cell imaging were used to study the interactions between tumor cells, macrophages and CD3 T cells in vitro. The role of exosomal miR-155-5p in tumor growth was evaluated in xenograft nude mice models and immune-competent mice models. Flow cytometry and flow sorting were used to determine the expression levels of miR-155-5p and PD-L1 in ascites and splenic macrophages, and the percentages of CD3 T cells subpopulations.The elevation of reactive oxygen species (ROS) greatly downregulated exosomal miR-155-5p expression in tumor cells. Neutralization of ROS with N-acetyl-L-cysteine (NAC) increased the levels of miR-155-5p in tumor exosomes that were taken up by macrophages, leading to reduction of macrophage migration and tumor spheroid infiltration. We further found that programmed death ligand 1 (PD-L1) is a functional target of miR-155-5p. Co-culture of macrophages pre-treated with NAC-derived tumor exosomes or exosomal miR-155-5p with T-lymphocytes leading to an increased percentage of CD8+ T-lymphocyte and a decreased CD3+ T cell apoptosis through PD-L1 downregulation. Tumor growth in nude mice was delayed by treatment with NAC-derived tumor exosomes. Delivery of tumor exo-miR-155-5p in immune-intact mice suppressed ovarian cancer progression and macrophage infiltration, and activated CD8+ T cell function. It is of note that exo-miR-155-5p inhibited tumor growth more potently than the PD-L1 antibody, suggesting that in addition to PD-L1, other pathways may also be targeted by this approach.Our findings demonstrate a novel mechanism, ROS-induced down-regulation of miR-155-5p, by which tumors modulate the microenvironment that favors tumor growth. Understanding of the negative impact of ROS on the tumor immune response will improve current therapeutic strategies. Targeting miR-155-5p can be an alternative approach to prevent formation of an immunosuppressive TME through downregulation of PD-L1 and other immunosuppressive factors.

10.1186/s13046-022-02244-1

Cite

Citations (71)

Plasma ω‑3 and ω‑6 fatty acids in thyroid diseases

Oncology Letters (2018)

Xiang Li Hui Li Jing Zhao Qi Dai Chaoran Huang

The incidences of nodular goiter (NG), thyroid adenoma (TA), and thyroid cancer (TC) are increasing rapidly; however, the etiologies of these diseases remain unclear. The present study aimed to evaluate the differences in plasma fatty acids among these three thyroid diseases to facilitate etiological research. Four ω-3 and seven ω-6 polyunsaturated fatty acids were measured from 97 TC, 14 TA and 11 NG patient plasma samples with gas chromatography-flame ionization detector. Fatty acids levels were expressed as the percentage of each fatty acid out of the total fatty acids evaluated. The present study identified that the level of 22:6n-3 [median, interquartile range (IQR)] was significantly increased in TA (5.2%, 4.3-6.4%) compared with NG (3.6%, 3.1-4.6%) and TC patients (4.2%, 3.2-4.8%). Though not statistically significant, the levels of 20:5n-3 and 22:5n-3 demonstrated a similar pattern. The level of 22:4n-6 expressed (median, IQR) was significantly increased in NG patients (0.21%, 0.18-0.26%) compared with TA (0.16%, 0.15-0.18%) and TC (0.17%, 0.14-0.22%) patients. Furthermore the fatty acids 18:3n-6, 20:2n-6, 20:3n-6, 20:4:6, and 22:5n-6 demonstrated a similar but statistically insignificant pattern. This suggests that different fatty acids exhibit various etiological roles in NG, TA and TC and warrant further study.

Interquartile range

Etiology

10.3892/ol.2018.9288

Cite

Citations (2)

A Hierarchy-driven Multi-label Network with Label Constraints for Post-operative Complication Prediction of Lung Cancer^*

2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC) (2023)

Danqing Hu Bing Liu Xiang Li Hui Chen Rui Guo

Lung cancer is one of the most dangerous cancers all over the world. Surgical resection remains the only potentially curative option for patients with lung cancer. However, this invasive treatment often causes various complications, which seriously endanger patient health. In this study, we proposed a novel multi-label network, namely a hierarchy-driven multi-label network with label constraints (HDMN-LC), to predict the risk of complications of lung cancer patients. In this method, we first divided all complications into pulmonary and cardiovascular complication groups and employed the hierarchical cluster algorithm to analyze the hierarchies between these complications. After that, we employed the hierarchies to drive the network architecture design so that related complications could share more hidden features. And then, we combined all complications and employed an auxiliary task to predict whether any complications would occur to impose the bottom layer to learn general features. Finally, we proposed a regularization term to constrain the relationship between specific and combined complication labels to improve performance. We conducted extensive experiments on real clinical data of 593 patients. Experimental results indicate that the proposed method outperforms the single-label, multi-label baseline methods, with an average AUC value of 0.653. And the results also prove the effectiveness of hierarchy-driven network architecture and label constraints. We conclude that the proposed method can predict complications for lung cancer patients more effectively than the baseline methods.Clinical relevance—This study presents a novel multi-label network that can more accurately predict the risk of specific postoperative complications for lung cancer patients. The method can help clinicians identify high-risk patients more accurately and timely so that interventions can be implemented in advance to ensure patient safety

Regularization

10.1109/embc40787.2023.10339943

Cite

Citations (1)

Identification of EGFR R776H germline mutations in a patient with multifocal lung adenocarcinoma: a case report and literature review

Respiratory Medicine Case Reports (2024)

Tianli Wang Zheng Qin Cong Deng Xiang Li Jia Huang

The advancement of molecular pathology techniques has led to the discovery of rare

Identification

10.1016/j.rmcr.2024.102051

Cite

Citations (1)