Juanjuan Huang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Juanjuan Huang has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
Guofeng Ji
Department of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
1 shared publication- Guoqing Wang
The First Affiliated Hospital of Xinjiang Medical University
1 shared publication - Haochen Yao
Key Laboratory and Engineering Laboratory of Lymphatic Surgery Jilin Province, China-Japan Union Hospital, Jilin University, Changchun, 130033, China
1 shared publication - Jiali Sun
Children's Hospital Affiliated to Shandong University, Department of Vascular anomalies and Interventional Radiology, Shandong, China
1 shared publication - Na Shen
Chinese Academy of Sciences
1 shared publication - Tingting Zheng
Department of Microbiology, School of Preclinical Medicine, Guangxi Medical University, Nanning 530021, China
1 shared publication
Latest Publications
- Open Access
Transcriptome Analysis of Natural Killer Cells in Response to Newcastle Disease Virus Infected Hepatocellular Carcinoma Cells
When tumor cells are infected by the Newcastle disease virus (NDV), the lysis of tumor cells by natural killer (NK) cells is enhanced, which may be related to the enhanced NK cell activation effect. To better understand the intracellular molecular mechanisms involved in NK cell activation, the transcriptome profiles of NK cells stimulated by NDV-infected hepatocellular carcinoma (HCC) cells (NDV group) and control (NC group, NK cells stimulated by HCC cells) were analyzed. In total, we identified 1568 differentially expressed genes (DEGs) in the NK cells of the NDV group compared to the control, including 1389 upregulated and 179 downregulated genes. Functional analysis showed that DEGs were enriched in the immune system, signal transmission, cell growth, cell death, and cancer pathways. Notably, 9 genes from the IFN family were specifically increased in NK cells upon NDV infection and identified as potential prognosis markers for patients with HCC. A qRT-PCR experiment was used to confirm the differential expression of IFNG and the other 8 important genes. The results of this study will improve our understanding of the molecular mechanisms of NK cell activation.
Open AccessTranscriptome Analysis of Natural Killer Cells in Response to Newcastle Disease Virus Infected Hepatocellular Carcinoma Cells
When tumor cells are infected by the Newcastle disease virus (NDV), the lysis of tumor cells by natural killer (NK) cells is enhanced, which may be related to the enhanced NK cell activation effect. To better understand the intracellular molecular mechanisms involved in NK cell activation, the transcriptome profiles of NK cells stimulated by NDV-infected hepatocellular carcinoma (HCC) cells (NDV group) and control (NC group, NK cells stimulated by HCC cells) were analyzed. In total, we identified 1568 differentially expressed genes (DEGs) in the NK cells of the NDV group compared to the control, including 1389 upregulated and 179 downregulated genes. Functional analysis showed that DEGs were enriched in the immune system, signal transmission, cell growth, cell death, and cancer pathways. Notably, 9 genes from the IFN family were specifically increased in NK cells upon NDV infection and identified as potential prognosis markers for patients with HCC. A qRT-PCR experiment was used to confirm the differential expression of IFNG and the other 8 important genes. The results of this study will improve our understanding of the molecular mechanisms of NK cell activation.
- 11 April 2022
- Published by American Chemical Society (ACS) in Nano Letters
- Vol. 22 (8) , 3328-3339
Cisplatin Nanoparticles Promote Intratumoral CD8+ T Cell Priming via Antigen Presentation and T Cell Receptor Crosstalk
Nanomedicines are highly promising for cancer therapy due to their minimal side effects. However, little is known regarding their host immune response, which may limit their clinical efficacy and applications. Here, we find that cisplatin (CDDP)-loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) elicit a strong antitumor CD8+ T cell-mediated immune response in a tumor-bearing mouse model compared to free CDDP. Mechanistically, the sustained retention of CDDP-NPs results in persistent tumor MHC-I overexpression, which promotes the formation of MHC-I-antigen peptide complex (pMHC-I), enhances the interaction between pMHC-I and T cell receptor (TCR), and leads to the activation of TCR signaling pathway and CD8+ T cell-mediated immune response. Furthermore, CDDP-NPs upregulate the costimulatory OX40 on intratumoral CD8+ T cells, and synergize with the agonistic OX40 antibody (aOX40) to suppress tumor growth by 89.2%. Our study provides a basis for the efficacy advantage of CDDP-based nanomedicines and immunotherapy.
- 11 April 2022
- Published by American Chemical Society (ACS) in Nano Letters
- Vol. 22 (8) , 3328-3339
Cisplatin Nanoparticles Promote Intratumoral CD8+ T Cell Priming via Antigen Presentation and T Cell Receptor Crosstalk
Nanomedicines are highly promising for cancer therapy due to their minimal side effects. However, little is known regarding their host immune response, which may limit their clinical efficacy and applications. Here, we find that cisplatin (CDDP)-loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) elicit a strong antitumor CD8+ T cell-mediated immune response in a tumor-bearing mouse model compared to free CDDP. Mechanistically, the sustained retention of CDDP-NPs results in persistent tumor MHC-I overexpression, which promotes the formation of MHC-I-antigen peptide complex (pMHC-I), enhances the interaction between pMHC-I and T cell receptor (TCR), and leads to the activation of TCR signaling pathway and CD8+ T cell-mediated immune response. Furthermore, CDDP-NPs upregulate the costimulatory OX40 on intratumoral CD8+ T cells, and synergize with the agonistic OX40 antibody (aOX40) to suppress tumor growth by 89.2%. Our study provides a basis for the efficacy advantage of CDDP-based nanomedicines and immunotherapy.