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Article ; Online: Radiofrequency ablation plays double role in immunosuppression and activation of PBMCs in recurrent hepatocellular carcinoma.

Zhao, Yang / Yang, Tongwang / Ouyang, Yabo / Rao, Wei / Liu, Kai / Zheng, Jiasheng / Lv, Fudong / Shi, Ying / Wang, Feng / Liu, Dongjie / Qiao, Luxin / Xia, Zhenying / Zhang, Yushi / Chen, Dexi / Wang, Wenjing

Frontiers in immunology

2024 Volume 15, Page(s) 1339213

Abstract: Background: Radiofrequency ablation (RFA) is the primary curative treatment for hepatocellular carcinoma (HCC) patients who are not eligible for surgery. However, the effects of RFA on the global tumor immune response remain unclear.: Method: In this ...

Abstract	Background: Radiofrequency ablation (RFA) is the primary curative treatment for hepatocellular carcinoma (HCC) patients who are not eligible for surgery. However, the effects of RFA on the global tumor immune response remain unclear. Method: In this study, we examined the phenotypic and functional changes in peripheral blood mononuclear cells (PBMCs) from recurrent HCC patients who had undergone two RFA treatments using mass cytometry and high-throughput mRNA assays. Results: We observed significant increase in monocytes and decrease in T cell subpopulations three days after the first RFA treatment and three days after the second RFA treatment. The down-regulation of GZMB, GZMH, GZMK, and CD8A, which are involved in the cytotoxic function of T cells, was observed following RFA. Furthermore, the population of CD8 effector and memory T cells (CD8 Teff and CD8 Tem) significantly decreased after RFA. The expression of CD5 and CD161 in various T cell subpopulations also showed significant reductions. Additionally, elevated secretion of VEGF was observed in monocytes, B cells, regulatory T cells (Tregs), and CD4 naive T cells. Conclusion: In recurrent HCC patients, serum components derived from radiofrequency therapy can enhance the antigen-presenting capacity of monocytes. However, they also inhibit the anti-cancer immune response by reducing the population of CD8 effector and memory T cells and suppressing the activation of T cells, as well as down-regulating the expression of CD161 and CD5 in various T cell subpopulations. These tumor-derived components also contribute to an immunosuppressive microenvironment by promoting the secretion of VEGF in monocytes, Tregs, B cells, and CD4 naive T cells.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/pathology ; Liver Neoplasms/pathology ; Leukocytes, Mononuclear ; Vascular Endothelial Growth Factor A ; Catheter Ablation ; Radiofrequency Ablation ; Immunosuppression Therapy ; Tumor Microenvironment
Chemical Substances	Vascular Endothelial Growth Factor A
Language	English
Publishing date	2024-01-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1339213
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: POU2F2-IL-31 Autoregulatory Circuit Converts Hepatocytes into the Origin Cells of Hepatocellular Carcinoma.

Yuan, Chunwang / Pang, Lijun / Wang, Wenjing / Ouyang, Yabo / Guo, Xianghua / Liu, Kai

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2021 Volume 8, Issue 13, Page(s) e2004683

Abstract: Hepatocellular carcinoma (HCC) originates from fully differentiated hepatocytes, but the decisive events for converting hepatocytes to the cells of origin for HCC are still unclear. Liver cancer stem cells (LCSCs) cause HCC but are not bona fide cells of ...

Abstract	Hepatocellular carcinoma (HCC) originates from fully differentiated hepatocytes, but the decisive events for converting hepatocytes to the cells of origin for HCC are still unclear. Liver cancer stem cells (LCSCs) cause HCC but are not bona fide cells of origin. Here, the expressions of POU2F2 and IL-31 are identified in macroscopically normal livers of diethylnitrosamine-challenged mice. An autoregulatory circuit formed by mutual induction between POU2F2 and IL-31 drives hepatocytes to progress to LCSCs by acquiring stemness, as well as stimulates them to in vivo grow and malignantly progress. The development of the autoregulatory circuit is a decisive event for converting hepatocytes into the cells of origin, since hepatocytes expressing the circuit have acquired tumorigenic potential before progressing to LCSCs. Nonetheless, acquiring stemness is still required for the cells of origin to initiate hepatocarcinogenesis. The circuit also occurs in human cirrhotic tissues, partially elucidating how premalignant lesions progress to HCC.
Language	English
Publishing date	2021-05-02
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202004683
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Corrigendum to "Usnea Acid as Multidrug Resistance (MDR) Reversing Agent against Human Chronic Myelogenous Leukemia K562/ADR Cells via an ROS Dependent Apoptosis".

Wang, Wenjing / Niu, Shubin / Qiao, Luxin / Wei, Feili / Yin, Jiming / Wang, Shanshan / Ouyang, Yabo / Chen, Dexi

BioMed research international

2021 Volume 2021, Page(s) 9808613

Abstract: This corrects the article DOI: 10.1155/2019/8727935.]. ...

Abstract	[This corrects the article DOI: 10.1155/2019/8727935.].
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2021/9808613
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Article ; Online: POU2F2‐IL‐31 Autoregulatory Circuit Converts Hepatocytes into the Origin Cells of Hepatocellular Carcinoma

Chunwang Yuan / Lijun Pang / Wenjing Wang / Yabo Ouyang / Xianghua Guo / Kai Liu

Advanced Science, Vol 8, Iss 13, Pp n/a-n/a (2021)

2021

Abstract: Abstract Hepatocellular carcinoma (HCC) originates from fully differentiated hepatocytes, but the decisive events for converting hepatocytes to the cells of origin for HCC are still unclear. Liver cancer stem cells (LCSCs) cause HCC but are not bona fide ...

Abstract	Abstract Hepatocellular carcinoma (HCC) originates from fully differentiated hepatocytes, but the decisive events for converting hepatocytes to the cells of origin for HCC are still unclear. Liver cancer stem cells (LCSCs) cause HCC but are not bona fide cells of origin. Here, the expressions of POU2F2 and IL‐31 are identified in macroscopically normal livers of diethylnitrosamine‐challenged mice. An autoregulatory circuit formed by mutual induction between POU2F2 and IL‐31 drives hepatocytes to progress to LCSCs by acquiring stemness, as well as stimulates them to in vivo grow and malignantly progress. The development of the autoregulatory circuit is a decisive event for converting hepatocytes into the cells of origin, since hepatocytes expressing the circuit have acquired tumorigenic potential before progressing to LCSCs. Nonetheless, acquiring stemness is still required for the cells of origin to initiate hepatocarcinogenesis. The circuit also occurs in human cirrhotic tissues, partially elucidating how premalignant lesions progress to HCC.
Keywords	hepatocellular carcinoma ; IL‐31 ; liver cancer stem cells ; origin cells ; p53 ; POU2F2 ; Science ; Q
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Corrigendum to “Usnea Acid as Multidrug Resistance (MDR) Reversing Agent against Human Chronic Myelogenous Leukemia K562/ADR Cells via an ROS Dependent Apoptosis”

Wenjing Wang / Shubin Niu / Luxin Qiao / Feili Wei / Jiming Yin / Shanshan Wang / Yabo Ouyang / Dexi Chen

BioMed Research International, Vol

2021 Volume 2021

Keywords	Medicine ; R
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Immunogenicity profiling and distinct immune response in liver transplant recipients vaccinated with SARS-CoV-2 inactivated vaccines.

Duan, Binwei / Zhang, Gongming / Wang, Wenjing / Yin, Jiming / Liu, Mengcheng / Zhang, Jing / Chen, Dexi / Ouyang, Yabo / Li, Guangming

Frontiers in immunology

2022 Volume 13, Page(s) 954177

Abstract: SARS-CoV-2 vaccination has been recommended for liver transplant (LT) recipients. However, our understanding of inactivated vaccine stimulation of the immune system in regulating humoral and cellular immunity among LT recipients is inadequate. Forty-six ... ...

Abstract	SARS-CoV-2 vaccination has been recommended for liver transplant (LT) recipients. However, our understanding of inactivated vaccine stimulation of the immune system in regulating humoral and cellular immunity among LT recipients is inadequate. Forty-six LT recipients who received two-dose inactivated vaccines according to the national vaccination schedule were enrolled. The clinical characteristics, antibody responses, single-cell peripheral immune profiling, and plasma cytokine/chemokine/growth factor levels were recorded. Sixteen (34.78%) LT recipients with positive neutralizing antibody (nAb) were present in the Type 1 group. Fourteen and 16 LT recipients with undetected nAb were present in the Type 2 and Type 3 groups, respectively. Time from transplant and lymphocyte count were different among the three groups. The levels of anti-RBD and anti-S1S2 decreased with decreasing neutralizing inhibition rates. Compared to the Type 2 and Type 3 groups, the Type 1 group had an enhanced innate immune response. The proportions of B, DNT, and CD3+CD19+ cells were increased in the Type 1 group, whereas monocytes and CD4+ T cells were decreased. High CD19, high CD8+CD45RA+ cells, and low effector memory CD4+/naïve CD4+ cells of the T-cell populations were present in the Type 1 group. The Type 1 group had higher concentrations of plasma CXCL10, MIP-1 beta, and TNF-alpha. No severe adverse events were reported in all LT recipients. We identified the immune responses induced by inactivated vaccines among LT recipients and provided insights into the identification of immunotypes associated with the responders.
MeSH term(s)	Antibodies, Neutralizing ; Antibody Formation ; COVID-19/prevention & control ; COVID-19 Vaccines ; Humans ; Liver Transplantation ; SARS-CoV-2 ; Tumor Necrosis Factor-alpha ; Vaccines, Inactivated ; Viral Vaccines
Chemical Substances	Antibodies, Neutralizing ; COVID-19 Vaccines ; SARS-CoV-2 inactivated vaccines ; Tumor Necrosis Factor-alpha ; Vaccines, Inactivated ; Viral Vaccines
Language	English
Publishing date	2022-09-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.954177
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Article ; Online: Enriched high‑throughput reverse transcription‑quantitative PCR template preparation without pre‑amplification.

Yang, Tongwang / Ouyang, Yabo / Gao, Yuxue / Liu, Daojie / Zang, Yunjin / Chen, Dexi

Molecular medicine reports

2020 Volume 22, Issue 4, Page(s) 3541–3548

Abstract: A cDNA template with a high concentration is required to generate a high number of copies for accurate downstream high‑throughput reverse transcription‑quantitative PCR screening. However, with the traditional method, pre‑amplification is not widely ... ...

Abstract	A cDNA template with a high concentration is required to generate a high number of copies for accurate downstream high‑throughput reverse transcription‑quantitative PCR screening. However, with the traditional method, pre‑amplification is not widely available. In the present study, a novel strategy to resolve the pre‑amplification limitation has been developed. Total RNA was extracted using a commercially available RNeasy Micro kit then, the cDNA was synthesized using SuperScript® III First‑Strand Synthesis system. PCR inhibitors (proteins and soluble salt ions) in the enriched cDNA were removed using saturated phenol‑chloroform extraction. Finally, genes were evaluated using PCR amplification and the BioMark™ HD system. The positive detection rate of individual target gene expression reached 70.18%; however, it markedly decreased to 35.42% using PCR amplification without prior dilution. Next, the reverse transcription product was purified using saturated phenol‑chloroform extraction, and the positive detection rate increased to 97.04%. Notably, the positive detection rate of cDNA prepared using this method of high‑throughput and traditional PCR (97.04 vs. 96.6%) was not significantly different. In conclusion, the results demonstrate the novel method was an easy and reproducible method for performing robust and highly accurate targeted amplification.
MeSH term(s)	Adult ; Aged ; Cell Line, Tumor ; Female ; Gene Expression Profiling/methods ; Hep G2 Cells ; Hepatitis B/diagnosis ; Hepatitis B/genetics ; High-Throughput Screening Assays ; Humans ; Male ; Middle Aged ; Real-Time Polymerase Chain Reaction/methods
Language	English
Publishing date	2020-07-30
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2469505-1
ISSN	1791-3004 ; 1791-2997
ISSN (online)	1791-3004
ISSN	1791-2997
DOI	10.3892/mmr.2020.11389
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Article ; Online: RNA Sequencing Analyses Reveal the Potential Mechanism of Pulmonary Injury Induced by Gallium Arsenide Particles in Human Bronchial Epithelioid Cells

Yabo Ouyang / Xiaodong Liu / Haibing Li / Shiwei Cui / Huifang Yan / Xingfu Pan

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 11

Abstract: Abstract Extensive use of gallium arsenide (GaAs) has led to increased exposure to humans working in the semiconductor industry. This study employed physicochemical characterization of GaAs obtained from a workplace, cytotoxicity analysis of damage ... ...

Abstract	Abstract Extensive use of gallium arsenide (GaAs) has led to increased exposure to humans working in the semiconductor industry. This study employed physicochemical characterization of GaAs obtained from a workplace, cytotoxicity analysis of damage induced by GaAs in 16HBE cells, RNA-seq and related bioinformatic analysis, qRT-PCR verification and survival analysis to comprehensively understand the potential mechanism leading to lung toxicity induced by GaAs. We found that GaAs-induced abnormal gene expression was mainly related to the cellular response to chemical stimuli, the regulation of signalling, cell differentiation and the cell cycle, which are involved in transcriptional misregulation in cancer, the MAPK signalling pathway, the TGF-β signalling pathway and pulmonary disease-related pathways. Ten upregulated genes (FOS, JUN, HSP90AA1, CDKN1A, ESR1, MYC, RAC1, CTNNB1, MAPK8 and FOXO1) and 7 downregulated genes (TP53, AKT1, NFKB1, SMAD3, CDK1, E2F1 and PLK1) related to GaAs-induced pulmonary toxicity were identified. High expression of HSP90AA1, RAC1 and CDKN1A was significantly associated with a lower rate of overall survival in lung cancers. The results of this study indicate that GaAs-associated toxicities affected the misregulation of oncogenes and tumour suppressing genes, activation of the TGF-β/MAPK pathway, and regulation of cell differentiation and the cell cycle. These results help to elucidate the molecular mechanism underlying GaAs-induced pulmonary injury.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: RNA Sequencing Analyses Reveal the Potential Mechanism of Pulmonary Injury Induced by Gallium Arsenide Particles in Human Bronchial Epithelioid Cells.

Ouyang, Yabo / Liu, Xiaodong / Li, Haibing / Cui, Shiwei / Yan, Huifang / Pan, Xingfu

Scientific reports

2020 Volume 10, Issue 1, Page(s) 8685

Abstract: Extensive use of gallium arsenide (GaAs) has led to increased exposure to humans working in the semiconductor industry. This study employed physicochemical characterization of GaAs obtained from a workplace, cytotoxicity analysis of damage induced by ... ...

Abstract	Extensive use of gallium arsenide (GaAs) has led to increased exposure to humans working in the semiconductor industry. This study employed physicochemical characterization of GaAs obtained from a workplace, cytotoxicity analysis of damage induced by GaAs in 16HBE cells, RNA-seq and related bioinformatic analysis, qRT-PCR verification and survival analysis to comprehensively understand the potential mechanism leading to lung toxicity induced by GaAs. We found that GaAs-induced abnormal gene expression was mainly related to the cellular response to chemical stimuli, the regulation of signalling, cell differentiation and the cell cycle, which are involved in transcriptional misregulation in cancer, the MAPK signalling pathway, the TGF-β signalling pathway and pulmonary disease-related pathways. Ten upregulated genes (FOS, JUN, HSP90AA1, CDKN1A, ESR1, MYC, RAC1, CTNNB1, MAPK8 and FOXO1) and 7 downregulated genes (TP53, AKT1, NFKB1, SMAD3, CDK1, E2F1 and PLK1) related to GaAs-induced pulmonary toxicity were identified. High expression of HSP90AA1, RAC1 and CDKN1A was significantly associated with a lower rate of overall survival in lung cancers. The results of this study indicate that GaAs-associated toxicities affected the misregulation of oncogenes and tumour suppressing genes, activation of the TGF-β/MAPK pathway, and regulation of cell differentiation and the cell cycle. These results help to elucidate the molecular mechanism underlying GaAs-induced pulmonary injury.
MeSH term(s)	Arsenicals ; Bronchi/cytology ; Cell Line ; Cell Survival/drug effects ; Down-Regulation/drug effects ; Epithelioid Cells/cytology ; Epithelioid Cells/drug effects ; Epithelioid Cells/metabolism ; Gallium/toxicity ; Humans ; Lung Injury/metabolism ; Lung Injury/pathology ; Protein Interaction Maps/drug effects ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; RNA/chemistry ; RNA/metabolism ; Sequence Analysis, RNA ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Up-Regulation/drug effects
Chemical Substances	Arsenicals ; FOS protein, human ; Proto-Oncogene Proteins c-fos ; TP53 protein, human ; Tumor Suppressor Protein p53 ; gallium arsenide (27FC46GA44) ; RNA (63231-63-0) ; Gallium (CH46OC8YV4)
Language	English
Publishing date	2020-05-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-65518-8
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Article ; Online: RDIVpSGP motif of ASPP2 binds to 14-3-3 and enhances ASPP2/k18/14-3-3 ternary complex formulation to promote BRAF/MEK/ERK signal inhibited cell proliferation in hepatocellular carcinoma.

Yang, Tongwang / Zhu, Cunle / Shi, Ying / Shen, Yuntai / Gao, Yuxue / Zhang, Bowen / Jin, Rifeng / Liu, Daojie / Ouyang, Yabo / Liu, Xiaoni / Wang, Wenjing / Yang, Pengxiang / Xu, Qingguo / Cai, Jinzhen / Chen, Dexi

Cancer gene therapy

2022 Volume 29, Issue 11, Page(s) 1616–1627

Abstract: The Apoptosis Stimulating Protein of p53 2 (ASPP2) is a heterozygous insufficient tumor suppressor; however, its molecular mechanism(s) in tumor suppression is not completely understood. ASPP2 plays an essential role in cell growth, as shown by liver ... ...

Abstract	The Apoptosis Stimulating Protein of p53 2 (ASPP2) is a heterozygous insufficient tumor suppressor; however, its molecular mechanism(s) in tumor suppression is not completely understood. ASPP2 plays an essential role in cell growth, as shown by liver hepatocellular carcinoma (LIHC) RNA-seq assay using the Cancer Genome Atlas (TCGA) and High-Throughput-PCR assay using ASPP2 knockdown cells. These observations were further confirmed by in vivo and in vitro experiments. Mechanistically, N-terminus ASPP2 interacted with Keratin 18 (k18) in vivo and in vitro. Interestingly, the RDIVpSGP motif of ASPP2 associates with 14-3-3 and promotes ASPP2/k18/14-3-3 ternary-complex formation which promotes MEK/ERK signal activation by impairing 14-3-3 and BRAF association. Additionally, ASPP2-rAd injection promotes paclitaxel-suppressed tumor growth by suppressing cell proliferation in the BALB/c nude mice model. ASPP2 and k18 were preferentially downregulated in Hepatocellular Carcinoma (HCC), which predicted poor prognosis in HCC patients. Overall, these findings suggested that ASPP2 promoted BRAF/MEK/ERK signal activation by promoting the formation of an ASPP2/k18/14-3-3 ternary complex via the RDIVpSGP motif at the N terminus. Moreover, this study provides novel insights into the molecular mechanism of tumor suppression in HCC patients.
MeSH term(s)	Mice ; Animals ; Carcinoma, Hepatocellular/pathology ; Tumor Suppressor Protein p53/metabolism ; Proto-Oncogene Proteins B-raf ; Liver Neoplasms/metabolism ; Keratin-18/metabolism ; Mice, Nude ; 14-3-3 Proteins/genetics ; 14-3-3 Proteins/metabolism ; Apoptosis Regulatory Proteins/metabolism ; Cell Proliferation ; Apoptosis ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Cell Line, Tumor
Chemical Substances	Tumor Suppressor Protein p53 ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Keratin-18 ; 14-3-3 Proteins ; Apoptosis Regulatory Proteins ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2022-05-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1212513-1
ISSN	1476-5500 ; 0929-1903
ISSN (online)	1476-5500
ISSN	0929-1903
DOI	10.1038/s41417-022-00474-1
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