Juan Wang

Chinese Academy of Agricultural Sciences

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Jin Yang

Qingdao University

Nanping Wu

Zhuhai People's Hospital

Zongxing Yang

Jilin University

Linfang Cheng

Zhejiang University

Changzhong Jin

Zhejiang University

Wei Wang

Tongde Hospital of Zhejiang Province

Huan Deng

Xi'an Jiaotong University

Wensheng Deng

Wuhan University of Science and Technology

Shasha Zhao

Wuhan University of Science and Technology

Jingrong Ye

Beijing Center for Disease Prevention and Control

Cooperative Institutions

Zhejiang University

Sun Yat-sen University

Chinese Academy of Sciences

Anhui Medical University

Southern Medical University

Chinese Academy of Medical Sciences & Peking Union Medical College

Huazhong University of Science and Technology

BGI Group (China)

Peking University

Shandong University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Triptolide inhibits epithelial‑mesenchymal transition and induces apoptosis in gefitinib‑resistant lung cancer cells

Oncology Reports (2020)

Fangqiong Li Huaizhong Cui Xin Jin Xiaoting Gong Wei Wang

The epidermal growth factor receptor‑tyrosine kinase inhibitor (EGFR‑TKI), gefitinib, is used widely to treat non‑small cell lung cancer (NSCLC) with EGFR‑activating mutations. Unfortunately, the acquired drug resistance promoted by epithelial‑mesenchymal transition (EMT) markedly limits the clinical effects and remains a major barrier to a cure. Our previous isobaric tags for relative and absolute quantitation‑based proteomics analysis revealed that the E‑cadherin protein level was markedly upregulated by triptolide (TP). The present study aimed to determine whether TP reverses the gefitinib resistance of human lung cancer cells by regulating EMT. It was revealed that TP combined with gefitinib synergistically inhibited the migration and invasion of lung adenocarcinoma cell line A549; the combination treatment had a significantly better outcome than that of TP and gefitinib alone. Moreover, TP effectively increased the sensitivity of drug resistant A549 cells to gefitinib by upregulating E‑cadherin protein expression and downregulating the MMP9, SNAIL, and vimentin expression levels. The dysregulated E‑cadherin expression of gefitinib‑sensitive cells induced gefitinib resistance, which could be overcome by TP. Finally, TP combined with gefitinib significantly inhibited the growth of xenograft tumors induced using gefitinib‑resistant A549 cells, which was associated with EMT reversal and E‑cadherin signaling activation in vivo. The present results indicated that the combination of TP and TKIs may be a promising therapeutic strategy to treat patients with NSCLCs harboring EGFR mutations.

Triptolide

10.3892/or.2020.7542

Cite

Citations (19)

DOT1L-controlled cell-fate determination and transcription elongation are independent of H3K79 methylation

Proceedings of the National Academy of Sciences (2020)

Kaixiang Cao Michal Ugarenko Patrick A. Ozark Juan Wang Stacy A. Marshall

Significance DOT1L is a histone methyltransferase that catalyzes histone H3K79 methylation, a chromatin modification that is correlated with active transcription. Inhibition of DOT1L’s catalytic activity has been studied for cancer therapy; however, the mechanisms underlying its function in development and cancer pathogenesis remain elusive. To understand the catalytic-dependent and catalytic-independent functions of DOT1L, we generated catalytic dead and null DOT1L embryonic stem cells and found that DOT1L, but not its catalytic activity, is required for establishing the proper expression signature of neural progenitor cells, suggesting that DOTlL has biological functions that are independent of its methyltransferase activity. We propose that the loss/degradation of DOT1L could be beneficial for cancer therapeutics.

Cell fate determination

Histone Methylation

10.1073/pnas.2001075117

Cite

Citations (53)

Research Advances in the Roles of N6-Methyladenosine Modification in Ovarian Cancer

Cancer Control (2024)

Y Zhang Yufeng Ling Ying Zhou Xiu Shi Fangrong Shen

Ovarian cancer (OC) is the most lethal gynecological tumor, characterized by its insidious and frequently recurring metastatic progression. Owing to limited early screening methods, over 70% of OC cases are diagnosed at advanced stages, typically stage III or IV. Recently, N6-methyladenosine (m6A) modification has emerged as a hotspot of epigenetic research, representing a significant endogenous RNA modification in higher eukaryotes. Numerous studies have reported that m6A-related regulatory factors play pivotal roles in tumor development through diverse mechanisms. Moreover, recent studies have indicated the aberrant expression of multiple regulatory factors in OC. Therefore, this paper comprehensively reviews research advancements concerning m6A in OC, aiming to elucidate the regulatory mechanism of m6A-associated regulators on pivotal aspects, such as proliferation, invasion, metastasis, and drug resistance, in OC. Furthermore, it discusses the potential of m6A-associated regulators as early diagnostic markers and therapeutic targets, thus contributing to the diagnosis and treatment of OC.

N6-Methyladenosine

10.1177/10732748241256819

Cite

Citations (0)

Gut microbiota and stroke-associated pneumonia

Int J Cerebrovasc Dis (2018)

Qiuwan Liu Zhuqing Wu Xiaoqiang Wang Yue Hong Chi Zhang

Recent studies have shown that there is a mutual influence between gut microbiota and stroke. Stroke-associated pneumonia (SAP) is a common complication of stroke, which is closely associated with death and poor prognosis of patients. Gut microbiota translocation may be the source of infection of SAP, but the specific mechanism of gut microbiota and SAP remains unclear. This article reviews the relationship between gut microbiota and SAP in order to provide reference for the prevention and treatment of SAP. Key words: Stroke; Pneumonia; Gastrointestinal Microbiome; Inflammation; Immunity

Stroke

Gut microbiome

10.3760/cma.j.issn.1673-4165.2018.10.009

Cite

Citations (0)

The transcription factor Sp1 modulates RNA polymerase III gene transcription by controlling BRF1 and GTF3C2 expression in human cells

Journal of Biological Chemistry (2020)

Feixia Peng Ying Zhou Juan Wang Baoqiang Guo Yun Wei

Specificity protein 1 (Sp1) is an important transcription factor implicated in numerous cellular processes. However, whether Sp1 is involved in the regulation of RNA polymerase III (Pol III)-directed gene transcription in human cells remains unknown. Here, we first show that filamin A (FLNA) represses Sp1 expression as well as expression of TFIIB-related factor 1 (BRF1) and general transcription factor III C subunit 2 (GTF3C2) in HeLa, 293T, and SaOS2 cell lines stably expressing FLNA-silencing shRNAs. Both BRF1 promoter 4 (BRF1P4) and GTF3C2 promoter 2 (GTF3C2P2) contain putative Sp1-binding sites, suggesting that Sp1 affects Pol III gene transcription by regulating BRF1 and GTF3C2 expression. We demonstrate that Sp1 knockdown inhibits Pol III gene transcription, BRF1 and GTF3C2 expression, and the proliferation of 293T and HeLa cells, whereas Sp1 overexpression enhances these activities. We obtained a comparable result in a cell line in which both FLNA and Sp1 were depleted. These results indicate that Sp1 is involved in the regulation of Pol III gene transcription independently of FLNA expression. Reporter gene assays showed that alteration of Sp1 expression affects BRF1P4 and GTF3C2P2 activation, suggesting that Sp1 modulates Pol III-mediated gene transcription by controlling BRF1 and GTF3C2 gene expression. Further analysis revealed that Sp1 interacts with and thereby promotes the occupancies of TATA box-binding protein, TFIIAα, and p300 at both BRF1P4 and GTF3C2P2. These findings indicate that Sp1 controls Pol III-directed transcription and shed light on how Sp1 regulates cancer cell proliferation.

Transcription

RNA polymerase II

Sigma factor

General transcription factor

10.1074/jbc.ra119.011555

Cite

Citations (14)

T cell receptor rearrangement excision circles (TRECs) and CD31+ regulatory T cells for assessing recent thymic output in patients with chronic hepatitis B

Zhonghua weishengwuxue he mianyixue zazhi (2019)

Yongle Zhang Ke′nyu Pan Xinping Shi Juan Wang Xin Jin

Objective To evaluate the clinical value of combined detection of T cell receptor rearrangement excision circles (TRECs) and CD31+ regulatory T (Treg) cells for accessing the recent thymic output in patients with chronic hepatitis B. Methods Four groups involving 135 subjects were set up in this study as follows: mild chronic hepatitis B (Mild CHB, n=35), moderate chronic hepatitis B (Moderate CHB, n=35), severe chronic hepatitis B (Severe CHB, n=35) and healthy control (HCs, n=30) groups. CD4+ CD25+ Treg cells in these subjects were sorted out using magnetic cell separation. The ratio of peripheral CD31+ Treg cells to Treg cells in each group was analyzed by flow cytometry. Real-time PCR was performed to detect TRECs in CD4+ CD25+ Treg cells. The percentages of CD3+ , CD4+ and CD8+ T cell subsets were also measured. Results The ratios of CD31+ Treg/Treg cells and the numbers of TRECs in peripheral blood of the Moderate CHB and Severe CHB groups were significantly lower than those of the Mild CHB and HCs groups (P 0.05). No significant difference in the percentages of CD3+ , CD4+ or CD8+ T cell subsets was observed between the four groups (P>0.05). CD31+ Treg/Treg cell ratio had a positive correlation with the number of TRECs (r=0.551, P=0.014). Conclusions Both CD31+ Treg/Treg cell ratio and the number of TRECs were reduced in the peripheral blood of patients with moderate or severe CHB. CD31+ Treg/Treg cell ratio and the number of TRECs were positively correlated and could be used as new indices to evaluate recent thymus output. Key words: Chronic hepatitis B; CD4+ CD25+ regulatory T cell; CD31+ regulatory T cell; T cell receptor rearrangement excision circles

CD31

10.3760/cma.j.issn.0254-5101.2019.07.005

Cite

Citations (0)

Exploring the effect of Anshen Dingzhi prescription on hippocampal mitochondrial signals in single prolonged stress mouse model

Journal of Ethnopharmacology (2024)

Juan Wang Panpan Zhao Ping Cheng Zhengrong Zhang Shaojie Yang

10.1016/j.jep.2024.117713

Cite

Citations (14)

Diagnostic value of microRNA-106a-5p in patients with psoriasis and its regulatory role in inflammatory responses

Dermatologica Sinica (2021)

Xiaolin Miao Xinyun Tong Jingsang Hu Juan Wang

Background: Psoriasis is a multifactorial, recurring, and chronic inflammatory skin disease. Objectives: This study was designed to explore the potential role of microRNA-106a-5p (miR-106a-5p) in psoriasis. Methods: The expression levels of miR-106a-5p in the serum of psoriasis patients and healthy individuals were detected by quantitative real-time polymerase chain reaction. The diagnostic value of miR-106a-5p in serum was evaluated by the receiver operating characteristic (ROC) curve. The levels of interleukin-22 (IL-22), IL-17A, and tumor necrosis factor-alpha (TNF-alpha) were determined by enzyme-linked immunosorbent assay. Dual-luciferase reporter assay was used for the target gene verification. Results: The serum expression of miR-106a-5p was found to be upregulated in psoriasis patients. ROC curve showed that miR-106a-5p had high specificity and sensitivity in the diagnosis of psoriasis. The correlation between the serum expression level of miR-106a-5p and Psoriasis Area and Severity Index was positive. The relative expression levels of IL-17A, IL-22, and TNF-alpha in serum of psoriasis patients were significantly upregulated compared with that in healthy controls, and showed a positive association with serum miR-106a-5p levels. Cell experiments demonstrated that upregulation of miR-106a-5p could promote cell proliferation, and the levels of IL-22, IL-17A, and TNF-alpha were upregulated significantly in M5-induced HaCaT cells. Phosphatase and tensin homolog was proved to be the target gene of miR-106a-5p. Conclusion: Considering the novel and vital role in psoriasis progression, miR-106a-5p is expected to be a new potent target for the treatment of psoriasis. MiR-106-5p was expected to use for more immunity diseases research and therapy.

Tensin

HaCaT

10.4103/ds.ds_5_21

Cite

Citations (4)

CRF07_BC is associated with slow HIV disease progression in Chinese patients

Scientific Reports (2022)

Jingrong Ye Jing Chen Juan Wang Yuncong Wang Hui Xing

HIV subtypes convey important epidemiological information and possibly influence the rate of disease progression. In this study, HIV disease progression in patients infected with CRF01_AE, CRF07_BC, and subtype B was compared in the largest HIV molecular epidemiology study ever done in China. A national data set of HIV pol sequences was assembled by pooling sequences from public databases and the Beijing HIV laboratory network. Logistic regression was used to assess factors associated with the risk of AIDS at diagnosis ([AIDSAD], defined as a CD4 count < 200 cells/µL) in patients with HIV subtype B, CRF01_AE, and CRF07_BC. Of the 20,663 sequences, 9,156 (44.3%) were CRF01_AE. CRF07_BC was responsible for 28.3% of infections, followed by B (13.9%). In multivariable analysis, the risk of AIDSAD differed significantly according to HIV subtype (OR for CRF07_BC vs. B: 0.46, 95% CI 0.39─0.53), age (OR for ≥ 65 years vs. < 18 years: 4.3 95% CI 1.81─11.8), and transmission risk groups (OR for men who have sex with men vs. heterosexuals: 0.67 95% CI 0.6─0.75). These findings suggest that HIV diversity in China is constantly evolving and gaining in complexity. CRF07_BC is less pathogenic than subtype B, while CRF01_AE is as pathogenic as B.

10.1038/s41598-022-07518-4

Cite

Citations (22)

Research of EL-3 on anti-lung cancer mechanism

Journal of Traditional Chinese Medicine University of Hunan (2011)

Juan Wang

Objective To investigate the mechanism of extract of limax(EL-3) on anti-lung cancer.Methods(1) BrdU infiltration method was used to observe the inhibiting rates of EL-3 on the human lung cancer A549 cells.(2) The morphology of A549 cells apoptosis induced by EL-3 was determined and counted with the acridine orange/ethidium bromide(AO/EB) staining,and the cell cycle and apoptosis were analyzed with FCM.(3) The ladder-like DNA bands of apoptosis cells was observed by the DNA garose gelatin electrophoresis.(4) The protein expression levels of PCNA,VEGF and CD3 affected by EL-3 were detected with Immunochistochemical technique and DAB staining.Results(1) EL-3 using only in concentration 100 μg/mL to induce A549 cells,the inhibiting rate was 63.59%.,which was significant compared with black group(0) and solvent group(7.54%)(P0.01).(2) EL-3 was more effective combined with chemotherapeutics and enhanced the effect of CDDP on nucleic acid synthesis inhibition rate of A549.EL-3 in low,middle and high dose groups,the IR of DDP used only were increased to14.01% 44,5%,48.96% and 67.05%(P0.01);when IC50 in 20.62 μg/mL,EL-3 used with paclitaxel significantly improved the inhibition of A549 cell nucleic acidsynthesis.EL-3 in low,middle and high dose groups enhanced the IR of TAX used only on A549 cell were respectively increased from 21.79% to 58.35%,66.13% and 73.67%(P0.05),and the IC50 was 7.41 μg/mL.(3) EL-3 was effective to induce apoptosis in A549 cells;(4) EL-3 was effective to inhibit the expression of PCNA,VEGF and CD31 protein expression in rats.Conclusion anti-cancer mechanism of EL-3 is the multi-target,such as(1) inhibiting lung cancer cell nucleic acid synthesis;(2) inducing lung cancer cells apoptosis;and(3) inhibiting foci of angiogenesis and cancer cells to vascular wall adhesion.

Acridine orange

Ethidium bromide

IC50

Source

Cite

Citations (0)