8 results on '"Wu, Yihua"'
Search Results
2. Identification of a Novel Prognostic Classification Model in Epithelial Ovarian Cancer by Cluster Analysis
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Chen, Kelie, Niu, Yuequn, Wang, Shengchao, Fu, Zhiqin, Lin, Hui, Lu, Jiaoying, Meng, Xinyi, Yang, Bowen, Zhang, Honghe, Wu, Yihua, Xia, Dajing, and Lu, Weiguo
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ovarian cancer ,classification ,Cancer Management and Research ,inflammation ,prognosis ,heterogeneity ,Original Research ,cluster analysis - Abstract
Kelie Chen,1,2,* Yuequn Niu,3,* Shengchao Wang,1,* Zhiqin Fu,4 Hui Lin,1,2 Jiaoying Lu,2 Xinyi Meng,2 Bowen Yang,2 Honghe Zhang,1 Yihua Wu,1,2 Dajing Xia,1,2 Weiguo Lu1 1Department of Gynecologic Oncology, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310058, People’s Republic of China; 2Department of Toxicology, School of Public Health, School of Medicine, Zhejiang University, Hangzhou 310058, People’s Republic of China; 3Department of Thoracic Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, People’s Republic of China; 4Department of Gynecological Oncology, Zhejiang Cancer Hospital, Hangzhou 310022, People’s Republic of China*These authors contributed equally to this workCorrespondence: Dajing XiaDepartment of Toxicology, School of Public Health, School of Medicine, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, People’s Republic of ChinaTel/ Fax +86-0571-88208140Email dxia@zju.edu.cnWeiguo LuDepartment of Gynecologic Oncology, Women’s Hospital, School of Medicine, Zhejiang University, 1 Xueshi Road, Hangzhou, Zhejiang 310006, People’s Republic of ChinaTel +86-571-8706-1501Fax +86-571-87061878Email lbwg@zju.edu.cnBackground: Heterogeneity plays an essential role in ovarian cancer. Patients with different clinical features may manifest diverse patterns in diagnosis, treatment, and prognosis. The aim of the present study was to identify a novel ovarian cancer–classification model through cluster analysis and assess its significance in prognosis.Methods: Among patients diagnosed with ovarian cancer in the Women’s Hospital School of Medicine, Zhejiang University between January 2014 and May 2019, 328 patients were included in a K-mean cluster analysis and 176 patients followed up. Major clinical indicators, overall survival, and recurrence-free survival in different subgroups were compared.Results: Two clusters for ovarian cancer were identified and grouped as noninflammatory (n=247) and inflammatory subtypes (n=81). Compared with the noninflammatory subgroup, the inflammatory subgroup presented a statistically significantly higher level of median CRP (median (IQR) 20.4 [7.8– 47.3] vs 1.2 [0.4– 3.5], p< 0.001), neutrophil percentage (median (IQR) 76.9 [72.6– 81.3] vs 66.2 [61.0– 72.0], p< 0.001), leukocyte count (median (IQR) 8.9 [7.0– 10.0] vs 6.0 [5.1– 7.2], p< 0.001), fibrinogen (median (IQR) 5.0 [4.4– 6.0] vs 3.4 [2.9– 3.9], p< 0.001), and platelet count (median (IQR) 324 [270– 405] vs 229 [181.5– 269], p< 0.001). During a median follow-up of 52 months, 21 participants (16.3%) died in the noninflammatory group, while 14 (29.8%) died in the inflammatory group (HR 2.15, 95% CI 1.09– 4.23; p=0.024). Death/recurrence was observed in 38 (29.5%) patients from the noninflammatory group and 25 (53.2%) from the inflammatory group (HR 2.32, 95% CI 1.40– 3.85; p< 0.001).Conclusion: Our study revealed a novel classification model of ovarian cancer that features inflammation. Inflammation predicts shorter survival and poorer prognosis, suggesting the significance of inflammation in the management of ovarian cancer.Keywords: ovarian cancer, classification, heterogeneity, cluster analysis, inflammation, prognosis
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- 2020
3. High expression of RIPK2 is associated with Taxol resistance in serous ovarian cancer.
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Shen, Yuqing, Lin, Hui, Chen, Kelie, Ge, Wanzhong, Xia, Dajing, Wu, Yihua, and Lu, Weiguo
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OVARIAN cancer ,PACLITAXEL ,PROTEIN-protein interactions ,GENE expression ,TUMOR microenvironment ,CANCER cells - Abstract
Background: Taxol resistance in serous ovarian cancer is responsible for its poor prognosis, yet the underlying mechanism is still poorly understood. Thus, we probed the mechanism of Taxol resistance in serous ovarian cancer with multiple bioinformatic methods to provide novel insights into potential therapies. Methods: The differentially expressed genes (DEGs) in Taxol-sensitive and Taxol-resistant cell lines and their relationship with the overall survival (OS) and progression-free interval (PFI) of ovarian cancer patients were analyzed using gene expression datasets from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The role of receptor interacting serine/threonine kinase 2 (RIPK2) was validated via identification of its coexpressed genes, functional analysis and generation of a protein-protein interaction (PPI) network. The single sample gene set enrichment analysis (ssGSEA) was used to explore immune infiltration, and genomic alterations of RIPK2 were also analyzed via cBio Cancer Genomics Portal (cBioProtal). Results: RIPK2 was highly expressed in Taxol resistant ovarian cancer cell lines, and its high expression was also linked with shorter OS and PFI in serous ovarian cancer patients. The PPI network analysis and pathway analysis demonstrated that RIPK2 might participate in the positive regulation of NF-κB transcription factor activity. RIPK2 expression was related to tumor microenvironment alterations, which might participate in the formation of Taxol resistance. Conclusions: Our studies suggested that high expression of RIPK2 is related to Taxol resistance in serous ovarian cancer, and that RIPK2 induces Taxol resistance through NOD1/RIPK2/NF-κB inflammatory pathway activation and tumor microenvironment changes. [ABSTRACT FROM AUTHOR]
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- 2022
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4. Environmentally relevant concentration PFNA promotes degradation of SMAD7 to drive progression of ovarian cancer via TGF-β/SMADs signaling pathway.
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Zhong, Jiamin, Zhang, Lihuan, Chen, Kelie, Yuan, Xiaoyu, Cui, Zhenyan, Tang, Song, Zheng, Fang, Li, Ying, Héroux, Paul, Wu, Yihua, and Xia, Dajing
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PERFLUOROOCTANE sulfonate ,PERFLUOROOCTANOIC acid ,CANCER cell migration ,OVARIAN cancer ,FLUOROALKYL compounds - Abstract
Perfluorononanoic acid (PFNA), an acknowledged environmental endocrine disruptor, is increasingly utilized as a substitute for perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA). Despite its growing use, limited research has been conducted to investigate its potential impact on tumorigenesis and progression, and the potential molecular mechanisms. Earlier studies linked perfluoroalkyl and polyfluoroalkyl substances (PFAS) exposure to breast and gynecological cancer progression in humans, lacking a clear understanding of the underlying mechanisms, notably in ovarian cancer. Our investigation into PFNA's effects at environmental concentrations (0.25–2 mM) showed no significant impact on cell proliferation but a notable increase in invasion and migration of ovarian cancer cells. This led to alterations in epithelial-mesenchymal transition (EMT) markers, including Claudin1, Vimentin, and Snail. Notably, PFNA exposure activated the TGF-β/SMADs signaling pathway. Crucially, SMAD7 degradation through the ubiquitin-proteasome system emerged as PFNA's pivotal molecular target for inducing EMT, corroborated in mouse models. In summary, this study presented evidence that environmentally relevant concentrations of PFNA could induce SMAD7 degradation via the proteasome pathway, subsequently activating the TGF-β/SMADs signaling pathway, and promoting EMT in ovarian cancer. These results illuminated the association between PFNA exposure and metastasis of ovarian cancer. [Display omitted] • Environmental concentrations of PFNA enhances EMT in ovarian cancer cells. • PFNA induces SMAD7 degradation via TGF-β/SMADs signaling pathway. • PFNA exposure promotes ovarian tumor metastasis in vivo. • Targeting TGF-β/SMADs pathway could be a strategy to eliminate PFNA toxicity. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Erratum to: "Low Dose of Bisphenol A. Modulates Ovarian Cancer Gene Expression Profile and Promotes Epithelial to Mesenchymal Transition Via Canonical Wnt Pathway".
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Lin, Hui, Li, Hongyi, Lu, Guang, Chen, Zhifeng, Sun, Wenjie, Shi, Yu, Fu, Zhiqin, Huang, Bo, Zhu, Xinqiang, Lu, Weiguo, Xia, Dajing, and Wu, Yihua
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EPITHELIAL-mesenchymal transition ,GENE expression profiling ,CANCER genes ,OVARIAN cancer ,BISPHENOL A ,BISPHENOLS - Published
- 2020
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6. PFDA promotes cancer metastasis through macrophage M2 polarization mediated by Wnt/β-catenin signaling.
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Cui, Zhenyan, Liu, Zekun, Yuan, Xiaoyu, Lu, Kean, Li, Mengyao, Xu, Sinan, Chen, Kelie, Zheng, Fang, Li, Ying, Héroux, Paul, Wu, Yihua, and Xia, Dajing
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CANCER invasiveness , *CANCER cells , *METASTASIS , *TUMOR microenvironment , *FOOD industry - Abstract
Perfluoroundecanoic acid (PFDA) is extensively utilized in the textile and food processing industries and may have a tumor-promoting effect by modulating the tumor microenvironment. Macrophages play crucial roles in tumor microenvironment as key regulators of tumor immunity. However, further investigation is needed to elucidate how PFDA interacts with macrophages and contributes to tumor progression. In this study, we treated the macrophage cell line RAW264.7 with various concentrations of PFDA and found that RAW264.7 transitioned into an M2 tumor-promoting phenotype. Through bioinformatic analysis and subsequent verification of molecular assays, we uncovered that PFDA could activate β-catenin and enhance its nuclear translocation. Additionally, it was also observed that inhibiting β-catenin nuclear translocation partly attenuated RAW264.7 M2 polarization induced by PFDA. The conditioned medium derived from PFDA-pretreated RAW264.7 cells significantly promoted the migration and invasion abilities of human ovarian cancer cells. Furthermore, in vivo studies corroborated that PFDA-pretreated RAW264.7 could promote tumor metastasis, which could be mitigated by pretreatment with the β-catenin inhibitor ICG001. In conclusion, our study demonstrated that PFDA could promote cancer metastasis through regulating macrophage M2 polarization in a Wnt/β-catenin-dependent manner. [Display omitted] • PFDA promotes macrophage M2 polarization. • PFDA activates Wnt/β-catenin signaling and enhances β-catenin nuclear accumulation. • Activation of Wnt/β-catenin facilitates M2 polarization of macrophages. • PFDA-induced M2 phenotype macrophage accelerates tumor progression in vitro and in vivo. [ABSTRACT FROM AUTHOR]
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- 2024
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7. Low-dose BPA and its substitute BPS promote ovarian cancer cell stemness via a non-canonical PINK1/p53 mitophagic signaling.
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Yuan, Xiaoyu, Chen, Kelie, Zheng, Fang, Xu, Sinan, Li, Yating, Wang, Yuwei, Ni, Heng, Wang, Fang, Cui, Zhenyan, Qin, Yuheng, Xia, Dajing, and Wu, Yihua
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BISPHENOL A , *OVARIAN cancer , *CANCER cells , *CANCER stem cells , *P53 antioncogene , *WNT signal transduction , *METASTASIS , *CANCER invasiveness - Abstract
The environmental toxicity of bisphenol A (BPA) and its analog like bisphenol S (BPS) have drawn wide attention, but their roles in cancer progression remain controversial. Here, we investigated the effect of BPA/BPS on the development of ovarian cancer. Human internal BPA/BPS exposure levels were analyzed from NHANES 2013–2016 data. We treated human ovarian cancer cells with 0−1000 nM BPA/BPS and found that 100 nM BPA/BPS treatment significantly increased Cancer Stem Cell (CSC) markers expression including OCT4, NANOG and SOX2. Cancer cell stemness evaluation induced by BPA/BPS was notably attenuated by the knockdown of PINK1 or Mdivi-1 treatment. The activation of PINK1 initiated mitophagy by inhibiting p-p53 nuclear translocation in a non-canonical manner. In vivo studies validated that BPA/BPS-exposed mice have higher tumor metastasis incidence compared with the control group, while mitophagy inhibition blocked such a promotion effect. In addition, CSC markers such as SOX2 had been found to be overexpressed in the tumor tissues of BPA/BPS exposure group. Taken together, the findings herein first provide the evidence that environmentally relevant BPA/BPS exposure could enhance ovarian cancer cell stemness through a non-canonical PINK1/p53 mitophagic pathway, raising concerns about the potential population hazards of BPA and other bisphenol analogs. [Display omitted] • Environmental relevant BPA/BPS exposure enhances ovarian cancer cell stemness. • Low-dose BPA/BPS upregulates PINK1 expression. • p53 rather than Parkin pathway is activated under low-dose BPA/BPS exposure. • BPA/BPS promotes ovarian cancer in vivo metastasis in a mitophagy-dependent manner. [ABSTRACT FROM AUTHOR]
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- 2023
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8. Low-dose mono(2-ethylhexyl) phthalate promotes ovarian cancer development through PPARα-dependent PI3K/Akt/NF-κB pathway.
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Leng, Jing, Li, Hongyi, Niu, Yuequn, Chen, Kelie, Yuan, Xiaoyu, Chen, Hanwen, Fu, Zhiqin, Zhang, Lihuan, Wang, Fang, Chen, Chaoyi, Héroux, Paul, Yang, Jun, Zhu, Xinqiang, Lu, Weiguo, Xia, Dajing, and Wu, Yihua
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- 2021
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