15 results on '"Xu, Yingying"'
Search Results
2. ARHGAP39 is a prognostic biomarker involved in immune infiltration in breast cancer
- Author
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Yao, Litong, Li, Yuwei, Li, Siyuan, Wang, Mozhi, Cao, Hongyi, Xu, Ling, and Xu, Yingying
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- 2023
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3. A plasma SNORD33 signature predicts platinum benefit in metastatic triple-negative breast cancer patients
- Author
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Wang, Biyun, Zhao, Yannan, Li, Yi, Xu, Yingying, Chen, Yun, Jiang, Qiuyu, Yao, Dingjin, Zhang, Li, Hu, Xichun, Fu, Chaowei, Zhang, Si, and Chen, She
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- 2022
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4. Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest
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Zhao, Yannan, Peng, Huitong, Liang, Limiao, Li, Yi, Hu, Xichun, Wang, Biyun, Xu, Yingying, and Chen, She
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- 2022
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5. Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest
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She Chen, Xu Yingying, Yannan Zhao, Xichun Hu, Biyun Wang, Huitong Peng, Yi Li, and Limiao Liang
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Cancer Research ,Cell cycle checkpoint ,Paclitaxel ,Polarity (physics) ,Cell Cycle ,Apoptosis ,Breast Neoplasms ,Cell Cycle Proteins ,Cell Cycle Checkpoints ,medicine.disease ,Antineoplastic Agents, Phytogenic ,Microtubules ,chemistry.chemical_compound ,Breast cancer ,chemistry ,Oncology ,Tubulin ,Cell Line, Tumor ,Cancer research ,medicine ,Humans ,Female ,Adaptor Proteins, Signal Transducing ,Cell Proliferation - Abstract
Purpose Paclitaxel, belongs to tubulin-binding agents (TBAs), showed a great efficacy against breast cancer via stabilizing microtubules. Drug resistance limits its clinical application. Here we aimed to explore a role of Polarity protein Par3 in improving paclitaxel effectiveness.Methods Breast cancer specimens from 45 patients were collected to study the relationship between Par3 expression and paclitaxel efficacy. The Kaplan–Meier method was used for survival analysis. Cell viability was measured in breast cancer cells (SK-BR-3 and T-47D) with Par3 over-expression or knockdown. The flow cytometry assays were performed to measure cell apoptosis and cell cycle. BrdU incorporation assay and Hoechst 33258 staining were performed to measure cell proliferation and cell apoptosis, respectively. Immunofluorescence was used to detect microtubule structures. Results Par3 expression is associated with good response of paclitaxel in breast cancer patients. Consistently, Par3 overexpression significantly sensitizes breast cancer cells to paclitaxel by promoting cell apoptosis and reducing cell proliferation. In Par3 overexpressing cells upon paclitaxel treatment, we observed intensified cell cycle arrests at metaphase. Further exploration showed that Par3 overexpression stabilizes microtubules of breast cancer cells in response to paclitaxel, and resists to microtubules instability induced by nocodazole, a microtubule-depolymerizing agent. Conclusion Par3 facilitates polymeric forms of tubulin and stabilizes microtubule structure, which aggravates paclitaxel-induced delay at the metaphase-anaphase transition, leading to proliferation inhibition and apoptosis of breast cancer cells. Par3 has a potential role in sensitizing breast cancer cells to paclitaxel, which may provide a more precise assessment of individual treatment and novel therapeutic targets.
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- 2021
6. Overexpression of CRKL correlates with malignant cell proliferation in breast cancer
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Zhao, Tingting, Miao, Zhifeng, Wang, Zhenning, Xu, Yingying, Wu, Jianhua, Liu, Xingyu, You, Yi, and Li, Jiguang
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- 2013
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7. Expressions of MAGE-A10 and MAGE-A11 in breast cancers and their prognostic significance: a retrospective clinical study
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Lian, Yishui, Sang, Meixiang, Ding, Chunyan, Zhou, Xinliang, Fan, Xiaojie, Xu, Yingying, Lü, Weihua, and Shan, Baoen
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- 2012
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8. OLR1 is a prognostic factor and correlated with immune infiltration in breast cancer
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Xiangyu Sun, Xu Yingying, Xin Fu, Qiang Zhang, Pengfei Qiu, Cui Mingke, Shouping Xu, and Zhi-Dong Lv
- Subjects
Immunology ,Macrophage polarization ,Datasets as Topic ,Breast Neoplasms ,Biology ,Lymphocytes, Tumor-Infiltrating ,Immune system ,Breast cancer ,Downregulation and upregulation ,Biomarkers, Tumor ,OLR1 ,medicine ,Humans ,Immunology and Allergy ,Molecular Targeted Therapy ,KEGG ,Pharmacology ,Cancer ,Prognosis ,Scavenger Receptors, Class E ,medicine.disease ,Survival Analysis ,Biomarker (cell) ,Gene Expression Regulation, Neoplastic ,Lipoproteins, LDL ,Cancer research ,Female - Abstract
Oxidized low-density lipoprotein receptor 1 (OLR1), a key receptor for oxidized low-density lipoprotein (ox-LDL), plays a crucial role in cancer and inflammatory disease. However, the correlation between OLR1 expression and immune infiltration in breast cancer (BC) remain unclear. In this study, we comprehensively analyzed the expression level of OLR1 in BC tissues and explore the prognostic importance of OLR1 using quantitative real-time PCR, immunohistochemical analysis and different databases. The significantly enriched KEGG and GO pathways were used to identify the potential biological function of OLR1 via LinkedOmics analysis. Furthermore, we detected the correlation between OLR1 expression and a variety of immune infiltrating cells via Tumor Immune Estimation Resource database and GEPIA database. Our study revealed that OLR1 upregulation was observed in BC tissues and correlated with worse clinical outcomes and advanced clinicopathological factors. Meanwhile, OLR1 regulated various immunity-related pathways, especially the polarization of macrophages. Immunohistochemical analysis further confirmed the significant correlation between OLR1 expression and tumor infiltration of M2 macrophages as well as tumor-associated macrophages. OLR1 upregulation indicated poor prognosis in BC, possibly through inducing macrophage polarization and triggering immune evasion. Collectively, OLR1 may represent a potential therapeutic target for BC tailored therapy.
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- 2021
9. An Immune Model to Predict Prognosis of Breast Cancer Patients Receiving Neoadjuvant Chemotherapy Based on Support Vector Machine.
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Wang, Mozhi, Pang, Zhiyuan, Wang, Yusong, Cui, Mingke, Yao, Litong, Li, Shuang, Wang, Mengshen, Zheng, Yanfu, Sun, Xiangyu, Dong, Haoran, Zhang, Qiang, and Xu, Yingying
- Subjects
NEOADJUVANT chemotherapy ,SUPPORT vector machines ,BREAST cancer prognosis ,T helper cells ,CYTOTOXIC T cells - Abstract
Tumor microenvironment has been increasingly proved to be crucial during the development of breast cancer. The theory about the conversion of cold and hot tumor attracted the attention to the influences of traditional therapeutic strategies on immune system. Various genetic models have been constructed, although the relation between immune system and local microenvironment still remains unclear. In this study, we tested and collected the immune index of 262 breast cancer patients before and after neoadjuvant chemotherapy. Five indexes were selected and analyzed to form the prediction model, including the ratio values between after and before neoadjuvant chemotherapy of CD4
+ /CD8+ T cell ratio; lymphosum of T, B, and natural killer (NK) cells; CD3+ CD8+ cytotoxic T cell percent; CD16+ CD56+ NK cell absolute value; and CD3+ CD4+ helper T cell percent. Interestingly, these characters are both the ratio value of immune status after neoadjuvant chemotherapy to the baseline. Then the prediction model was constructed by support vector machine (accuracy rate = 75.71%, area under curve = 0.793). Beyond the prognostic effect and prediction significance, the study instead emphasized the importance of immune status in traditional systemic therapies. The result provided new evidence that the dynamic change of immune status during neoadjuvant chemotherapy should be paid more attention. [ABSTRACT FROM AUTHOR]- Published
- 2021
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10. Assessment of CPS + EG, Neo-Bioscore and Modified Neo-Bioscore in Breast Cancer Patients Treated With Preoperative Systemic Therapy: A Multicenter Cohort Study.
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Xu, Ling, Liu, Yinhua, Fan, Zhimin, Jiang, Zefei, Liu, Yunjiang, Ling, Rui, Zhang, Jianguo, Yu, Zhigang, Jin, Feng, Wang, Chuan, Cui, Shude, Wang, Shu, Mao, Dahua, Han, Bing, Wang, Tao, Zhang, Geng, Wang, Ting, Guo, Baoliang, Yu, Lixiang, and Xu, Yingying
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PROGRESSION-free survival ,CANCER patients ,TUMOR grading ,BREAST cancer ,CLINICAL trial registries - Abstract
This study was to assess the prognosis stratification of the clinical-pathologic staging system incorporating estrogen receptor (ER)-negative disease, the nuclear grade 3 tumor pathology (CPS + EG), Neo-Bioscore, and a modified Neo-Bioscore system in breast cancer patients after preoperative systemic therapy (PST). A retrospective multicenter cohort study was conducted from 12 participating hospitals' databases from 2006 to 2015. Five-year disease free survival (DFS), disease specific survival (DSS), and overall survival (OS) were calculated using Kaplan–Meier Method. Area under the curve (AUC) of the three staging systems was compared. Wald test and maximum likelihood estimates in Cox proportional hazards model were used for multivariate analysis. A total of 1,077 patients were enrolled. The CPS + EG, Neo-Bioscore, and modified Neo-Bioscore could all stratify the DFS, DSS, and OS (all P < 0.001). While in the same stratum of Neo-Bioscore scores 2 and 3, the HER2-positive patients without trastuzumab therapy had much poorer DSS (P = 0.013 and P values < 0.01, respectively) as compared to HER2-positive patients with trastuzumab therapy and HER2-negative patients. Only the modified Neo-Bioscore had a significantly higher stratification of 5-year DSS than PS (AUC 0.79 vs. 0.65, P = 0.03). So, the modified Neo-Bioscore could circumvent the limitation of CPS + EG or Neo-Bioscore. Clinical Trial Registration: ClinicalTrials.gov , identifier NCT03437837. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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11. Long non‐coding RNA‐CTD‐2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor.
- Author
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Wang, Mozhi, Wang, Mengshen, Wang, Zhenning, Yu, Xueting, Song, Yongxi, Wang, Chong, Xu, Yujie, Wei, Fengheng, Zhao, Yi, and Xu, Yingying
- Abstract
Breast cancer (BC) is an aggressive malignant disease in women worldwide with a high tendency to metastasize. However, important biomarkers for BC metastasis remain largely undefined. In the present study, we identified that long non‐coding RNA‐CTD‐2108O9.1 is downregulated in BC tissues and cells and acts as a metastatic inhibitor of BC. Mechanistic investigation determined that lncRNA‐CTD‐2108O9.1 represses metastasis by targeting leukemia inhibitory factor receptor (LIFR), which is designated as a metastasis suppressor in BC. Our study characterizes a significant tumor suppressor active in BC metastasis repression through the known metastasis inhibitor LIFR. [ABSTRACT FROM AUTHOR]
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- 2018
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12. Selective inhibition of breast cancer stem cells by gold nanorods mediated plasmonic hyperthermia.
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Xu, Yingying, Wang, Jing, Li, Xiaofan, Liu, Ying, Dai, Luru, Wu, Xiaochun, and Chen, Chunying
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BREAST cancer , *STEM cells , *GOLD nanoparticles , *FEVER , *CANCER radiotherapy , *CANCER chemotherapy - Abstract
Abstract: Cancer stem cells (CSCs) have been identified in a variety of cancers and emerged as a new target for cancer therapy. CSCs are resistant to many current cancer treatments, including chemotherapy and radiation therapy. Therefore, eradication of this cell population is a primary objective in cancer therapy. Here, we report gold nanorods (AuNRs) mediated photothermal treatment can selectively eliminate CSCs in MCF-7 breast cancer cells. It significantly reduced the aldehyde dehydrogenase positive (ALDH+) cells subpopulation and the mammosphere formation ability of treated cells. Also, the gene expression of stem cell markers was decreased. Cellular uptake assay revealed that polyelectrolyte conjugated AuNRs could be internalized by CSCs much more and faster than non cancer stem cells (NCSCs), which might be the main reason for the selective elimination of CSCs. We further loaded salinomycin (SA), a CSCs inhibitor with polyelectrolyte conjugated AuNRs to get a synergistic CSCs inhibition. Enhanced inhibition of CSCs was obtained by NIR light triggered drug release and hyperthermia. This CSCs-targeted thermo-chemotherapy platform provides a new combinatorial strategy for efficient inhibition of CSCs, which is promising to improve cancer treatment and may overcome the chemoresistance and recurrence of cancer. [Copyright &y& Elsevier]
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- 2014
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13. PROS1, a clinical prognostic biomarker and tumor suppressor, is associated with immune cell infiltration in breast cancer: A bioinformatics analysis combined with experimental verification.
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He, Tianyi, Sun, Xiangyu, Wu, Chen, Yao, Litong, Zhang, Yingfan, Liu, Shiyang, Jiang, Yuhan, Li, Yixiao, Wang, Mozhi, and Xu, Yingying
- Subjects
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BREAST cancer , *BIOMARKERS , *OVERALL survival , *PROGRAMMED cell death 1 receptors , *BREAST cancer prognosis , *EPITHELIAL-mesenchymal transition , *BREAST - Abstract
PROS1 is an encoding gene that can generate protein S. This protein is a glycoprotein found in plasma that conducts physiological functions with vitamin K. However, the impact of its expression remains absent in the progression and prognosis of breast cancer (BC). In this study, we comprehensively explored the expression of PROS1 in BC and its relationship with BC patient survival, prognosis, and other clinicopathological features. We investigated how PROS1 influenced the malignant biological behavior of BC cells. A series of enrichment analyses were conducted, and the immune landscape was explored in BC affected by PROS1. We also determined correlations between PROS1 and common drug sensitivities used for BC treatments. PROS1 had low expression in BC, which tended to result in poor survival of BC patients. Overexpressed PROS1 inhibited the migration and invasion of BC cells as well as the epithelial–mesenchymal transition process by downregulating SNAIL. Functional enrichment analyses revealed that PROS1 was more active in extracellular matrix (ECM) organization and structural constituent, ECM-receptor interaction, and other pathways with its related genes. PROS1 was also found to affect immune activity, including various immune cells infiltrating BC. BC patients with high PROS1 expression tended to have lower IC50 values of three common medications and obtained better efficacy. PROS1 can become a promising prognostic factor and a possible therapeutic target in BC patients and suppress BC cell metastatic potential. In addition, PROS1 is a crucial factor in immune infiltration in BC. • PROS1 is lowly expressed in BC and predicts a poor survival of BC patients. • Overexpressed PROS1 inhibits the migration and invasion of BC cells. • PROS1 is a new hub gene regulating the EMT process and immune infiltration in BC cells. • PROS1 can be a new drug-effect predictor for BC treatment. [ABSTRACT FROM AUTHOR]
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- 2023
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- View/download PDF
14. OLR1 is a prognostic factor and correlated with immune infiltration in breast cancer.
- Author
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Sun, Xiangyu, Fu, Xin, Xu, Shouping, Qiu, Pengfei, Lv, Zhidong, Cui, Mingke, Zhang, Qiang, and Xu, Yingying
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BREAST cancer , *PROGNOSIS , *TUMOR-infiltrating immune cells , *IMMUNOHISTOCHEMISTRY , *LIPOPROTEIN receptors - Abstract
• OLR1 was highly upregulated in the breast cancer compared with nontumor tissues. • High expression of OLR1 was significantly correlated with poor prognosis in breast cancer. • OLR1 markedly affected the immune infiltration level of breast cancer. Oxidized low-density lipoprotein receptor 1 (OLR1), a key receptor for oxidized low-density lipoprotein (ox-LDL), plays a crucial role in cancer and inflammatory disease. However, the correlation between OLR1 expression and immune infiltration in breast cancer (BC) remain unclear. In this study, we comprehensively analyzed the expression level of OLR1 in BC tissues and explore the prognostic importance of OLR1 using quantitative real-time PCR, immunohistochemical analysis and different databases. The significantly enriched KEGG and GO pathways were used to identify the potential biological function of OLR1 via LinkedOmics analysis. Furthermore, we detected the correlation between OLR1 expression and a variety of immune infiltrating cells via Tumor Immune Estimation Resource database and GEPIA database. Our study revealed that OLR1 upregulation was observed in BC tissues and correlated with worse clinical outcomes and advanced clinicopathological factors. Meanwhile, OLR1 regulated various immunity-related pathways, especially the polarization of macrophages. Immunohistochemical analysis further confirmed the significant correlation between OLR1 expression and tumor infiltration of M2 macrophages as well as tumor-associated macrophages. OLR1 upregulation indicated poor prognosis in BC, possibly through inducing macrophage polarization and triggering immune evasion. Collectively, OLR1 may represent a potential therapeutic target for BC tailored therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
15. LMO4 inhibits p53-mediated proliferative inhibition of breast cancer cells through interacting p53
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Zhou, Xinliang, Sang, Meixiang, Liu, Wei, Gao, Wei, Xing, Enhong, Lü, Weihua, Xu, Yingying, Fan, Xiaojie, Jing, Shaowu, and Shan, Baoen
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P53 antioncogene , *BREAST cancer treatment , *CANCER cells , *GENETIC transcription regulation , *DOXORUBICIN , *PROTEINS , *BIOLOGICAL assay - Abstract
Abstract: Aims: The LIM domain only proteins (LMOs) which consist of four members (LMO1–LMO4) are a family of nuclear transcription coregulators that are characterized by the exclusive presence of two tandem LIM domains and no other functional domains. They regulate gene transcription by functioning as “linker” or “scaffolding” proteins by virtue of their LIM domains and are involved in the formation of multiprotein complexes with several DNA-binding factors and transcriptional regulatory proteins. In the present study, we tried to find the physical interaction between p53 and LMO4, and the effect of LMO4 on p53-mediated proliferative inhibition of breast cancer cells. Main methods: FCM analysis was developed to detect the apoptosis of breast cancer cells after adriamycin (ADR) treatment. RT-PCR and Western blot analysis were performed to detect the expression of LMO4 and p53-related genes and proteins. Immunoprecipitation assay was used to detect the interaction between LMO4 and p53. Colony formation assay was developed to detect the proliferation of breast cancer cells. Key findings: We found that p53 was induced, but LMO4 was down-regulated in response to ADR. We also found that enforced expression of p53 inhibited the expression of LMO4, suggesting that LMO4 is a direct transcriptional target of p53. Furthermore, LMO4 can interact with p53 and inhibit p53-mediated inhibition of colony formation of breast cancer MDA-MB-453 cells. Significance: The present study showed that LMO4 is a direct target of p53 and inhibits p53-mediated proliferative inhibition of breast cancer cells through interacting p53. [Copyright &y& Elsevier]
- Published
- 2012
- Full Text
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