Ming Zhou

Hunan Cancer Hospital

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Guiyuan Li

Central South University

114

Wei Xiong

Central South University

Zhaoyang Zeng

Central South University

Bo Xiang

Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital

Xiayu Li

Zhejiang University

Xiaoling Li

National Institute of Environmental Health Sciences

Can Guo

Central South University

Zhaojian Gong

Second Xiangya Hospital of Central South University

Yong Li

Baylor College of Medicine

Qianjin Liao

Hunan Normal University

Cooperative Institutions

Central South University

483

Xiangya Hospital Central South University

204

Hunan Cancer Hospital

169

Third Xiangya Hospital

108

Sun Yat-sen University

Chinese Academy of Sciences

Second Xiangya Hospital of Central South University

Soochow University

Chinese Academy of Medical Sciences & Peking Union Medical College

Shanghai Jiao Tong University

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The role of microenvironment in tumor angiogenesis

Journal of Experimental & Clinical Cancer Research (2020)

Xianjie Jiang Jie Wang Xiangying Deng Fang Xiong Shanshan Zhang

Abstract Tumor angiogenesis is necessary for the continued survival and development of tumor cells, and plays an important role in their growth, invasion, and metastasis. The tumor microenvironment—composed of tumor cells, surrounding cells, and secreted cytokines—provides a conducive environment for the growth and survival of tumors. Different components of the tumor microenvironment can regulate tumor development. In this review, we have discussed the regulatory role of the microenvironment in tumor angiogenesis. High expression of angiogenic factors and inflammatory cytokines in the tumor microenvironment, as well as hypoxia, are presumed to be the reasons for poor therapeutic efficacy of current anti-angiogenic drugs. A combination of anti-angiogenic drugs and antitumor inflammatory drugs or hypoxia inhibitors might improve the therapeutic outcome.

Hypoxia

Tumor Hypoxia

10.1186/s13046-020-01709-5

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Citations (464)

Knockout of BRD7 results in impaired spermatogenesis and male infertility

Scientific Reports (2016)

Heran Wang Ran Zhao Chi Guo Shihe Jiang Jing Yang

Abstract BRD7 was originally identified as a novel bromodomain gene and a potential transcriptional factor. BRD7 was found to be extensively expressed in multiple mouse tissues but was highly expressed in the testis. Furthermore, BRD7 was located in germ cells during multiple stages of spermatogenesis, ranging from the pachytene to the round spermatid stage. Homozygous knockout of BRD7 (BRD7 −/− ) resulted in complete male infertility and spermatogenesis defects, including deformed acrosomal formation, degenerative elongating spermatids and irregular head morphology in postmeiotic germ cells in the seminiferous epithelium, which led to the complete arrest of spermatogenesis at step 13. Moreover, a high ratio of apoptosis was determined by TUNEL analysis, which was supported by high levels of the apoptosis markers annexin V and p53 in knockout testes. Increased expression of the DNA damage maker λH2AX was also found in BRD7 −/− mice, whereas DNA damage repair genes were down−regulated. Furthermore, no or lower expression of BRD7 was detected in the testes of azoospermia patients exhibiting spermatogenesis arrest than that in control group. These data demonstrate that BRD7 is involved in male infertility and spermatogenesis in mice, and BRD7 defect might be associated with the occurrence and development of human azoospermia.

10.1038/srep21776

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YB1 associates with oncogenetic roles and poor prognosis in nasopharyngeal carcinoma

Scientific Reports (2022)

Yuting Zhan Xianyong Chen Hongmei Zheng Jiadi Luo Yang Yang

Abstract Nasopharyngeal carcinoma (NPC) is the malignant tumor arising from the nasopharynx epithelium with ethnic and geographical distribution preference. Y-box binding protein-1 (YB1) is the highly expressed DNA/RNA-binding protein with cold shock domain, and enhanced YB1 expression was proved to be associated with many kinds of malignant tumors. There is no systematic study about the regulation of YB1 and cell proliferation, migration, invasion and stress granules (SGs) in NPC, and the relationship between YB1 expression and clinical characteristics and prognosis of NPC patients. We analyzed the mRNA expression of YBX1 in head and neck squamous carcinoma (HNSC) and NPC in databases, investigated the functions of YB1 in cell proliferation, migration and invasion and SGs formation of NPC cells, and detected expression of YB1 protein in a large scale of NPC samples and analyzed their association with clinicopathological features and prognostic significance of NPC patients. YBX1 mRNA was significantly high expression in HNSC and NPC by bioinformatic analysis, and higher expression of YBX1 mRNA indicated poorer prognosis of HNSC patients. Clinically, the expression of YB1 in NPC tissues was significantly higher than these in the control nasopharyngeal epithelial tissues. We further found that the expression of YB1 had an evidently positive relation with advanced clinical stages of patients with NPC. The overall survival rates (OS) were significantly lower for NPC patients with positive expression of YB1. Multivariate analysis confirmed that positive expression of YB1 was the independent poorer prognostic factor for patients with NPC. Moreover, compared with the immortalized nasopharyngeal epithelial cell line (NP69), the basal level of YB1 in NPC cell lines was significantly higher. Knocking down YB1 may inhibit Akt/mTOR pathway in NPC cells. Knocking down YB1 by small interfering RNAs can reduce the ability of proliferation, migration, invasion and SGs formation of NPC cells. The expression of YB1 in NPC cell lines or patients with NPC was significantly higher. The high expression of YB1 protein may act as one valuable independent biomarker to predict poor prognosis for patients with NPC. Knocking down YB1 may release the malignant phenotype of NPC cells.

10.1038/s41598-022-07636-z

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Citations (11)

[18F]SynVesT-1 and [18F]FDG quantitative PET imaging in the presurgical evaluation of MRI-negative children with focal cortical dysplasia type II

European Journal of Nuclear Medicine and Molecular Imaging (2024)

Ling Xiao Jinhui Yang Haoyue Zhu Ming Zhou Jian Li

Statistical parametric mapping

10.1007/s00259-024-06593-1

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Citations (2)

Abnormal X chromosome inactivation and tumor development

Cellular and Molecular Life Sciences (2020)

Dan Wang Le Tang Yingfen Wu Chunmei Fan Shanshan Zhang

XIST

Skewed X-inactivation

10.1007/s00018-020-03469-z

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Citations (44)

Protective effect of ginsenoside Rg1 on 661W cells exposed to oxygen-glucose deprivation/reperfusion via keap1/nrf2 pathway

International Journal of Ophthalmology (2023)

Ming Zhou Yiyu Xie Jiabei Zhou Xielan Kuang Huangxuan Shen

To construct an in vitro model of oxygen-glucose deprivation/reperfusion (OGD/R) induced injury to the optic nerve and to study the oxidative damage mechanism of ischemia-reperfusion (I/R) injury in 661W cells and the protective effect of ginsenoside Rg1.The 661W cells were treated with different concentrations of Na2S2O4 to establish OGD/R model in vitro. Apoptosis, intracellular reactive oxygen species (ROS) levels and superoxide dismutase (SOD) levels were measured at different time points during the reperfusion injury process. The injury model was pretreated with graded concentrations of ginsenoside Rg1. Real-time polymerase chain reaction (PCR) was used to measure the expression levels of cytochrome C (cyt C)/B-cell lymphoma-2 (Bcl2)/Bcl2 associated protein X (Bax), heme oxygenase-1 (HO-1), caspase9, nuclear factor erythroid 2-related factor 2 (nrf2), kelch-like ECH-associated protein 1 (keap1) and other genes. Western blot was used to detect the expression of nrf2, phosphorylated nrf2 (pnrf2) and keap1 protein levels.Compared to the untreated group, the cell activity of 661W cells treated with Na2S2O4 for 6 and 8h decreased (P<0.01). Additionally, the ROS content increased and SOD levels decreased significantly (P<0.01). In contrast, treatment with ginsenoside Rg1 reversed the cell viability and SOD levels in comparison to the Na2S2O4 treated group (P<0.01). Moreover, Rg1 reduced the levels of caspase3, caspase9, and cytC, while increasing the Bcl2/Bax level. These differences were all statistically significant (P<0.05). Western blot analysis showed no significant difference in the protein expression levels of keap1 and nrf2 with Rg1 treatment, however, Rg1 significantly increased the ratio of pnrf2/nrf2 protein expression compared to the Na2S2O4 treated group (P<0.001).The OGD/R process is induced in 661W cells using Na2S2O4. Rg1 inhibits OGD/R-induced oxidative damage and alleviates the extent of apoptosis in 661W cells through the keap1/nrf2 pathway. These results suggest a potential protective effect of Rg1 against retinal I/R injury.

Viability assay

KEAP1

10.18240/ijo.2023.07.04

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Additional file 4: of BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141

Figshare (2018)

Yukun Liu Ran Zhao Yanmei Wei Mengna Li Heran Wang

Table S3. Protein-Protein Interaction predictions for BRD7. (XLS 49 kb)

Negative feedback

10.6084/m9.figshare.6008966

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Abstract 2130: Overcoming chemotherapy resistance by targeting LDHA mediated glycolysis

Cancer Research (2011)

Zixing Liu Ming Zhou Yuhua Zhao Yan Ding Hao Liu

Abstract Taxol is one of the most effective chemotherapeutic agents for the treatment of patients with breast cancer. Despite impressive clinical responses initially, the majority of patients eventually develop resistance to Taxol. Lactate dehydrogenase-A (LDH-A) is one of the predominant isoforms of LDH expressed in breast tissue, which controls the conversion of pyruvate to lactate and plays an important role in glucose metabolism. In this study we investigated the role of LDH-A in mediating Taxol resistance in human breast cancer cells. Taxol-resistant subclones, derived from the cancer cell line MDA-MB-435, sustained continuous growth in high concentrations of Taxol while the Taxol-sensitive cells could not. The increased expression and activity of LDH-A were detected in Taxol-resistant cells when compared with their parental cells. The downregulation of LDH-A by siRNA significantly increased the sensitivity of Taxol-resistant cells to Taxol. A higher sensitivity to the specific LDH inhibitor, oxamate, was found in the Taxol-resistant cells. Furthermore, treating cells with the combination of Taxol and oxamate showed a synergistical inhibitory effect on Taxol-resistant breast cancer cells by promoting apoptosis in these cells. LDH-A plays an important role in Taxol resistance and inhibition of LDH-A re-sensitizes Taxol-resistant cells to Taxol. This supports that Warburg effect is a property of Taxol resistant cancer cells and may play an important role in the development of Taxol resistance. To our knowledge, this is the first report showing that the increased expression of LDH-A plays an important role in Taxol resistance of human breast cancer cells. This study provides valuable information for the future development and use of targeted therapies, such as oxamate, for the treatment of patients with Taxol-resistant breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2130. doi:10.1158/1538-7445.AM2011-2130

Lactate dehydrogenase A

Anaerobic glycolysis

Warburg Effect

10.1158/1538-7445.am2011-2130

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Citations (1)

785: A Living Human Tumor Bank Using an Orthotopic Xenograft Mouse Model: Feasability and Implications of Angiogenesis and Proliferation

The Journal of Urology (2004)

Louis S. Liou Ming Zhou Yuwei Wang Hui Xue Joseph A. DiDonato

You have accessJournal of UrologyDiscussed Poster, Monday, May 10, 2004, 8:00 am - 12:00 pm1 Apr 2004785: A Living Human Tumor Bank Using an Orthotopic Xenograft Mouse Model: Feasability and Implications of Angiogenesis and Proliferation Louis S. Liou, Ming Zhou, Yuwei Wang, Hui Xue, Joseph A. DiDonato, and Y.Z. Wang Louis S. LiouLouis S. Liou More articles by this author , Ming ZhouMing Zhou More articles by this author , Yuwei WangYuwei Wang More articles by this author , Hui XueHui Xue More articles by this author , Joseph A. DiDonatoJoseph A. DiDonato More articles by this author , and Y.Z. WangY.Z. Wang More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)38034-0AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "785: A Living Human Tumor Bank Using an Orthotopic Xenograft Mouse Model: Feasability and Implications of Angiogenesis and Proliferation." The Journal of Urology, 171(4S), p. 208 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 171Issue 4SApril 2004Page: 208 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Louis S. Liou More articles by this author Ming Zhou More articles by this author Yuwei Wang More articles by this author Hui Xue More articles by this author Joseph A. DiDonato More articles by this author Y.Z. Wang More articles by this author Expand All Advertisement PDF downloadLoading ...

10.1016/s0022-5347(18)38034-0

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RASSF1A suppresses melanoma development by modulating apoptosis and cell‐cycle progression

Journal of Cellular Physiology (2010)

Mei Yi Jianbo Yang Xiang Chen Ji Li Xiayu Li

The tumor suppressor candidate gene Ras association domain family 1, isoform A (RASSF1A) encodes a microtubule-associated protein that is implicated in the regulation of cell proliferation, migration, and apoptosis. Several studies indicate that down-regulation of RASSF1A resulting from promoter hypermethylation is a frequent epigenetic abnormality in malignant melanoma. In this study, we report that compared with melanocytes in normal skins or benign skin lesions, RASSF1A is down-regulated in melanoma tissues as well as cell lines, and its expression negatively correlates with lymph node metastasis. Following ectopic expression in RASSF1A-deficient melanoma A375 cell line, RASSF1A reduces cell viability, suppresses cell-cycle progression but enhances apoptotic cell death. In vivo, RASSF1A expression inhibits the tumorigenic potential of A375 cells in nude mice, which also correlates with decreased cell proliferation and increased apoptosis. On the molecular level, ectopic RASSF1A expression leads to differential expression of 209 genes, including 26 down-regulated and 183 up-regulated ones. Among different signaling pathways, activation of the apoptosis signal-regulating kinase 1 (ASK1)/p38 MAP kinase signaling is essential for RASSF1A-induced mitochondrial apoptosis, and the inhibition of the Akt/p70S6 kinase/eIF4E signaling is also important for RASSF1A-mediated apoptosis and cell-cycle arrest. This is the first study exploring the biological functions and the underlying mechanisms of RASSF1A during melanoma development. It also identifies potential targets for further diagnosis and clinical therapy.

Ectopic expression

10.1002/jcp.22568

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Citations (44)