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Cresca S, Parise A, Magistrato A. Assessing the Mechanism of Rac1b: An All-Atom Simulation Study of the Alternative Spliced Variant of Rac1 Small Rho GTPase. J Chem Inf Model 2024; 64:9474-9486. [PMID: 39632743 DOI: 10.1021/acs.jcim.4c01376] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/07/2024]
Abstract
The Rho GTPase family plays a key role in cell migration, cytoskeletal dynamics, and intracellular signaling. Rac1 and its splice variant Rac1b, characterized by the insertion of an Extraloop, are frequently associated with cancer. These small GTPases switch between an active GTP-bound state and an inactive GDP-bound state, a process that is regulated by specific protein modulators. Among them, the Guanine nucleotide exchange factor (GEF) protein DOCK5 specifically targets Rho GTPases, promoting their activation by facilitating the exchange of GDP for GTP. In this study, we performed cumulative 10-μs-long all-atom molecular dynamics simulations of Rac1 and Rac1b, in isolation and in complex with DOCK5 and ELMO1, to investigate the impact of the Rac1b Extraloop. Our findings reveal that this Extraloop decreases the GDP residence time as compared to Rac1, mimicking the effect of accelerated GDP/GTP exchange induced by DOCK5. Furthermore, both Rac1b Extraloop and the ELMO1 protein stabilize the GTPase/DOCK5 complex, contributing to facilitate GDP dissociation. This shifts the balance between the GPT- and GDP-bound state of Rac1b toward the active GTP-bound state, sending a prooncogenic signal. Besides broadening our understanding of the biological functions of small Rho GTPases, this study provides key information to exploit a previously unexplored therapeutic niche to counter Rac1b-associated cancer.
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Affiliation(s)
- Sofia Cresca
- Theory Department, National Institute of Chemistry, Hajdrihova 19, 1000 Ljubljana, Slovenia
- Consiglio Nazionale delle Ricerche (CNR)-IOM, c/o International School for Advanced Studies (SISSA/ISAS), via Bonomea 265, 34136 Trieste, Italy
| | - Angela Parise
- Consiglio Nazionale delle Ricerche (CNR)-IOM, c/o International School for Advanced Studies (SISSA/ISAS), via Bonomea 265, 34136 Trieste, Italy
| | - Alessandra Magistrato
- Consiglio Nazionale delle Ricerche (CNR)-IOM, c/o International School for Advanced Studies (SISSA/ISAS), via Bonomea 265, 34136 Trieste, Italy
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2
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Shan DD, Zheng QX, Wang J, Chen Z. Small nucleolar RNA host gene 3 functions as a novel biomarker in liver cancer and other tumour progression. World J Gastroenterol 2022; 28:1641-1655. [PMID: 35581965 PMCID: PMC9048787 DOI: 10.3748/wjg.v28.i16.1641] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/18/2022] [Revised: 02/09/2022] [Accepted: 03/16/2022] [Indexed: 02/06/2023] Open
Abstract
Cancer has become the most life-threatening disease in the world. Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs, especially long noncoding RNAs (lncRNAs), have significant effects in human cancers. LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes. Small nucleolar RNA host gene 3 (SNHG3) is a novel lncRNA and has been reported to be differentially expressed in various tumors, such as liver cancer, gastric cancer, and glioma. However, the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood. In this review, we summarize the results of SNHG3 studies in humans, animal models, and cells to underline the expression and role of SNHG3 in cancer. SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis. SNHG3 expression in lung adenocarcinoma remains controversial. Concurrently, SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms, including competing endogenous RNA effects. A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.
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Affiliation(s)
- Dan-Dan Shan
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
| | - Qiu-Xian Zheng
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
| | - Jing Wang
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
| | - Zhi Chen
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
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3
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Major Role for Cellular MicroRNAs, Long Noncoding RNAs (lncRNAs), and the Epstein-Barr Virus-Encoded BART lncRNA during Tumor Growth
In Vivo. mBio 2022; 13:e0065522. [PMID: 35435703 PMCID: PMC9239068 DOI: 10.1128/mbio.00655-22] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
Abstract
This study assessed the effects of Epstein-Barr virus (EBV) and one form of virally encoded BART long noncoding RNAs (lncRNAs) on cellular expression in epithelial cells grown in vitro and as tumors in vivo determined by high-throughput RNA sequencing of mRNA and small RNAs. Hierarchical clustering based on gene expression distinguished the cell lines from the tumors and distinguished the EBV-positive tumors and the BART tumors from the EBV-negative tumors. EBV and BART expression also induced specific expression changes in cellular microRNAs (miRs) and lncRNAs. Multiple known and predicted targets of the viral miRs, the induced cellular miRs, and lncRNAs were identified in the altered gene set. The changes in expression in vivo indicated that the suppression of growth pathways in vivo reflects increased expression of cellular miRs in all tumors. In the EBV and BART tumors, many of the targets of the induced miRs were not changed and the seed sequences of the nonfunctional miRs were found to have homologous regions within the BART lncRNA. The inhibition of these miR effects on known targets suggests that these induced miRs have reduced function due to sponging by the BART lncRNA. This composite analysis identified the effects of EBV on cellular miRs and lncRNAs with a functional readout through identification of the simultaneous effects on gene expression. Major shifts in gene expression in vivo are likely mediated by effects on cellular noncoding RNAs. Additionally, a predicted property of the BART lncRNA is to functionally inhibit the induced cellular miRs.
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Paul U, Banerjee S. The functional significance and cross-talk of non-coding RNAs in triple negative and quadruple negative breast cancer. Mol Biol Rep 2022; 49:6899-6918. [PMID: 35235157 DOI: 10.1007/s11033-022-07288-2] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/08/2021] [Accepted: 02/18/2022] [Indexed: 12/13/2022]
Abstract
One of the leading causes of cancer-related deaths worldwide is breast cancer, among which triple-negative breast cancer (TNBC) is the most malignant and lethal subtype. This cancer accounts for 10-20% of all breast cancer deaths. Proliferation, tumorigenesis, and prognosis of TNBC are affected when the androgen receptor (AR) is not expressed, and it is classified as quadruple negative breast cancer (QNBC). Non-coding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play a significant role in tumorigenesis by virtue of their oncogenic and tumor-suppressive properties. To regulate tumorigenesis, miRNAs interact with their target mRNAs and modulate their expression, whereas lncRNAs can either act alone or interact with miRNAs or other molecules through various signaling pathways. Conversely, circRNAs regulate tumorigenesis by acting as miRNA sponges predominantly. Recently, non-coding RNAs were studied comprehensively for their roles in tumor proliferation, progression, and metastasis. As a result of existing studies and research progress, non-coding RNAs have been implicated in TNBC, necessitating their use as biomarkers for future diagnostic applications. In this review, the non-coding RNAs are explicitly implicated in the regulation of breast cancer, and their cross-talk between TNBC and QNBC is also discussed.
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Affiliation(s)
- Utpalendu Paul
- School of Bio Science and Technology, Vellore Institute of Technology (VIT), Vellore, Tamil Nadu, 632014, India
| | - Satarupa Banerjee
- School of Bio Science and Technology, Vellore Institute of Technology (VIT), Vellore, Tamil Nadu, 632014, India.
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Xie Y, Rong L, He M, Jiang Y, Li H, Mai L, Song F. LncRNA SNHG3 promotes gastric cancer cell proliferation and metastasis by regulating the miR-139-5p/MYB axis. Aging (Albany NY) 2021; 13:25138-25152. [PMID: 34898477 PMCID: PMC8714158 DOI: 10.18632/aging.203732] [Citation(s) in RCA: 21] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/15/2021] [Accepted: 11/23/2021] [Indexed: 12/27/2022]
Abstract
The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity in vitro and constrained in vivo GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR-139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.
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Affiliation(s)
- Yan Xie
- Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China.,Qinggang Senior Care Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
| | - Li Rong
- Department of Gastroenterology, Bishan Hospital of Chongqing, Chongqing 402760, China
| | - Min He
- Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
| | - Yuyou Jiang
- Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
| | - Haiyu Li
- Chongqing Public Health Medical Center, Chongqing 400036, China
| | - Li Mai
- Department of Laboratory Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
| | - Fangzhou Song
- Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
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Dong C, Rao N, Du W, Gao F, Lv X, Wang G, Zhang J. mRBioM: An Algorithm for the Identification of Potential mRNA Biomarkers From Complete Transcriptomic Profiles of Gastric Adenocarcinoma. Front Genet 2021; 12:679612. [PMID: 34386038 PMCID: PMC8354214 DOI: 10.3389/fgene.2021.679612] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/12/2021] [Accepted: 05/06/2021] [Indexed: 12/09/2022] Open
Abstract
Purpose In this work, an algorithm named mRBioM was developed for the identification of potential mRNA biomarkers (PmBs) from complete transcriptomic RNA profiles of gastric adenocarcinoma (GA). Methods mRBioM initially extracts differentially expressed (DE) RNAs (mRNAs, miRNAs, and lncRNAs). Next, mRBioM calculates the total information amount of each DE mRNA based on the coexpression network, including three types of RNAs and the protein-protein interaction network encoded by DE mRNAs. Finally, PmBs were identified according to the variation trend of total information amount of all DE mRNAs. Four PmB-based classifiers without learning and with learning were designed to discriminate the sample types to confirm the reliability of PmBs identified by mRBioM. PmB-based survival analysis was performed. Finally, three other cancer datasets were used to confirm the generalization ability of mRBioM. Results mRBioM identified 55 PmBs (41 upregulated and 14 downregulated) related to GA. The list included thirteen PmBs that have been verified as biomarkers or potential therapeutic targets of gastric cancer, and some PmBs were newly identified. Most PmBs were primarily enriched in the pathways closely related to the occurrence and development of gastric cancer. Cancer-related factors without learning achieved sensitivity, specificity, and accuracy of 0.90, 1, and 0.90, respectively, in the classification of the GA and control samples. Average accuracy, sensitivity, and specificity of the three classifiers with machine learning ranged within 0.94–0.98, 0.94–0.97, and 0.97–1, respectively. The prognostic risk score model constructed by 4 PmBs was able to correctly and significantly (∗∗∗p < 0.001) classify 269 GA patients into the high-risk (n = 134) and low-risk (n = 135) groups. GA equivalent classification performance was achieved using the complete transcriptomic RNA profiles of colon adenocarcinoma, lung adenocarcinoma, and hepatocellular carcinoma using PmBs identified by mRBioM. Conclusions GA-related PmBs have high specificity and sensitivity and strong prognostic risk prediction. MRBioM has also good generalization. These PmBs may have good application prospects for early diagnosis of GA and may help to elucidate the mechanism governing the occurrence and development of GA. Additionally, mRBioM is expected to be applied for the identification of other cancer-related biomarkers.
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Affiliation(s)
- Changlong Dong
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
| | - Nini Rao
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
| | - Wenju Du
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
| | - Fenglin Gao
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
| | - Xiaoqin Lv
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
| | - Guangbin Wang
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
| | - Junpeng Zhang
- Center for Informational Biology, School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,School of Life Sciences and Technology, University of Electronic Science and Technology of China, Chengdu, China.,Key Laboratory for NeuroInformation of the Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
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Liang J, Oyang L, Rao S, Han Y, Luo X, Yi P, Lin J, Xia L, Hu J, Tan S, Tang L, Pan Q, Tang Y, Zhou Y, Liao Q. Rac1, A Potential Target for Tumor Therapy. Front Oncol 2021; 11:674426. [PMID: 34079763 PMCID: PMC8165220 DOI: 10.3389/fonc.2021.674426] [Citation(s) in RCA: 59] [Impact Index Per Article: 14.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/01/2021] [Accepted: 04/29/2021] [Indexed: 12/20/2022] Open
Abstract
RAS-related C3 botulinum toxin substrate 1 (Rac.1) is one of the important members of Rho GTPases. It is well known that Rac1 is a cytoskeleton regulation protein that regulates cell adhesion, morphology, and movement. Rac1 is highly expressed in different types of tumors, which is related to poor prognosis. Studies have shown that Rac1 not only participates in the tumor cell cycle, apoptosis, proliferation, invasion, migration and angiogenesis, but also participates in the regulation of tumor stem cell, thus promoting the occurrence of tumors. Rac1 also plays a key role in anti-tumor therapy and participates in immune escape mediated by the tumor microenvironment. In addition, the good prospects of Rac1 inhibitors in cancer prevention and treatment are exciting. Therefore, Rac1 is considered as a potential target for the prevention and treatment of cancer. The necessity and importance of Rac1 are obvious, but it still needs further study.
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Affiliation(s)
- Jiaxin Liang
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Linda Oyang
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Shan Rao
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Yaqian Han
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Xia Luo
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Pin Yi
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Jinguan Lin
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Longzheng Xia
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Jiaqi Hu
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Shiming Tan
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Lu Tang
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.,University of South China, Hengyang, China
| | - Qing Pan
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.,University of South China, Hengyang, China
| | - Yanyan Tang
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.,Clinical Research Center for Wound Healing in Hunan Province, Changsha, China
| | - Yujuan Zhou
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
| | - Qianjin Liao
- Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.,Clinical Research Center for Wound Healing in Hunan Province, Changsha, China
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Xu B, Mei J, Ji W, Bian Z, Jiao J, Sun J, Shao J. LncRNA SNHG3, a potential oncogene in human cancers. Cancer Cell Int 2020; 20:536. [PMID: 33292213 PMCID: PMC7640707 DOI: 10.1186/s12935-020-01608-x] [Citation(s) in RCA: 37] [Impact Index Per Article: 7.4] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2020] [Accepted: 10/15/2020] [Indexed: 02/06/2023] Open
Abstract
Long noncoding RNAs (lncRNAs) are composed of > 200 nucleotides; they lack the ability to encode proteins but play important roles in a variety of human tumors. A large number of studies have shown that dysregulated expression of lncRNAs is related to tumor oncogenesis and progression. Emerging evidence shows that SNHG3 is a novel oncogenic lncRNA that is abnormally expressed in various tumors, including osteosarcoma, liver cancer, lung cancer, etc. SNHG3 primarily competes as a competitive endogenous RNA (ceRNA) that targets tumor suppressor microRNAs (miRNAs) and ceRNA mechanisms that regulate biological processes of tumors. In addition, abnormal expression of SNHG3 is significantly correlated with patient clinical features. Upregulation of SNHG3 contributes to biological functions, including tumor cell proliferation, migration, invasion and EMT. Therefore, SNHG3 may represent a potential diagnostic and prognostic biomarker, as well as a novel therapeutic target.
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Affiliation(s)
- Bin Xu
- Department of Neurosurgery, Wuxi People's Hospital Affiliated to Nanjing Medical University, No. 299 Qing Yang Road, Wuxi, 214023, Jiangsu, China
| | - Jie Mei
- Department of Oncology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, P. R. China
| | - Wei Ji
- Department of Neurosurgery, Wuxi People's Hospital Affiliated to Nanjing Medical University, No. 299 Qing Yang Road, Wuxi, 214023, Jiangsu, China
| | - Zheng Bian
- Department of Neurosurgery, Wuxi People's Hospital Affiliated to Nanjing Medical University, No. 299 Qing Yang Road, Wuxi, 214023, Jiangsu, China
| | - Jiantong Jiao
- Department of Neurosurgery, Wuxi People's Hospital Affiliated to Nanjing Medical University, No. 299 Qing Yang Road, Wuxi, 214023, Jiangsu, China
| | - Jun Sun
- Department of Neurosurgery, Wuxi People's Hospital Affiliated to Nanjing Medical University, No. 299 Qing Yang Road, Wuxi, 214023, Jiangsu, China.
| | - Junfei Shao
- Department of Neurosurgery, Wuxi People's Hospital Affiliated to Nanjing Medical University, No. 299 Qing Yang Road, Wuxi, 214023, Jiangsu, China.
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