Zhuanyi Yang1, Zhiquan Yang1, Zhongliang Hu2,3, Bo Li2,3, Dingyang Liu1, Xiaoyu Chen1, Ying Wang2,3, Deyun Feng2,3. 1. Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China. 2. Department of Pathology, School of Basic Medical Science, Central South University, Changsha, China. 3. Department of Pathology, Xiangya Hospital, Central South University, Changsha, China.
Abstract
BACKGROUND: Uridine diphosphate-N-acetylglucosamine pyrophosphorylase-1-like-1 (UAP1L1) is involved in protein glycosylation and promotes proliferation in some tumors. By analyzing the publicly available Gene Expression Omnibus (GEO) database, we found that UAP1L1 displayed a significant change between paired glioma and normal brain tissues. The purpose of this study was to investigate the expression and functional role of UAP1L1 in glioma. METHODS: To determine the expression level of UAP1L1 in glioma, immunohistochemistry (IHC) staining was performed in tissue microarrays of 160 gliomas and 24 normal brain tissues. The correlation between UAP1L1 expression and the outcomes of glioma patients was analyzed. Human glioblastoma cell lines, U251 and U87, were employed in this study. Endogenous UAP1L1 expression in U251 and U87 cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). A lentiviral short hairpin RNA (shRNA) vector (shUAP1L1) was constructed and used to infect U251 and U87 cells to knock down the expression of UAP1L1. We performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, flow cytometry, human apoptosis antibody array, and in vivo subcutaneous xenograft model to investigate the biological functions of UAP1L1. RESULTS: We revealed that UAP1L1 expression was obviously upregulated in the glioma tissues. The increased UAP1L1 expression level was clinically associated with higher tumor grades and poorer patient prognoses. Moreover, we demonstrated that UAP1L1 knockdown suppressed proliferation and increased apoptosis of glioma cells in vitro. In the xenograft mouse model, we further verified that UAP1L1 knockdown could attenuate the growth of glioma cells in vivo. CONCLUSIONS: These results indicated that UAP1L1 may play an oncogene-like role in glioma, especially in high grade glioma, and thus may be of clinical importance as a future therapeutic target. 2021 Annals of Translational Medicine. All rights reserved.
BACKGROUND: Uridine diphosphate-N-acetylglucosamine pyrophosphorylase-1-like-1 (UAP1L1) is involved in protein glycosylation and promotes proliferation in some tumors. By analyzing the publicly available Gene Expression Omnibus (GEO) database, we found that UAP1L1 displayed a significant change between paired glioma and normal brain tissues. The purpose of this study was to investigate the expression and functional role of UAP1L1 in glioma. METHODS: To determine the expression level of UAP1L1 in glioma, immunohistochemistry (IHC) staining was performed in tissue microarrays of 160 gliomas and 24 normal brain tissues. The correlation between UAP1L1 expression and the outcomes of glioma patients was analyzed. Human glioblastoma cell lines, U251 and U87, were employed in this study. Endogenous UAP1L1 expression in U251 and U87 cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). A lentiviral short hairpin RNA (shRNA) vector (shUAP1L1) was constructed and used to infect U251 and U87 cells to knock down the expression of UAP1L1. We performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, flow cytometry, human apoptosis antibody array, and in vivo subcutaneous xenograft model to investigate the biological functions of UAP1L1. RESULTS: We revealed that UAP1L1 expression was obviously upregulated in the glioma tissues. The increased UAP1L1 expression level was clinically associated with higher tumor grades and poorer patient prognoses. Moreover, we demonstrated that UAP1L1 knockdown suppressed proliferation and increased apoptosis of glioma cells in vitro. In the xenograft mouse model, we further verified that UAP1L1 knockdown could attenuate the growth of glioma cells in vivo. CONCLUSIONS: These results indicated that UAP1L1 may play an oncogene-like role in glioma, especially in high grade glioma, and thus may be of clinical importance as a future therapeutic target. 2021 Annals of Translational Medicine. All rights reserved.
Authors: C Peneff; P Ferrari; V Charrier; Y Taburet; C Monnier; V Zamboni; J Winter; M Harnois; F Fassy; Y Bourne Journal: EMBO J Date: 2001-11-15 Impact factor: 11.598
Authors: Marta Baro; Cecilia Lopez Sambrooks; Amanda Quijano; W Mark Saltzman; Joseph Contessa Journal: Clin Cancer Res Date: 2018-07-02 Impact factor: 12.531
Authors: Yuk Kien Chong; Edwin Sandanaraj; Lynnette W H Koh; Moogaambikai Thangaveloo; Melanie S Y Tan; Geraldene R H Koh; Tan Boon Toh; Grace G Y Lim; Joanna D Holbrook; Oi Lian Kon; Mahendran Nadarajah; Ivan Ng; Wai Hoe Ng; Nguan Soon Tan; Kah Leong Lim; Carol Tang; Beng Ti Ang Journal: J Natl Cancer Inst Date: 2015-11-07 Impact factor: 13.506