KAI WANG^2,#, FENGTIAN ZHANG^1,3,4,#, CHANGLONG WEN⁵, ZHIHUA HUANG⁶, ZHIHAO HU¹, YUWEN ZHANG¹, FUQIANG HU^2,*, LIJUAN WEN^1,6,*

Oncology Research, Vol.29, No.5, pp. 351-363, 2021, DOI:10.32604/or.2022.025696 - 10 October 2022

Abstract The blood-brain barrier (BBB) is an essential component in regulating and maintaining the homeostatic microenvironment of the central nervous system (CNS). During the occurrence and development of glioblastoma (GBM), BBB is pathologically destroyed with a marked increase in permeability. Due to the obstruction of the BBB, current strategies for GBM therapeutics still obtain a meager success rate and may lead to systemic toxicity. Moreover, chemotherapy could promote pathological BBB functional restoration, which results in significantly reduced intracerebral transport of therapeutic agents during multiple administrations of GBM and the eventual failure of GBM chemotherapy. The effective More >

Hengzhou Lin, Dahui Zuo, Jiabin He, Tao Ji, Jianzhong Wang, Taipeng Jiang

Oncology Research, Vol.28, No.6, pp. 591-603, 2020, DOI:10.3727/096504020X15982623243955

Abstract The long noncoding RNA WEE2 antisense RNA 1 (WEE2-AS1) plays an oncogenic role in hepatocellular carcinoma and triple negative breast cancer progression. In this study, we investigated the expression and roles of WEE2-AS1 in glioblastoma (GBM). Furthermore, the molecular mechanisms behind the oncogenic actions of WEE2-AS1 in GBM cells were explored in detail. WEE2-AS1 expression was detected using quantitative real-time polymerase chain reaction. The roles of WEE2-AS1 in GBM cells were evaluated by the cell counting kit-8 assay, flow cytometric analysis, Transwell cell migration and invasion assays, and tumor xenograft experiments. WEE2-AS1 expression was evidently… More >

Sarah A. Scuderi^*, Marika Lanza^*, Giovanna Casili^*, Francesca Esposito^†, Cristina Colarossi^‡, Dario Giuffrida^‡, Paterniti Irene^*, Salvatore Cuzzocrea^*,* Emanuela Esposito^*, Michela Campolo^*

Oncology Research, Vol.28, No.7-8, pp. 779-790, 2020, DOI:10.3727/096504021X16161478258040

Abstract Glioma are common malignant brain tumors, among which glioblastoma multiforme (GBM) has the worst prognosis. Different studies of GBM revealed that targeting nuclear factor B (NF- B) induced an attenuation tumor proliferation and prolonged cell survival. TBK1 {TANK [TRAF (TNF (tumor-necrosis-factor) receptorassociated factor)-associated NF- B activator]-binding kinase 1} is a serine/threonine protein kinase, and it is a member of the I B kinase (IKK) family involved in NF- B pathway activation. The aim of this study was to investigate the potential effect of BX795, an inhibitor of TBK1, in an in vitro and ex vivo… More >

Shihui Liu, Xiuxiu Li, Sujing Zhuang

Oncology Research, Vol.27, No.2, pp. 165-171, 2019, DOI:10.3727/096504018X15193506006164

Abstract miR-30c has been acknowledged as a tumor suppressor in various human cancers, such as ovarian cancer, gastric cancer, and prostate cancer. However, the role of miR-30c in glioblastoma (GBM) needs to be investigated. In our study, we found that the expression of miR-30c was significantly downregulated in GBM tissues and cell lines. We found that overexpression of miR-30c inhibited cellular proliferation of GBM cells in vitro and in vivo. More GBM cells were arrested in the G₀ phase after miR-30c overexpression. Moreover, we showed that miR-30c overexpression suppressed the migration and invasion of GBM cells. Mechanistically, More >

Yongtao Li^*, Fanyu Chen^*, Jiancheng Chu^*, Chao Wu^*, Yuan Li^†, Heng Li^†, Hongxin Ma^*

Oncology Research, Vol.27, No.8, pp. 911-921, 2019, DOI:10.3727/096504019X15516966905337

Abstract To date, miR-148-3p and DNMT1–recombinant human runt-related transcription factor 3 (RUNX3) axis have been linked to cell proliferation, migration, and invasion; however, their roles and relationships in human glioblastoma multiforme (GBM) are still not clear. Here we found that the expression of miR-148-3p in glioma tissues was decreased compared with adjacent nontumor tissues and correlated with WHO grade, tumor size, and prognosis as well as DNMT1 and RUNX3 expressions. Compared with NHA cells, the expression of miR- 148-3p in U87 and U251 cells was also downregulated and accompanied with upregulation of DNMT1 and hypermethylation level… More >

Jie Xu^*1, Zhongzhou Su^*1, Qiuping Ding^†, Liang Shen^*, Xiaohu Nie^*, Xuyan Pan^*, Ai Yan^*, Renfu Yan^*, Yue Zhou^*, Liqin Li^‡, Bin Lu^*

Oncology Research, Vol.27, No.7, pp. 819-826, 2019, DOI:10.3727/096504018X15478559215014

Abstract Human glioblastoma multiforme (GBM) accounts for the majority of human brain gliomas. Several TMEM proteins, such as TMEM 45A, TMEM 97, and TMEM 140, are implicated in human brain gliomas. However, the roles of TMEM168 in human GBM remain poorly understood. Herein we found that mRNA levels of TMEM168 were overexpressed in GBM patients (n=85) when compared with healthy people (n=10), which was also supported by data from The Cancer Genome Atlas (TCGA). Kaplan–Meier analysis of Gene Expression Omnibus dataset GSE16011 suggested that enhanced TMEM168 expression was associated with shorter survival time. To investigate whether and… More >

Yan Gao, Yongchuan Xu, Jue Wang, Xue Yang, Lulu Wen, Juan Feng

Oncology Research, Vol.27, No.3, pp. 341-347, 2019, DOI:10.3727/096504018X15228909735079

Abstract Long noncoding RNAs (lncRNAs) have been acknowledged as important regulators in various human cancers. lncRNA MNX1-AS1 has been shown to be an oncogene in epithelial ovarian cancer. However, the function of MNX1-AS1 in glioblastoma (GBM) remains largely unknown. Here we found that the expression of MNX1-AS1 was significantly upregulated in GBM tissues and cell lines. Knockdown of MNX1-AS1 significantly inhibited the proliferation, migration, and invasion of GBM cells. In terms of mechanism, we found that MNX1-AS1 could bind to miR-4443 in GBM cells. Overexpression of miR-4443 significantly inhibited the expression of MNX1-AS1 and vice versa. More >

Xuejian Liu^*1, Xia Wu^*1, Yanming Wang^†, Yuhua Li^*, Xiangli Chen^*, Wenchuan Yang^*, Lihua Jiang^*

Oncology Research, Vol.27, No.4, pp. 415-422, 2019, DOI:10.3727/096504018X15155538502359

Abstract Cluster of differentiation 47 (CD47) overexpression is common in various malignancies. This study investigated whether CD47 promotes human glioblastoma invasion and, if so, the underlying mechanisms involved. CD47 expression was found to be stronger in tissues of patients with glioblastoma and in various cancer cell lines than in normal controls. CD47 downregulation via siRNA suppressed invasion in vitro, whereas CD47 overexpression through plasmid transfection exerted the opposite effect. However, overexpression or knocking down of CD47 had no effect on cell proliferation. Moreover, CD47 expression was related to Akt phosphorylation at the cellular molecular level. Suppression More >

Gloria B. Kim^1,†, Qiong Wei^2,†, Virginia Aragon-Sanabria¹, Sulin Zhang², Jian Yang¹, Cheng Dong^1,*

Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 15-15, 2019, DOI:10.32604/mcb.2019.07137

Abstract Most cells survive and grow by attaching and spreading on a substrate. They generate internal tension that contracts the cell body and thus exert tractions on the underlying substrate through focal adhesions. Traction force also plays a critical role in many biological processes, such as inflammation, metastasis, and angiogenesis. Thus, measuring the cell traction force provides valuable information on understanding the underlying mechanism of these biological processes. Here, a traction force microscopy (TFM) method using super thin hydrogels composed of immobilized fluorescent beads was utilized to quantify the mechanical forces generated during the transmigration of… More >

Ning Wang^*1, Yang Zhang^†1, Huaxin Liang^‡

Oncology Research, Vol.26, No.8, pp. 1275-1283, 2018, DOI:10.3727/096504018X15185735627746

Abstract The dysregulation of microRNA (miRNA) expression is closely related with tumorigenesis and tumor development in glioblastoma (GBM). In this study, we found that miRNA-598 (miR-598) expression was significantly downregulated in GBM tissues and cell lines. Restoring miR-598 expression inhibited cell proliferation and invasion in GBM. Moreover, we validated that metastasis associated in colon cancer-1 (MACC1) is a novel target of miR-598 in GBM. Restoring MACC1 expression reversed the inhibitory effects of miR-598 overexpression on GBM cells. In addition, miR-598 overexpression suppressed Met/ AKT pathway activation in GBM. Our results provided compelling evidence that miR-598 serves More >