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Cancers
Special Issues
Invasion in Glioblastoma
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Invasion in Glioblastoma

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (20 June 2024) | Viewed by 3702

Special Issue Editor

Prof. Dr. Deni S. Galileo

E-Mail Website
Guest Editor
Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA
Interests: glioblastoma; stem cells; chick embryo; confocal microscopy; adhesion proteins; L1CAM; integrins; cell motility; cell invasion

Special Issue Information

Dear Colleagues,

One of the most important attributes of glioblastoma (GBM) is its extreme cell invasiveness into surrounding brain tissue, which is arguably the reason why surgical resection and other treatments are ineffective. This Special Issue of Cancers focuses on invasion in glioblastoma and is aimed at creating a thorough view of this characteristic of the deadliest primary brain cancer. We will consider all aspects of invasion in glioblastoma for this Issue, including the routes of GBM cell invasion, genetics of invasion, intrinsic cellular mechanisms controlling invasion, extracellular and microenvironmental cues that influence cell invasion, in vivo models for studying GBM cell invasion, in vitro approaches to studying invasion, imaging GBM cell invasion, mathematical modeling of invasion, and potential therapeutic approaches to inhibiting invasion. Original research articles, review articles, and short communications will be considered for inclusion in this Special Issue.

Prof. Dr. Deni S. Galileo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glioblastoma
  • invasion
  • glioblastoma stem cells
  • xenograft models
  • cell invasiveness

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Published Papers (2 papers)

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Research

20 pages, 11125 KiB  
Article
QSOX1 Modulates Glioblastoma Cell Proliferation and Migration In Vitro and Invasion In Vivo
by Reetika Dutt, Colin Thorpe and Deni S. Galileo
Cancers 2024, 16(21), 3620; https://doi.org/10.3390/cancers16213620 - 26 Oct 2024
Viewed by 909
Abstract
Background: Quiescin Sulfhydryl Oxidase 1 (QSOX1) is an enzyme that catalyzes the oxidation of free thiols to generate disulfide bonds in a variety of proteins, including the cell surface and extracellular matrix. QSOX1 has been reported to be upregulated in a number [...] Read more.
Background: Quiescin Sulfhydryl Oxidase 1 (QSOX1) is an enzyme that catalyzes the oxidation of free thiols to generate disulfide bonds in a variety of proteins, including the cell surface and extracellular matrix. QSOX1 has been reported to be upregulated in a number of cancers, and the overexpression of QSOX1 has been correlated with aggressive cancers and poor patient prognosis. Glioblastoma (GBM) brain cancer has been practically impossible to treat effectively, with cells that rapidly invade normal brain tissue and escape surgery and other treatment. Thus, there is a crucial need to understand the multiple mechanisms that facilitate GBM cell invasion and to determine if QSOX1 is involved. Methods and Results: Here, we investigated the function of QSOX1 in human glioblastoma cells using two cell lines derived from T98G cells, whose proliferation, motility, and invasiveness has been shown by us to be dependent on disulfide bond-containing adhesion and receptor proteins, such as L1CAM and the FGFR. We lentivirally introduced shRNA to attenuate the QSOX1 protein expression in one cell line, and a Western blot analysis confirmed the decreased QSOX1 expression. A DNA content/cell cycle analysis using flow cytometry revealed 27% fewer knockdown cells in the S-phase of the cell cycle, indicating a reduced proliferation. A cell motility analysis utilizing our highly quantitative SuperScratch time-lapse microscopy assay revealed that knockdown cells migrated more slowly, with a 45% decrease in migration velocity. Motility was partly rescued by the co-culture of knockdown cells with control cells, indicating a paracrine effect. Surprisingly, knockdown cells exhibited increased motility when assayed using a Transwell migration assay. Our novel chick embryo orthotopic xenograft model was used to assess the in vivo invasiveness of knockdown vs. control cells, and tumors developed from both cell types. However, fewer invasive knockdown cells were observed after about a week. Conclusions: Our results indicate that an experimental reduction in QSOX1 expression in GBM cells leads to decreased cell proliferation, altered in vitro migration, and decreased in vivo invasion. Full article
(This article belongs to the Special Issue Invasion in Glioblastoma)
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20 pages, 6735 KiB  
Article
Comparative Analysis of the GNAI Family Genes in Glioblastoma through Transcriptomics and Single-Cell Technologies
by Ahmad Raza, Meng-Chi Yen, Gangga Anuraga, Iram Shahzadi, Muhammad Waqar Mazhar, Hoang Dang Khoa Ta, Do Thi Minh Xuan, Sanskriti Dey, Sachin Kumar, Adrian Wangsawijaya Santoso, Bianca Tobias William and Chih-Yang Wang
Cancers 2023, 15(20), 5112; https://doi.org/10.3390/cancers15205112 - 23 Oct 2023
Cited by 3 | Viewed by 2386
Abstract
Glioblastoma multiforme (GBM) is one of the most aggressive cancers with a low overall survival rate. The treatment of GBM is challenging due to the presence of the blood–brain barrier (BBB), which hinders drug delivery. Invasive procedures alone are not effective at completely [...] Read more.
Glioblastoma multiforme (GBM) is one of the most aggressive cancers with a low overall survival rate. The treatment of GBM is challenging due to the presence of the blood–brain barrier (BBB), which hinders drug delivery. Invasive procedures alone are not effective at completely removing such tumors. Hence, identifying the crucial pathways and biomarkers for the treatment of GBM is of prime importance. We conducted this study to identify the pathways associated with GBM. We used The Cancer Genome Atlas (TCGA) GBM genomic dataset to identify differentially expressed genes (DEGs). We investigated the prognostic values of the guanine nucleotide-binding protein G(i) alpha subunit (GNAI) family of genes in GBM using a Chinese Glioma Genome Atlas (CGGA) dataset. Within this dataset, we observed the association in the tumor microenvironment between the gene expression of GNAI subunit 3 (GNAI3) and a poor prognosis. MetaCore and gene ontology (GO) analyses were conducted to explore the role of GNAI3 in co-expressed genes and associated signaling pathways using a transcript analysis. Notable pathways included “Cytoskeleton remodeling regulation of actin cytoskeleton organization by the kinase effectors of Rho GTPases” and “Immune response B cell antigen receptor (BCR) pathway”. A single-cell analysis was used to assess GNAI3 expression in GBM. The results demonstrated that GNAI family genes, specifically GNAI3, were significantly associated with carcinogenesis and malignancy in GBM patients. Our findings suggest that the GNAI3 gene holds potential as a prognostic biomarker for GBM. Full article
(This article belongs to the Special Issue Invasion in Glioblastoma)
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