Elucidation of the genetic and epigenetic landscape alterations in RNA binding proteins in glioblastoma

Bhargava, Shruti; Patil, Vikas; Mahalingam, Kulandaivelu; Somasundaram, Kumaravel

doi:10.18632/oncotarget.14287

Cited by 29 publications

(31 citation statements)

References 81 publications

(80 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More information on known cancer susceptibility genes and regions have been summarized by Parsons et al (2008), Li et al (2016), and Bhargava et al (2017) for GB (Bahrami et al, 2018; Tan et al, 2018) for CC (Collins, 2011; Michailidou et al, 2015) for BC, and (Martinez-Gonzalez et al, 2018; Benafif and Eeles, 2016) for PCa.…”

Section: Micrornasmentioning

confidence: 99%

MicroRNAs, Hypoxia and the Stem-Like State as Contributors to Cancer Aggressiveness

et al. 2019

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are small non-coding RNA molecules that play key regulatory roles in cancer acting as both oncogenes and tumor suppressors. Due to their potential roles in improving cancer prognostic, predictive, diagnostic and therapeutic approaches, they have become an area of intense research focus in recent years. Several studies have demonstrated an altered expression of several miRNAs under hypoxic condition and even shown that the hypoxic microenvironment drives the selection of a more aggressive cancer cell population through cellular adaptations referred as the cancer stem-like cell. These minor fractions of cells are characterized by their self-renewal abilities and their ability to maintain the tumor mass, suggesting their crucial roles in cancer development. This review aims to highlight the interconnected role between miRNAs, hypoxia and the stem-like state in contributing to the cancer aggressiveness as opposed to their independent contributions, and it is based in four aggressive tumors, namely glioblastoma, cervical, prostate, and breast cancers.

show abstract

Section: Micrornasmentioning

confidence: 99%

MicroRNAs, Hypoxia and the Stem-Like State as Contributors to Cancer Aggressiveness

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Concerning the present findings, the expression of AHNAK is down-regulated in human breast cancer 12 , melanoma 21 , Burkitt lymphoma, colon carcinoma, and neuroblastoma 9 ; but up-regulated in mesothelioma 22 , laryngeal carcinoma 23 and invasive ductal carcinoma 24 . Meanwhile, researches showed that AHNAK mutation was considered as a prognostic factor related to the poor survival of patients with melanoma 21 , laryngeal carcinoma 23 , triple-negative breast cancer 25 and glioblastoma 26 .…”

Section: Introductionmentioning

confidence: 99%

AHNAK as a Prognosis Factor Suppresses the Tumor Progression in Glioma

Zhao¹,

Xiao²,

Yuan

et al. 2017

J. Cancer

View full text Add to dashboard Cite

Purpose: AHNAK is originally identified as a giant protein based on the estimated size of approximately 700 kDa. The aim of this study is to identify the role of AHNAK in the pathogenesis of glioma.Methods: We tested AHNAK mRNA level in a panel of six human glioma cell lines, and in 30 cases of normal brain tissues and 73 cases of glioma tissue samples using a qRT-PCR method. Further, we analyzed the relationship of AHNAK expression with clinicopathological characteristics in glioma patients. Meanwhile, we analyzed the relationship of expression of AHNAK and survival of glioma patients in survival analyses. Then, in vitro, we analyzed the biological effects of AHNAK in glioma cell lines (U87 and U251) including proliferation assay, cell transwell assay, and apoptosis. And in vivo, we examined the effects of AHNAK on tumor growth using xenograft model of human glioma cells in nude mice. Then we examined the expression of Ki-67-positive cells in these tumors.Results: We found that the mRNA levels of AHNAK were down-regulated in 4 of 6 human glioma cell lines, especially in U87 and U251 cell lines. Meanwhile, in glioma patients, a negative correlation was found between the expression of AHNAK and the glioma histopathology. And a low expression of AHNAK was a significant and independent prognostic factor for poor survival of glioma patients. Through over expression of AHNAK in both of U87 and U251, we demonstrated that overexpression of AHNAK could inhibit glioma cell proliferation and invasion, induce apoptosis, and inhibit in vivo glioma tumor growth and ki-67 expression.Conclusions: The AHNAK acts as a potential tumor suppressor. Our study provides a preclinical basis for developing AHNAK as a reliable clinical prognostic indicator for glioma patients, and a new biomarker for treatment response, and a potentially therapeutic target in glioma management options.

show abstract

“…Accordingly, it may be expected that new types of GBMs will be identified in the future based on unique molecular changes as proposed recently [4,5]. Finally, since the detailed description of genetic and epigenetic changes in GBM was not the primary focus of the present work, interested readers will find more in-depth information in several other published reports [8][9][10].…”

Section: Molecular Classification Of Gbmmentioning

confidence: 89%

Biology of Glioblastoma Multiforme—Exploration of Mitotic Catastrophe as a Potential Treatment Modality

Vitovcova

Skarkova

Rudolf

et al. 2020

IJMS

View full text Add to dashboard Cite

Glioblastoma multiforme (GBM) represents approximately 60% of all brain tumors in adults. This malignancy shows a high biological and genetic heterogeneity associated with exceptional aggressiveness, leading to a poor survival of patients. This review provides a summary of the basic biology of GBM cells with emphasis on cell cycle and cytoskeletal apparatus of these cells, in particular microtubules. Their involvement in the important oncosuppressive process called mitotic catastrophe will next be discussed along with select examples of microtubule-targeting agents, which are currently explored in this respect such as benzimidazole carbamate compounds. Select microtubule-targeting agents, in particular benzimidazole carbamates, induce G2/M cell cycle arrest and mitotic catastrophe in tumor cells including GBM, resulting in phenotypically variable cell fates such as mitotic death or mitotic slippage with subsequent cell demise or permanent arrest leading to senescence. Their effect is coupled with low toxicity in normal cells and not developed chemoresistance. Given the lack of efficient cytostatics or modern molecular target-specific compounds in the treatment of GBM, drugs inducing mitotic catastrophe might offer a new, efficient alternative to the existing clinical management of this at present incurable malignancy.

show abstract

Elucidation of the genetic and epigenetic landscape alterations in RNA binding proteins in glioblastoma

Cited by 29 publications

References 81 publications

MicroRNAs, Hypoxia and the Stem-Like State as Contributors to Cancer Aggressiveness

MicroRNAs, Hypoxia and the Stem-Like State as Contributors to Cancer Aggressiveness

AHNAK as a Prognosis Factor Suppresses the Tumor Progression in Glioma

Biology of Glioblastoma Multiforme—Exploration of Mitotic Catastrophe as a Potential Treatment Modality

Contact Info

Product

Resources

About