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Cancer: Brain Cancers
Drug: Temodar

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Total 27 results found since Jan 2013.

Combination of B7H6-siRNA and temozolomide synergistically reduces stemness and migration properties of glioblastoma cancer cells
This study aimed to understand the potential role and molecular mechanism of the combination therapy of B7H6-siRNA and temozolomide in glioblastoma cancer. U87 cells were treated with B7H6-siRNA and temozolomide, separately and in combination. Cell viability, stemness, cell migration, and apoptosis were measured. The results of this work presented the synergistic effect of B7H6-siRNA and temozolomide in inhibiting the cancerous features of the U87 cell line. Down-regulating B7H6-siRNA expression inhibited the cell viability of U87 glioblastoma cancer cells and increased their sensitivity to temozolomide. In addition, a not...
Source: Experimental Cell Research - May 29, 2023 Category: Cytology Authors: Nadia Allahyarzadeh Khiabani Mohammad Amin Doustvandi Fateme Mohammadnejad Elnaz Salmani Hassan Kohal Neda Boushehri Mahdi Jafarlou Behzad Baradaran Source Type: research

MicroRNA-640 Inhibition Enhances the Chemosensitivity of Human Glioblastoma Cells to Temozolomide by Targeting Bcl2 Modifying Factor
Biochem Genet. 2022 Aug 19. doi: 10.1007/s10528-022-10264-x. Online ahead of print.ABSTRACTGlioblastoma (GBM) is the most malignant and challenging type of astrocytoma and also notoriously acknowledged as the most common primary brain tumor globally. Currently, chemotherapy is the most master therapy for tumor and is essential in clinical treatment for GBM. Nevertheless, the characterization of chemotherapy resistance seriously hinders clinical chemotherapy treatment. Accordingly, there are imperious demands for the exploitation of novel chemosensitizer to promote the efficacy of chemotherapy. Our current study was conduct...
Source: Biochemical Genetics - August 19, 2022 Category: Genetics & Stem Cells Authors: Shu Jiang Chao Luo Yongli Chen Jing Chen Shuang Tao Quan Zou Chunzhi He Shanwu Dong Source Type: research

Kill two birds with one stone: Engineered exosome-mediated delivery of cholesterol modified YY1-siRNA enhances chemoradiotherapy sensitivity of glioblastoma
In this study, we utilize the engineering technology to generate T7 peptide-decorated exosome (T7-exo). T7 is a peptide specifically binding to the transferrin receptor. T7-exo shows excellent packaging and protection of cholesterol-modified Cy3-siYY1 while quickly releasing payloads in a cytoplasmic reductive environment. The engineered exosomes T7-siYY1-exo could deliver more effciently to GBM cells both in vitro and in vivo. Notably, in vitro experiments demonstrate that T7-siYY1-exo can enhance chemoradiotherapy sensitivity and reverse therapeutic resistance. Moreover, T7-siYY1-exo and TMZ/IR exert synergistic anti-GBM...
Source: Frontiers in Pharmacology - August 19, 2022 Category: Drugs & Pharmacology Source Type: research

Anti-Proliferative Effects of E2F1 Suppression in Glioblastoma Cells
Glioblastoma (GBM) is an aggressive malignant brain tumor; surgery, radiation, and temozolomide still remain the main treatments. There is evidence that E2F1 is overexpressed in various types of cancer, including GBM. E2F1 is a transcription factor that controls the cell cycle progression and regulates DNA damage responses and the proliferation of pluripotent and neural stem cells. To test the potentiality of E2F1 as molecular target for GBM treatment, we suppressed theE2F1 gene (siRNA) in the U87MG cell line, aiming to inhibit cellular proliferation and modulate the radioresistance of these cells. Following E2F1 suppressi...
Source: Cytogenetic and Genome Research - September 3, 2021 Category: Genetics & Stem Cells Source Type: research

TRIM66 Overexpression Promotes Glioma Progression and Regulates Glucose Uptake Through cMyc/GLUT3 Signaling
CONCLUSION: TRIM66 was upregulated in human gliomas, where it promoted cell growth and chemoresistance. Our data also identified novel roles of TRIM66 in glioma progression. TRIM66 upregulates glucose uptake and mitochondrial function through the cMyc/GLUT3 signaling, which makes it a potential therapeutic target.PMID:34234562 | PMC:PMC8256720 | DOI:10.2147/CMAR.S293728
Source: Cell Research - July 8, 2021 Category: Cytology Authors: Yuequn Song Lifang Meng Jian Yu Zhi Cao Jizhou Sun Hongyu Zhao Source Type: research

Cancers, Vol. 13, Pages 944: Identification and Validation of ERK5 as a DNA Damage Modulating Drug Target in Glioblastoma
wn Spencer J. Collis Brain tumours kill more children and adults under 40 than any other cancer, with approximately half of primary brain tumours being diagnosed as high-grade malignancies known as glioblastomas. Despite de-bulking surgery combined with chemo-/radiotherapy regimens, the mean survival for these patients is only around 15 months, with less than 10% surviving over 5 years. This dismal prognosis highlights the urgent need to develop novel agents to improve the treatment of these tumours. To address this need, we carried out a human kinome siRNA screen to identify potential drug targets that augment the e...
Source: Cancers - February 24, 2021 Category: Cancer & Oncology Authors: Natasha Carmell Ola Rominiyi Katie N. Myers Connor McGarrity-Cottrell Aurelie Vanderlinden Nikita Lad Eva Perroux-David Sherif F. El-Khamisy Malee Fernando Katherine G. Finegan Stephen Brown Spencer J. Collis Tags: Article Source Type: research

The guanine nucleotide exchange factor, LARG, and RhoC play a role in glioblastoma cell invasion and resistance.
Abstract Glioblastoma (GBM) is the most common primary malignant brain cancer in adults. A hallmark of GBM is aggressive invasion of tumor cells into the surrounding normal brain. The current standard of care therapy, as well as targeted therapies, have largely failed to specifically address this issue. Therefore, identifying key regulators of GBM cell migration and invasion is of particular interest. The leukemia-associated RhoGEF (LARG) has previously been implicated in cell invasion in other tumor types; however, the role of LARG in GBM pathobiology remains undefined. Here, we report that the expression level o...
Source: The American Journal of Pathology - July 17, 2020 Category: Pathology Authors: Ding Z, Dong Z, Yang Y, Fortin Ensign SP, Sabit H, Nakada M, Ruggieri R, Kloss JM, Symons M, Tran NL, Loftus JC Tags: Am J Pathol Source Type: research

TROY signals through JAK1-STAT3 to promote glioblastoma cell migration and resistance.
Abstract Glioblastoma (GBM) is the most common primary malignant brain tumor in adults and carries a discouraging prognosis. Its aggressive and highly infiltrative nature renders the current standard treatment of maximal surgical resection, radiation, and chemotherapy relatively ineffective. Identifying the signaling pathways that regulate GBM migration/invasion and resistance is required to develop more effective therapeutic regimens to treat GBM. Expression of TROY, an orphan receptor of the TNF receptor superfamily, increases with glial tumor grade, inversely correlates with patient overall survival, stimulates...
Source: Neoplasia - July 2, 2020 Category: Cancer & Oncology Authors: Ding Z, Kloss JM, Tuncali S, Tran NL, Loftus JC Tags: Neoplasia Source Type: research

CD73 as a target to improve temozolomide chemotherapy effect in glioblastoma preclinical model
AbstractGlioblastoma is the most devastating primary brain tumor and effective therapies are not available. Treatment is based on surgery followed by radio and chemotherapy with temozolomide (TMZ), but TMZ increases patient survival only by 2  months. CD73, an enzyme responsible for adenosine production, emerges as a target for glioblastoma treatment. Indeed, adenosine causes tumor-promoting actions and CD73 inhibition increases sensitivity to TMZ in vitro. Here, a cationic nanoemulsion to nasal delivery of siRNA CD73 (NE-siRNA CD73) ai ming glioblastoma treatment was employed alone or in combination with TMZ. In vitro, t...
Source: Cancer Chemotherapy and Pharmacology - May 15, 2020 Category: Cancer & Oncology Source Type: research

A HIF-independent, CD133-mediated mechanism of cisplatin resistance in glioblastoma cells
ConclusionsFrom our data we conclude that the mechanisms underlying hypoxia-induced CD133-mediated cisplatin resistance may be instrumental for the design of new GBM treatment strategies.
Source: Cellular Oncology - February 28, 2018 Category: Cancer & Oncology Source Type: research

CSIG-24. REGULATION OF Fn14 EXPRESSION BY EGFRvIII-STAT SIGNALING ENHANCES GLIOBLASTOMA CELL INVASION AND SURVIVAL
Glioblastoma Multiforme (GBM) is the most common malignant brain tumor in adults. Most GBM patients succumb to the disease less than one-year post diagnosis due to the highly invasive nature of the tumor, which prevents complete surgical resection and gives rise to tumor recurrence. The invasive phenotype also confers radio-and chemoresistant properties to the tumor cells; therefore, there is a need to develop new therapeutics that target drivers of GBM invasion. Amplification of EGFR is observed in over 50% of GBM tumors, of which half concurrently overexpress the variant EGFRvIII, and expression of both receptors confers...
Source: Neuro-Oncology - November 6, 2016 Category: Cancer & Oncology Authors: Roos, A., Mayo, Z., Sonnemann, H., Lambert, G., Dhruv, H., Winkles, J., Berens, M., Tran, N., Sabir, M. Tags: CELL SIGNALING AND SIGNALING PATHWAYS Source Type: research

P06.20 EGFRvIII: a predictive marker for Temozolomide response in O6-methylguanine-DNA methyltransferase negative glioblastoma cells and tumor xenografts
Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults with an estimated 5-year survival of less 10%. The current standard of care involves maximal tumor resection followed by radiation and chemotherapy with the alkylating agent temozolomide (TMZ). Epigenetic silencing of the O6-methylguanine-DNA methyltransferase (MGMT) gene predicts response to TMZ therapy, but does not explain all of the heterogeneity in responses observed in the clinic. The establishment of additional molecular biomarkers, is therefore of significant interest.The aim of the present study was to analyze the impact of endogenous...
Source: Neuro-Oncology - September 20, 2016 Category: Cancer & Oncology Authors: Struve, N., Brend, T., Ott, L., Petersen, C., Rothkamm, K., Short, S. C., Kriegs, M. Tags: P06 Biomarkers Source Type: research