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Cancer: Glioma
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Total 18 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

A Nanoparticle-Conjugated Anti-TBK1 siRNA Induces Autophagy-Related Apoptosis and Enhances cGAS-STING Pathway in GBM Cells
CONCLUSION: The rGO-PEG could be an efficient system facilitating the delivery of specific siRNA. TBK1si/rGO-PEG could be a novel strategy for the treatment of GBM.PMID:34931127 | PMC:PMC8684524 | DOI:10.1155/2021/6521953
Source: Evidence-based Complementary and Alternative Medicine - December 21, 2021 Category: Complementary Medicine Authors: Shengchao Xu Xi Yan Lu Tang Gan Dai Chengke Luo Source Type: research

EZH2 as a new therapeutic target in brain tumors: Molecular landscape, therapeutic targeting and future prospects
Biomed Pharmacother. 2021 Dec 11;146:112532. doi: 10.1016/j.biopha.2021.112532. Online ahead of print.ABSTRACTBrain tumors are responsible for high mortality and morbidity worldwide. The brain tumor treatment depends on identification of molecular pathways involved in progression and malignancy. Enhancer of zeste homolog 2 (EZH2) has obtained much attention in recent years in field of cancer therapy due to its aberrant expression and capacity in modulating expression of genes by binding to their promoter and affecting methylation status. The present review focuses on EZH2 signaling in brain tumors including glioma, gliobla...
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - December 15, 2021 Category: Drugs & Pharmacology Authors: Mahshid Deldar Abad Paskeh Atefeh Mehrabi Mohammad Hossein Gholami Amirhossein Zabolian Ehsan Ranjbar Hossein Saleki Adnan Ranjbar Mehrdad Hashemi Yavuz Nuri Ertas Kiavash Hushmandi Sepideh Mirzaei Milad Ashrafizadeh Ali Zarrabi Saeed Samarghandian Source Type: research

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
In conclusion, our research results indicate that DAPT activates PI3K/AKT/Cdc42 signaling by non-canonical Notch pathway, and the activated Cdc42 promotes the filopodia formation and inhibits lamellipodia assembly, resulting in reduced migration of breast cancer cells. The results imply that non-canonical Notch signaling may play a very important role in the rapid response of cells to the extracellular signals. Author Contributions LG, JD, and LL designed the study and wrote and revised the manuscript. LL and LZ performed most of the experiments and data analysis. SZ, X-YZ, P-XM, Y-DM, Y-YW, YC, S-JT, and Y-JZ assisted i...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development
Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroi...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin
Conclusion: Our results provide novel evidence that HDGF interacts with DDX5 and promotes the progression of EC through the induction of β-catenin. Introduction Endometrial cancer (EC) comprises the most common malignancy involving the female genital tract and the fourth most common malignancy in women after breast, lung, and colorectal cancers (1). In 2012, approximately 320,000 new cases of EC were diagnosed worldwide and the incidence is increasing (2). Currently, endometrial carcinogenesis is thought to be a multi-step process involving the coordinated interaction of hormonal regulation, gene mutation, ad...
Source: Frontiers in Oncology - April 10, 2019 Category: Cancer & Oncology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Overcoming resistance to TRAIL-induced apoptosis in solid tumor cells by simultaneously targeting death receptors, c-FLIP and IAPs.
This study provides a rationale for the development of TRAIL-induced apoptosis-based cancer therapies. PMID: 27210546 [PubMed - as supplied by publisher]
Source: International Journal of Oncology - May 15, 2016 Category: Cancer & Oncology Authors: Huang Y, Yang X, Xu T, Kong Q, Zhang Y, Shen Y, Wei Y, Wang G, Chang KJ Tags: Int J Oncol Source Type: research

Nucleic-Acid Delivery Using Lipid Nanocapsules.
In conclusion, LNCs are very good candidates to deliver nucleic acids to cells in the course of anti-cancer therapies. PMID: 27033510 [PubMed - as supplied by publisher]
Source: Current Pharmaceutical Biotechnology - March 31, 2016 Category: Biotechnology Authors: Lagarce F, Passirani C Tags: Curr Pharm Biotechnol Source Type: research

Abstract 680: Identification of GLI1 antagonists for breast cancer therapy
Conclusion: Several agents showed efficacy in in vitro BC cancer models demonstrating that GLI inhibitors may be a valid therapeutic approach for targeting GLI-dependent BC cancers.[1] Z. Thomas, W. Gibson, J. Sexton, K. Aird, S. Ingram, A. Aldrich, H. Lyerly, G. Devi, K. Williams, Targeting GLI1 expression in human inflammatory breast cancer cells enhances apoptosis and attenuates migration. British Journal of Cancer 104 (2011) 1575-1586.[2] K.P. Williams, J.L. Allensworth, S.M. Ingram, G.R. Smith, A.J. Aldrich, J. Z Sexton, G. R Devi, Quantitative high-throughput efficacy profiling of approved oncology drugs in inflammat...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Oladapo, H., Fleming, J. M., Addo, K., Tarpley, M., Ehe, B., Ingram, S., Sauer, S., Devi, G., Williams, K. P. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 5328: Protein phosphatase 2A activity is a major determinant of therapy response in cancer cells
Protein phosphatase 2A (PP2A) dephosphorylates majority of Ser/Thr phosphorylated proteins. Consequently, PP2A is an antagonist of multiple oncogenic pathways and PP2A reactivation may provide an alternative route to target these pathways. Importantly, because PP2A reactivation would result in simultaneous dephosphorylation of both collateral and downstream effectors of kinase pathways, it might circumvent commonly encountered kinase inhibitor resistance mechanisms.To systematically study the role of PP2A in cancer therapy response we used RNAi targeting against PP2A inhibitor proteins CIP2A, PME-1 and SET (PP2A reactivati...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Kauko, O., Imanishi, S., Kaur, A., Laajala, D., Kulesskiy, E., Jumppanen, M., Corthals, G., Aittokallio, T., Wennerberg, K., Westermarck, J. Tags: Experimental and Molecular Therapeutics Source Type: research