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Cancer: Glioma

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Total 625 results found since Jan 2013.

CD44 expression in the tumor periphery predicts the responsiveness to bevacizumab in the treatment of recurrent glioblastoma
In this research, we analyze a relationship between CD44 expression and responsiveness to Bev and elucidate the role of CD44 in anti ‐VEGF therapy. These results indicate CD44 will be a useful biomarker for predicting responsiveness to bevacizumab and may serve as a therapeutic target in both primary and recurrent GBMs. AbstractAntiangiogenic therapy with bevacizumab (Bev), a monoclonal antibody targeting vascular endothelial growth factor (VEGF), is a common treatment for recurrent glioblastoma (GBM), but its survival benefit is limited. Resistance to Bev is thought to be a major cause of ineffectiveness on Bev therapy....
Source: Cancer Medicine - February 5, 2021 Category: Cancer & Oncology Authors: Masahiro Nishikawa, Akihiro Inoue, Takanori Ohnishi, Hajime Yano, Yonehiro Kanemura, Shohei Kohno, Shiro Ohue, Saya Ozaki, Shirabe Matsumoto, Satoshi Suehiro, Yawara Nakamura, Seiji Shigekawa, Hideaki Watanabe, Riko Kitazawa, Junya Tanaka, Tags: ORIGINAL RESEARCH Source Type: research

MicroRNA ‑186‑5p downregulation inhibits osteoarthritis development by targeting MAPK1
In conclusion, the present results indicated that miR‑186‑5p could attenuate IL‑1β‑induced chondrocyte inflammation damage by increasing MAPK1 expression, suggesting that miR‑186‑5p may be used as a potential therapeutic target for OA.PMID:33537828 | DOI:10.3892/mmr.2021.11892
Source: Molecular Medicine Reports - February 4, 2021 Category: Molecular Biology Authors: Qing Li Mingjie Wu Guofang Fang Kuangwen Li Wengang Cui Liang Li Xia Li Junsheng Wang Yanhong Cang Source Type: research

MiR-489 inhibits proliferation and apoptosis of glioblastoma multiforme cells via regulating TWIST1 expression.
CONCLUSIONS: MiR-489 can repress the proliferation and promote the apoptosis of glioma cells by targeting TWIST1. PMID: 33455101 [PubMed - in process]
Source: Journal of B.U.ON. - January 20, 2021 Category: Cancer & Oncology Tags: J BUON Source Type: research

p53 affects epigenetic signature on SOCS1 promoter in response to TLR4 inhibition.
Abstract Suppressor of cytokine signaling (SOCS1) functions as a negative regulator of toll-like receptor (TLR) induced inflammatory signaling. As silencing of SOCS1 is concomitant with elevated TLR4 levels in glioblastoma, we investigated the effect of TLR4 inhibition on SOCS1 expression. Pharmacological inhibition of TLR4 signaling by TAK242 or its siRNA-mediated knockdown in p53 mutant or wild-type glioma cells resulted in either increased or decreased SOCS1 expression and promoter activity, respectively. Genetic manipulation of p53 indicated that SOCS1 expression upon TLR4 inhibition is dependent on p53 mutati...
Source: Cytokine - January 18, 2021 Category: Molecular Biology Authors: Sheikh T, Sen E Tags: Cytokine Source Type: research

Regulation of temozolomide resistance in glioma cells via the RIP2/NF- κB/MGMT pathway.
CONCLUSION: We report that the RIP2/NF-κB/MGMT signaling pathway is involved in the regulation of TMZ resistance. Interference with NF-κB or MGMT activity could constitute a novel strategy for the treatment of RIP2-positive TMZ-resistant glioma. PMID: 33460245 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - January 18, 2021 Category: Neuroscience Authors: Hu YH, Jiao BH, Wang CY, Wu JL Tags: CNS Neurosci Ther Source Type: research

Effect of Ras-guanine nucleotide release factor 1-mediated H-Ras/ERK signaling pathway on glioma.
CONCLUSION: Ras-GRF1 was upregulated in glioma tissues and correlated with its malignancy and prognosis. Silencing Ras-GRF1, through mediating H-Ras/ERK pathway, may suppress the growth and metastasis of glioma. PMID: 33412149 [PubMed - as supplied by publisher]
Source: Brain Research - January 4, 2021 Category: Neurology Authors: Pan YH, Chen J, Sun C, Ma JF, Li X Tags: Brain Res Source Type: research

TRPM7 Induces Tumorigenesis and Stemness Through Notch Activation in Glioma
In this study, we determined the major contributor(s) to TRPM7 mediated glioma stemness by further deciphering each individual Notch signaling. We first determined whether TRPM7 is an oncotarget in glioblastoma multiforme (GBM) using the Oncomine database. Next, we determined whether TRPM7 silencing by siRNA TRPM7 (siTRPM7) induces cell growth arrest or apoptosis to reduce glioma cell proliferation using cell cycle analysis and annexin V staining assay. We then examined the correlations between the expression of TRPM7 and Notch signaling activity as well as the expression of GSC markers CD133 and ALDH1 in GBM by downregula...
Source: Frontiers in Pharmacology - December 14, 2020 Category: Drugs & Pharmacology Source Type: research

Cancers, Vol. 12, Pages 3260: Improving Radiation Response in Glioblastoma Using ECO/siRNA Nanoparticles Targeting DNA Damage Repair
Camphausen Radiation therapy is a mainstay in the standard of care for glioblastoma (GBM), thus inhibiting the DNA damage response (DDR) is a major strategy to improve radiation response and therapeutic outcomes. Small interfering RNA (siRNA) therapy holds immeasurable potential for the treatment of GBM, however delivery of the siRNA payload remains the largest obstacle for clinical implementation. Here we demonstrate the effectiveness of the novel nanomaterial, ECO (1-aminoethylimino[bis(N-oleoylcysteinylaminoethyl) propionamide]), to deliver siRNA targeting DDR proteins ataxia telangiectasia mutated and DNA-dependen...
Source: Cancers - November 4, 2020 Category: Cancer & Oncology Authors: Jennifer A. Lee Nadia Ayat Zhanhu Sun Philip J. Tofilon Zheng-Rong Lu Kevin Camphausen Tags: Article Source Type: research

Transmembrane protein 45A regulates the proliferation, migration, and invasion of glioma cells through nuclear factor kappa-B
In conclusion, TMEM45A is an oncogenic gene in glioma. The proliferation, migration, and invasion of gliomas could be effectively impeded by inhibition of TMEM45A, and the cancer-promoting effect of TMEM45A on gliomas was involved with the NFκB pathway.
Source: Anti-Cancer Drugs - September 18, 2020 Category: Cancer & Oncology Tags: Preclinical Reports Source Type: research

Expression of Rab3b in Human Glioma: Influence on Cell Proliferation and Apoptosis.
CONCLUSION: Rab3b expression levels are significantly related to the progression of gliomas. Moreover, Rab3b silencing not only significantly inhibits cell proliferation in gliomas via cell cycle arrest but also promotes cell apoptosis by upregulating the expression levels of apoptosis-related proteins, however these preliminary in vitro results warrant validation on in vivo studies. PMID: 32940170 [PubMed - as supplied by publisher]
Source: Current Pharmaceutical Design - September 16, 2020 Category: Drugs & Pharmacology Authors: Luo Q, Liu Y, Yuan Z, Huang L, Diao B Tags: Curr Pharm Des Source Type: research

Involvement of SNARE Protein Interaction for Non-classical Release of DAMPs/Alarmins Proteins, Prothymosin Alpha and S100A13.
Abstract Prothymosin alpha (ProTα) is involved in multiple cellular processes. Upon serum-free stress, ProTα lacking a signal peptide sequence is non-classically released from C6 glioma cells as a complex with Ca2+-binding cargo protein S100A13. Thus, ProTα and S100A13 are conceived to be members of damage-associated molecular patterns (DAMPs)/alarmins. However, it remains to be determined whether stress-induced release of ProTα and S100A13 involves SNARE proteins in the mechanisms underlying membrane tethering of the multiprotein complex. In the present study, we used C6 glioma cells as a model of ProTα rele...
Source: Cellular and Molecular Neurobiology - August 26, 2020 Category: Cytology Authors: Matsunaga H, Halder SK, Ueda H Tags: Cell Mol Neurobiol Source Type: research

Silencing of Long Non-Coding RNA (LncRNA) Non-Coding RNA Activated by DNA Damage (NORAD) Inhibits Proliferation, Invasion, Migration, and Promotes Apoptosis of Glioma Cells via Downregulating the Expression of AKR1B1.
CONCLUSIONS These findings demonstrated that NORAD silencing suppressed proliferation, invasion, and migration and boosted apoptosis of glioma cells via downregulating the AKR1B1 expression, which may provide a potential therapeutic target for glioma treatment. PMID: 32778640 [PubMed - in process]
Source: Medical Science Monitor - August 13, 2020 Category: Research Tags: Med Sci Monit Source Type: research

Blockade of CD73 delays glioblastoma growth by modulating the immune environment
This study indicates that CD73 knockdown using a nanotechnological approach to perform nasal delivery of siRNA-CD73 to CNS can potentially regulate the glioblastoma immune microenvironment and delay tumor growth by inducing apoptosis.
Source: Cancer Immunology, Immunotherapy - August 13, 2020 Category: Cancer & Oncology Source Type: research

Targeting CD146 using folic acid-conjugated nanoparticles and suppression of tumor growth in a mouse glioma model.
CONCLUSIONS: CD146 is a potential therapeutic target, and folic acid-conjugated NPs delivering siRNA may facilitate gene therapy in malignant gliomas. PMID: 32707539 [PubMed - as supplied by publisher]
Source: Journal of Neurosurgery - July 23, 2020 Category: Neurosurgery Authors: Fukui N, Yawata T, Nakajo T, Kawanishi Y, Higashi Y, Yamashita T, Aratake T, Honke K, Ueba T Tags: J Neurosurg 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