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Condition: Ataxia
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Total 67 results found since Jan 2013.
Abstract 5193: Ataxia telangiectasia mutated relates to epithelial-mesenchymal transition in colorectal cancer
Conclusions: ATM might be a critical regulator of EMT in colorectal cancer invasion.Citation Format: Hidena Takahashi, Masashi Tsuruta, Hirotoshi Hasegawa, Koji Okabayashi, Ryo Seishima, Shimpei Matsui, Toru Yamada, Takayuki Kondo, Takehiro Shimada, Mutsuhito Matsuda, Masashi Yahagi, Yusuke Yoshikawa, Yusuke Asada, Kiyoaki Sugiura, Yoshiyuki Suzuki, Yuki Tajima, Junpei Nakadai, Yuko Kitagawa. Ataxia telangiectasia mutated relates to epithelial-mesenchymal transition in colorectal cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Takahashi, H., Tsuruta, M., Hasegawa, H., Okabayashi, K., Seishima, R., Matsui, S., Yamada, T., Kondo, T., Shimada, T., Matsuda, M., Yahagi, M., Yoshikawa, Y., Asada, Y., Sugiura, K., Suzuki, Y., Tajima, Y., Nakadai, J., Kitagawa, Y. Tags: Tumor Biology Source Type: research
Genome-Engineering Tools to Establish Accurate Reporter Cell Lines That Enable Identification of Therapeutic Strategies to Treat Friedreich's Ataxia
Friedreich’s ataxia is a neurodegenerative disease caused by deficiency of the mitochondrial protein frataxin. This deficiency results from expansion of a trinucleotide repeat in the first intron of the frataxin gene. Because this repeat expansion resides in an intron and hence does not alter the amino acid sequence of the frataxin protein, gene reactivation could be of therapeutic benefit. High-throughput screening for frataxin activators has so far met with limited success because current cellular models may not accurately assess endogenous frataxin gene regulation. Here we report the design and validation of genom...
Source: Journal of Biomolecular Screening - June 19, 2015 Category: Molecular Biology Authors: Villasenor, R., Miraglia, L., Romero, A., Tu, B., Punga, T., Knuckles, P., Duss, S., Orth, T., Buhler, M. Tags: Original Research Source Type: research
PTEN-Deficient Tumor Cells Are Dependent on ATM Signaling
In this study, we took an siRNA screening strategy to identify other tumor suppressors that, when inhibited, similarly sensitized cells to ATM inhibition. In this manner, we determined that PTEN and ATM were synthetically lethal when jointly inhibited. PTEN-deficient cells exhibited elevated levels of reactive oxygen species, increased endogenous DNA damage, and constitutive ATM activation. ATM inhibition caused catastrophic DNA damage, mitotic cell cycle arrest, and apoptosis specifically in PTEN-deficient cells in comparison with wild-type cells. Antioxidants abrogated the increase in DNA damage and ATM activation in PTE...
Source: Cancer Research - May 31, 2015 Category: Cancer & Oncology Authors: McCabe, N., Hanna, C., Walker, S. M., Gonda, D., Li, J., Wikstrom, K., Savage, K. I., Butterworth, K. T., Chen, C., Harkin, D. P., Prise, K. M., Kennedy, R. D. Tags: Priority Reports Source Type: research
RNF8 plays an important role in the radioresistance of human nasopharyngeal cancer cells in vitro.
Authors: Wang M, Chen X, Chen H, Zhang X, Li J, Gong H, Shiyan C, Yang F
Abstract
Tumor residue or recurrence is common after radiation therapy for nasopharyngeal cancer (NPC) since the tumor cells can repair irradiation-induced DNA damage. The ubiquitination cascade mediates the assembly of repair and signaling proteins at sites of DNA double-strand breaks (DSBs). Ring finger protein 8 (RNF8) is an E3 ubiquitin ligase that triggers ubiquitination at the site of DSBs. The present study aimed to identify whether and how RNF8 small interfering RNA (siRNA) treatment enhances the radiosensitivity of irradiated human ...
Source: Oncology Reports - May 9, 2015 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
Resveratrol analogue (E)-8-acetoxy-2-2-(3,4-diacetoxyphenyl)ethenyl-quinazoline induces G2/M cell cycle arrest through the activation of ATM/ATR in human cervical carcinoma HeLa cells.
Authors: Kim JY, Choi HE, Lee HH, Shin JS, Shin DH, Choi JH, Lee YS, Lee KT
Abstract
Styrylquinazolines are synthetic analogues of resveratrol and have been suggested to cause anti-inflammatory activity by modulating prostaglandin E2 (PGE2) production. In the present study, we evaluated cytotoxic effects of various styrylquinazoline derivatives and found that (E)-8-acetoxy-2-[2-(3,4-diacetoxyphenyl)ethenyl]-quinazoline (8-ADEQ) most potently inhibited the proliferation of the human cervical carcinoma HeLa cells. Exploring the growth-inhibitory mechanisms of 8-ADEQ, we found that it causes a cell cycle arrest at the...
Source: Oncology Reports - April 1, 2015 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
MutL homolog 1 contributes to temozolomide-induced autophagy via ataxia-telangiectasia mutated in glioma.
Abstract
In the present study, mutL homolog 1 (MLH1) small interfering (si)RNA, KU‑55933, an ataxia‑telangiectasia mutated (ATM) inhibitor, and compound C, an adenosine monophosphate‑activated protein kinase (AMPK) inhibitor, were used to investigate the mechanisms underlying temozolomide (TMZ)‑induced autophagy and to determine the role of MLH1 and ATM in autophagy. MLH1 siRNA and KU‑55933 inhibited the phosphorylation of AMPK and ULK1 and reduced the levels of autophagy. MLH1 siRNA inhibited the phosphorylation of ATM and attenuated TMZ cytotoxicity, whereas the inhibition of ATM‑AMPK augmented TM...
Source: Molecular Medicine - February 3, 2015 Category: Molecular Biology Authors: Zou Y, Wang Q, Wang W Tags: Mol Med Rep Source Type: research
ATR and ATM Loss-of-Function
Mechanisms to maintain genomic integrity are essential for cells to remain viable. Not surprisingly, disruption of key DNA damage response pathway factors, such as ataxia telangiectasia-mutated (ATM)/ataxia telangiectasia and RAD3-related (ATR) results in loss of genomic integrity. Here, a synthetic lethal siRNA-screening approach not only confirmed ATM but identified additional replication checkpoint proteins, when ablated, enhanced ATR inhibitor (ATRi) response in a high-content -H2AX assay. Cancers with inactivating ATM mutations exhibit impaired DNA double-stranded break (DSB) repair and rely on compensatory repair pat...
Source: Molecular Cancer Research - January 15, 2015 Category: Cancer & Oncology Authors: Menezes, D. L., Holt, J., Tang, Y., Feng, J., Barsanti, P., Pan, Y., Ghoddusi, M., Zhang, W., Thomas, G., Holash, J., Lees, E., Taricani, L. Tags: DNA Damage and Repair Source Type: research
Ataxia telangiectasia mutated inhibits oxidative stress-induced apoptosis by regulating heme oxygenase-1 expression.
In conclusion, ATM induces HO-1 expression via activation of PKC-δ and NF-κB and inhibits oxidative stress-induced apoptosis. A loss of HO-1 induction may explain why AT patients are vulnerable to oxidative stress.
PMID: 25592228 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - January 12, 2015 Category: Biochemistry Authors: Yu JH, Cho SO, Lim JW, Kim N, Kim H Tags: Int J Biochem Cell Biol Source Type: research
The catalytic topoisomerase II inhibitor dexrazoxane induces DNA breaks, ATF3 and the DNA damage response in cancer cells
Conclusions and ImplicationsSimilar to TOP2A poisons, DRZ induces DNA double‐strand breaks followed by activation of DNA damage response. The DNA damage‐triggered ATF3 controls the level of p53 accumulation as well as double‐strand breaks generation and is proposed to serve as a switch between DNA damage and cell death following DRZ treatment. These findings suggest a mechanistic explanation for the diverse clinical observations associated with DRZ.
Source: British Journal of Pharmacology - December 17, 2014 Category: Drugs & Pharmacology Authors: Shiwei Deng, Tiandong Yan, Teodora Nikolova, Dominik Fuhrmann, Andrea Nemecek, Ute Gödtel‐Armbrust, Bernd Kaina, Leszek Wojnowski Tags: Research Paper Source Type: research
An ATM-MPG Axis Promotes Resistance to Alkylating Agents Research Articles
This article is highlighted in the In This Issue feature, p. 1103
Source: Cancer Discovery - September 30, 2014 Category: Cancer & Oncology Authors: Agnihotri, S., Burrell, K., Buczkowicz, P., Remke, M., Golbourn, B., Chornenkyy, Y., Gajadhar, A., Fernandez, N. A., Clarke, I. D., Barszczyk, M. S., Pajovic, S., Ternamian, C., Head, R., Sabha, N., Sobol, R. W., Taylor, M. D., Rutka, J. T., Jones, C., Di Tags: Preclinical Intervention, Preclinical Intervention: In Vitro: Drugs, Mechanisms Research Articles Source Type: research
A hormone-dependent feedback-loop controls androgen receptor levels by limiting MID1, a novel translation enhancer and promoter of oncogenic signaling
Conclusion:
Promotion of AR, in addition to enhancement of the Akt-, NFkappaB-, and Hh-pathways by sustained MID1-upregulation during androgen deprivation therapy provides a powerful proliferative scenario for PCa progression into castration resistance. Thus MID1 represents a novel, multi-faceted player in PCa and a promising target to treat castration resistant prostate cancer.
Source: Molecular Cancer - June 9, 2014 Category: Cancer & Oncology Authors: Andrea KöhlerÜmmühan DemirEva KicksteinSybille KraussJohanna AignerBeatriz Aranda-OrgillésAntonios KaragiannidisClemens AchmüllerHuajie BuAndrea WunderlichMichal-Ruth SchweigerGeorg SchaeferSusann SchweigerHelmut KlockerRainer Schneider Source Type: research
Coenzyme Q10, Statin, and Spinocerebellar Ataxias (I11-1.008)
CONCLUSIONS:CoQ10 is associated with better clinical outcome in SCA1, 2, and 3 whereas statins are associated with worse clinical outcome in SCA6. These drug exposures did not appear to influence clinical progression within 2 years. CoQ10 and statins may have only symptomatic effects or require a longer period of time for disease modification.Study Supported by:American Brain Foundation Research Fellowship, Rare Disease Clinical Research Network RC1NS068897, and NINDS K08 NS083738.Disclosure: Dr. Kuo has nothing to disclose. Dr. Lo has nothing to disclose. Dr. Figueroa has nothing to disclose. Dr. Pulst has received person...
Source: Neurology - April 9, 2014 Category: Neurology Authors: Kuo, S.-H., Lo, R., Figueroa, K., Pulst, S., Perlman, S., Wilmot, G., Gomez, C., Schmahmann, J., Paulson, H., Shakkottai, V., Ying, S., Zesiewicz, T., Bushara, K., Geschwind, M., Xia, G., Subramony, S., Ashizawa, T. Tags: Proteinopathy in Neurodegenerative Disease Poster Presentations Source Type: research
Coenzyme Q10, Statin, and Spinocerebellar Ataxias (P6.047)
CONCLUSIONS:CoQ10 is associated with better clinical outcome in SCA1, 2, and 3 whereas statins are associated with worse clinical outcome in SCA6. These drug exposures did not appear to influence clinical progression within 2 years. CoQ10 and statins may have only symptomatic effects or require a longer period of time for disease modification.Study Supported by:American Brain Foundation Research Fellowship, Rare Disease Clinical Research Network RC1NS068897, and NINDS K08 NS083738.Disclosure: Dr. Kuo has nothing to disclose. Dr. Lo has nothing to disclose. Dr. Figueroa has nothing to disclose. Dr. Pulst has received person...
Source: Neurology - April 9, 2014 Category: Neurology Authors: Kuo, S.-H., Lo, R., Figueroa, K., Pulst, S., Perlman, S., Wilmot, G., Gomez, C., Schmahmann, J., Paulson, H., Shakkottai, V., Ying, S., Zesiewicz, T., Bushara, K., Geschwind, M., Xia, G., Subramony, S., Ashizawa, T. Tags: Movement Disorders: Spinocerebellar Ataxias Source Type: research
cAMP signaling inhibits radiation-induced ATM phosphorylation leading to the augmentation of apoptosis in human lung cancer cells
Conclusions:
cAMP signaling inhibits radiation-induced ATM activation by PKA-dependent activation of PP2A, and this signaling mechanism augments radiation-induced apoptosis by reducing ATM-dependent activation of NF-kappaB in lung cancer cells.
Source: Molecular Cancer - February 24, 2014 Category: Cancer & Oncology Authors: Eun-Ah ChoEui-Jun KimSahng-June KwakYong-Sung Juhnn Source Type: research
Prodegenerative IκBα expression in oligodendroglial α-synuclein models of multiple system atrophy.
Abstract
Multiple system atrophy is a progressive, neurodegenerative disease characterized by parkinsonism, ataxia, autonomic dysfunction, and accumulation of α-synuclein in oligodendrocytes. To understand how α-synuclein aggregates impact oligodendroglial homeostasis, we investigated an oligodendroglial cell model of α-synuclein dependent degeneration and identified responses linked to the NF-κB transcription factor stress system. Coexpression of human α-synuclein and the oligodendroglial protein p25α increased the expression of IκBα mRNA and protein early during the degenerative process and this was depe...
Source: Neurobiology of Disease - December 17, 2013 Category: Neurology Authors: Kragh CL, Gysbers AM, Rockenstein E, Murphy K, Halliday GM, Masliah E, Jensen PH Tags: Neurobiol Dis Source Type: research
