Begell House Inc.
Critical Reviews™ in Eukaryotic Gene Expression
CRE
1045-4403
23
4
2013
Skeletal Muscle Adaptations to Cancer and its Treatment: Their Fundamental Basis and Contribution to Functional Disability
283-297
10.1615/CritRevEukaryotGeneExpr.2013007650
Hirak
Der-Torossian
Department of Surgery, University of Vermont, College of Medicine, Burlington, VT
Marion E.
Couch
Department of Surgery, University of Vermont, College of Medicine, Burlington, VT
Kim
Dittus
Department of Surgery, University of Vermont, College of Medicine, Burlington, VT
Michael J.
Toth
Departments of Medicine and Molecular Physiology and Biophysics, University of Vermont, College of Medicine, Burlington, VT
myofilaments
atrophy
cachexia
oxidative metabolism
Cancer is a physically disabling condition. Functional disability, defined as an inability or impaired ability to perform simple tasks of daily life, afflicts a large majority of the cancer population and dramatically impacts
patient well-being, negatively affecting treatment decisions, quality of life, and clinical outcomes. Our current understanding of the fundamental mechanisms underlying physical disability in cancer patients, however, is limited. This review will evaluate how cancer and cancer treatments and their pathological sequelae alter skeletal muscle structure and function to promote functional disability. Briefly, factors associated with cancer and its treatment can diminish skeletal muscle size and contractile function, which lead to a reduced physiological capacity for work and, in turn, functional disability. We outline the clinical evidence for the involvement of each of these factors in disability
in cancer patients and then review structural and functional evidence at various anatomic levels to explore the tissue, cellular, and molecular mechanisms underlying cancer-related disability.
Emerging Biomedicines Based on Bacteriophages
299-308
10.1615/CritRevEukaryotGeneExpr.2013006578
Jianlong
Yan
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University, Beibei, Chongqing 400715, China
Xiangyu
Fan
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Enviroment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University.
Jianping
Xie
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Key Laboratory of Ecoenvironments in Three Gorges Reservoir Region, Ministry of Education,
School of Life Sciences, Southwest University, Beibei, Chongqing 400715, China
bacteriophage
endolysin
holin
engineered bacteriophage
Bacteriophage is bacterial virus widespread in the biosphere. Bacteriophages and their encoded endolysin
(or lysin), holin, and other small proteins are intensively pursed as novel therapeutic agents to complement and tackle the increasing antibiotics resistance. Moreover, the delivery system based on bacteriophage and the diagnostic method based on engineered bacteriophage were also promising new avenues to drug delivery and diagnosis.
TCF7L2 rs12255372 (G > T) Polymorphism Contributes to Breast Carcinogenesis: Evidence from a Meta-Analysis
309-316
10.1615/CritRevEukaryotGeneExpr.2013007820
Zexing
Wang
The Second People's Hospital of Wuhu Affiliated to Wannan Medical College
Qun
Zhang
Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China
Fengxia
Chen
Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China
Yanru
Wang
Department of Medical Oncology, Jinling Hospital, School of Medicine, Southern Medical University, Guangzhou, 510282, China
Weiwei
Nie
Department of Medical Oncology, Jinling Hospital, School of Medicine, Southern Medical University, Guangzhou, 510282, China
Bin
Yang
Department of Ultrosound, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China
Xiaoxiang
Guan
Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002; Department of Medical Oncology, Jinling Hospital, School of Medicine, Southern Medical University, Guangzhou, 510282, China
TCF7L2
polymorphism
breast cancer
susceptibility
Studies on the association between the TCF7L2 rs12255372 polymorphism and breast cancer risk have reported conflicting results. To characterize the relationship between this polymorphism and breast cancer risk, we
conducted a comprehensive literature search for relevant studies and performed a meta-analysis. A total of four studies including 5280 cases and 6026 controls were eligible for our analysis. Overall, we did find that this polymorphism correlates with breast cancer risk [TT versus GG: odds ratio (OR) = 1.19, 95% confidence interval (CI) = 1.02−1.40; GT versus GG: OR = 1.10, 95% CI = 1.01−1.19; T versus G: OR = 1.12, 95% CI = 1.05−1.19]. Furthermore, in the subgroup analysis by ethnicity, we did also find that this polymorphism associated with an increased breast cancer risk in white individuals (T versus G: OR = 1.11, 95% CI = 1.04−1.18). In summary, this meta-analysis suggests that the rs12255372 T allele is a low-penetrant risk factor for breast carcinogenesis. In the future, larger-scale and more well-designed studies based on homogeneous breast cancer patients are needed to validate our findings, especially in Asians.
Bacteriophage Inspired Antibiotics Discovery against Infection Involved Biofilm
317-326
10.1615/CritRevEukaryotGeneExpr.2013007717
Xiangyu
Fan
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Enviroment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University.
Wu
Li
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University, Chongqing, China
Fei
Zheng
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University, Beibei, Chongqing 400715, China
Jianping
Xie
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Key Laboratory of Ecoenvironments in Three Gorges Reservoir Region, Ministry of Education,
School of Life Sciences, Southwest University, Beibei, Chongqing 400715, China
Phage
Bacterial biofilm
Extracellular DNA
Polysaccharide depolymerases
Phage therapy
Drug design
Bacterial biofilm profoundly influences the fate of bacteria within and the outcome of related infection,
and is closely associated with antibiotics resistance and bacterial persistence. Bacteriophages represent a new
promising alternative to combat biofilm-related infection. The interplay between phages and biofilms is complex.
Some phages or their components can inhibit the host bacteria biofilm via diverse mechanisms, while other phages
can facilitate the host biofilm formation through phage-mediated lysis and extracellular DNA release. In this paper, we summarize the role of bacteriophages in the biofilm formation, and the application of phages to the control of bacterial persisters and infectious biofilms, in particular, the phage-inspired antibiotics discovery.
Progress of FtsZ Inhibitors as Novel Antibiotics Leads
327-338
10.1615/CritRevEukaryotGeneExpr.2013007742
Weiling
Hong
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University, Chongqing 400715, China
Jianping
Xie
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Key Laboratory of Ecoenvironments in Three Gorges Reservoir Region, Ministry of Education,
School of Life Sciences, Southwest University, Beibei, Chongqing 400715, China
antibiotics target
antibiotic resistant
FtsZ inhibitors
novel antibiotics
Bacterial cell division is an attractive target for new antibiotics. FtsZ is a major cytoskeletal protein
widespread among archaea and bacteria. FtsZ has a filament-forming GTPase and a structural homologue of eukaryotic
tubulin. FtsZ has been validated as a target for antibiotics. This review summarizes the chemical features, binding sites, mechanisms of action, and minimum inhibitory concentration of FtsZ inhibitors.
XRCC1 Arg194Trp and Arg280His Polymorphisms in Bladder Cancer Susceptibility: A Meta-Analysis
339-354
10.1615/CritRevEukaryotGeneExpr.2013007781
Chuan
Liu
Department of Oncology, Changhai Hospital, Second Military Medical University, P.R.China
Qinghua
Yin
Department of Oncology, the First People's Hospital of Yueyang, P.R.China
Lian
Li
Yueyang Second People's Hospital, 263 Baling Road, Yueyang, People's Republic of China, 414000
Guangjun
Jiao
Musculoskeletal Tumor Center, People's Hospital, Peking University, Beijing, P.R. China
Mei
Wang
Department of Oncology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai, People's Republic of China, 200433; School of Medicine, Jiangsu University, Zhenjiang 212013, China
Yajie
Wang
Department of Oncology, Changhai Hospital, Second Military Medical University, P.R.China
meta-analysis
XRCC1
Arg194Trp
Arg280His
bladder cancer
The XRCC1 Arg194Trp and Arg280His polymorphisms were likely to be involved with the development of bladder cancer. However, there had been inconsistent reports of association. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed,
Embase, and Web of Science for relevant articles with a time limit of April 25, 2013. Summary odds ratios (ORs)
with 95% confidence intervals (CIs) were used to assess the strength of association between the two polymorphisms and bladder cancer susceptibility using a random-effects model. This meta-analysis including 14 case-control studies evaluated the associations between the two XRCC1 polymorphisms and bladder cancer susceptibility. Overall, for Arg194Trp, significant associations were found in TT versus CC (OR = 1.78, 95% CI = 1.12−2.82) and the recessive
model (OR = 1.71, 95% CI = 1.11−2.65); for Arg280His, significant associations were also found in AG versus GG (OR = 1.63, 95% CI = 1.24−2.13) and the dominant model (OR = 1.39, 95% CI = 1.07−1.82). When stratified by ethnicity, in Asian population, significant associations were found for Arg194Trp polymorphism in TT versus CC (OR = 2.99, 95% CI = 1.48−6.06), the dominant model (OR = 1.33, 95% CI = 1.03−1.72) and the recessive model (OR = 2.72, 95% CI = 1.36−5.45), and for Arg280His in GA versus GG (OR = 2.13, 95% CI = 1.63−2.97), but no significant associations were found in no-Asian population. This meta-analysis suggested that XRCC1 Arg194Trp and Arg280His polymorphisms were risk factors for increasing bladder cancer in Asian population.
Mechanism of Neurotoxicity of Prion and Alzheimer's Disease−Related Proteins: Molecular Insights from Bioinformatically Identified ω-Conotoxin-Like Pharmacophores
355-373
10.1615/CritRevEukaryotGeneExpr.2013007950
Emanuele
Bellacchio
Research Laboratories, Bambino Gesu Children's Hospital, IRCCS, V.le F. Baldelli 41, 00146 Rome, Italy
Alzheimer's disease
prion diseases
neurodegenerative disorders
N-type calcium channels
omega-conotoxin
molecular modeling
bioinformatics
Prion diseases are fatal neurodegenerative disorders caused by altered forms of the prion protein (PrPc). It was reported that dysregulation of cellular Ca2+ homeostasis is recurrent in these diseases and that scrapie-infected cells exhibit Ca2+ perturbation via specific impairment of N-type calcium channels. However, it is not known whether such dysfunction is secondary to the broad neuronal damage accompanying prion diseases or whether it underlies pathological interactions of prions with calcium channels. In this research, we examined this latter possibility by searching for channel binding signatures in PrPc through structural comparison with known N-type channel blockers. To this aim, a computational method devised by us to recognize similar distributions of basic residues in protein structures enabled us to find that the bioactive groups representing the pharmacophores of ω-conotoxins GVIA and MVIIA can be overlaid onto similar residues within the PrPc globular domain. This finding, together with the knowledge that Ca2+ homeostasis disruption is common to other neurodegenerative disorders, led us to search for and identify an ω-conotoxin-like pharmacophore also in the Alzheimer's Aβ(1-42) peptide. These results point to the potential ability of prions and Aβ(1-42) to bind calcium channels as the elusive neurotoxic mechanism common to seemingly unrelated fatal neuropathies.