It should be noted that if INPs act at a click here transcriptional level in Chlamydia, they might not affect the secretion of all effectors to the same extent. Therefore, at this stage INPs should only be used cautiously to assess the mechanism of secretion of a given chlamydial protein. Down-regulation of transcription could perhaps also be due to feedback inhibition resulting from blocking T3S activity [24]. If, in Chlamydia, either the transcription of T3S associated genes or the assembly of the T3S AZD1152 ic50 machinery are inhibited, addition of the drugs at the end of one cycle of infection is expected to affect the next round of infection. This is

exactly what was observed when looking at the progeny of C. trachomatis infected cells treated with INP0341 24 hours post infection [19]. In this experiment, although the inclusions formed upon late INP0341 treatment were as abundant as in control cells, there was a decrease in the infectious

progeny, suggesting that EBs formed in the presence of INPs might be defective in their ability to secrete type selleck III effectors. However, due to the asynchronicity of the Chlamydia developmental cycle, we can not definitively rule out that the decrease in the formation of infectious EBs when the drug is added late in the cycle is not due to the now well documented reduction of RB multiplication upon INP treatment. Conclusion In the present study we demonstrate that small molecule inhibitors of Yersinia T3S have a strong inhibitory effect on Chlamydia growth but

fail to inhibit Chlamydia invasion. Teicoplanin INPs had no significant effect on C. trachomatis L2 and C. caviae GPIC entry into epithelial cells. Moreover, recruitment of actin and small GTPases to bacterial entry sites was not altered. These results suggest that in the presence of INPs pivotal events in early Chlamydia biogenesis following entry must be affected which could account for the observed inhibition of Chlamydia growth. The inability of INPs to interfere with the entry mechanism suggest that the drug might not affect the translocation process per se. We believe that the identification of the mode of action of INPs on type III secretion in genetically tractable bacteria will clarify this issue. Methods Cells, bacterial strains, antibodies and plasmids HeLa cells were grown as described [11]. The Chlamydia trachomatis L2 strain 434 (VR-902B) was from the ATCC and the GPIC strain of C. caviae was obtained from Dr. R. Rank (University of Arkansas). Plasmids coding for HA-tagged Arf6, GFP-tagged Rac and GFP-tagged Cdc42 were kindly given by Drs. Ph. Chavrier (Institut Curie, Paris), G. Tran van Nhieu (Institut Pasteur, Paris) and E. Caron (Imperial College, London), respectively. The mouse anti-Chlamydia antibody (unlabelled and FITC-conjugated) was purchased from Argene, Biosoft.

4-fold with a V diff confidence score of >0.7, while phosphoglycerate mutase and triosephosphate isomerase increased by ~1.4-fold, but only with a V diff confidence score of >0.2. While Raman et al.

(2011) observed a decrease in mRNA expression of ATP-dependent phosphofuctokinase Cthe_1261 and PPi-dependent phosphofructokinase Cthe_0389 during transition to stationary phase, we did not observe any changes in protein levels. However, we did observe a decrease in phosphoglycerate mutase Cthe_0946 and an increase in Cthe_1292, consistent with cellulose grown C. thermocellum mRNA profiles [37]. Energy storage Glycogen, an energy and selleck carbon storage compound, is commonly synthesized during periods of slow or no growth, especially in carbon excess, and is often associated with sporulation [71, 72]. Glucose-1-P adenylyltransferase (Cthe_3166 and Cthe_3167), involved in the synthesis of the primary glucosyl donor ADP-glucose, was detected in exponential phase cell-free extracts using shotgun 2D-HPLC-MS/MS (Figure  2b, Additional file 4). Of the two genes encoding glycogen synthase (Cthe_1284 and Cthe_0282), which catalyzes α-1,4-glucosyl linkages to a pre-existing α-1,4-glucan, levels of Cthe_1284 were ~15-fold higher than that of Cthe_0282, suggesting p38 MAPK activity it is the primary glycogen synthase in C. thermocellum. While the

level of 1,4-α-glucan branching enzyme, required for catalyzing α-1,6-glucosyl linkages, was below our threshold cutoff in shotgun analysis, it was detected in 4-plex analysis. A putative 1,4-α-glycogen debranching enzyme and α-glucan phosphorylase, required for glycogen breakdown, was also detected in exponential phase cultures. On the basis of simultaneous glucose-1-P

adenylyltransferase, glycogen synthase, and glycogen phosphorylase activities in C. cellulolyticum cell-free extracts, Guedon et al. have proposed that glycogen synthesis and glycogenolysis can occur simultaneously [73]. While allosteric regulation of these enzymes has been demonstrated in E. coli[71], the effect of allosteric regulators on these enzymes was not studied in C. cellulolyticum. Alternatively, Selleckchem ZD1839 the simultaneous detection of enzymes involved in glycogen synthesis as well as glycogen breakdown may be a consequence of metabolic heterogeneity within the culture, where some cells are expressing AP26113 in vivo pathways for glycogen synthesis while others are expression pathways capable of glycogenolysis. While this type of cell-to-cell variation has been observed in Bacillus subtilis[74], it cannot be verified using proteomics as these variations are homogenized as one examines bulk mixtures of cells. We observed a 3.5-fold increase in glycogen synthase Cthe_0282 and a 2.5-fold increase in 1,4-α-branching enzyme in stationary phase, suggesting that glycogen synthesis is favoured during stationary phase.

On the contrary 1 patient had local residual tumor evidenced by renal mass persistence and pathological contrast enhancement with nodular feature in the cryoablated area (TA 14,3 sec; TTP 38,3 sec; WIR 11,56/sec; PCE 301,23 HU) compared to normal ipsilateral

cortex (TA 13,8 sec; TTP 44,4 sec; WIR 9,41; PCE 374,18 HU). The VX-680 clinical trial mean BV value at the same residual tumour area was 140,68 ± 24,48 mL/100 g (vs. BV of 116,14 ± 14,27 in normal parenchyma), BF and PS mean values respectively were 562,72 ± 97,96 mL/100 g/min (vs. 393,8 ± 59,01 mL/100 g/min in normal parenchyma) and 73,52 ± 28,1 mL/100 g/min (vs. 41,88 ± 19,89 mL/100 g/min in normal parenchyma). MTT was 15 ± 0,1 sec (vs. 17,69 ± 0,4 sec in normal parenchyma). At a six months postoperative follow-up, 11 patients (73%) underwent CT guided percutaneous core needle biopsy. Two/Three needle cores were obtained per patient with a spring loaded, 18 gauge TSA HDAC price core biopsy device. According to pCT results with one case of persistent disease, of 25 needle cores obtained, two specimen of RCC were identified in 1 patients. This patient was scheduled for salvage laparoscopic

cryoablation and is currently under image monitoring without actual evidence of local residual or metastatic disease at the 12 months follow-up. In the remaining 23 needle cores available, a varying evidence of irreversible cell death was depicted including: hemosiderin deposits in 10 (43%), coagulative necrosis in 8 (35%), and fibrosis in 5 (22%) cores. Discussion Perfusion imaging is a non-invasive functional technique firstly introduced by Miles [16, 17] and implemented for the evaluation of neoplastic disease on account of its diagnostic and prognostic value as observed for treatment response of lymphoma [18] and head-and-neck

ADP ribosylation factor cancer [19], for predictive malignancy value in pulmonary solitary nodule [20], for monitoring of hemodynamic changes after anti-angiogenic therapy [21]. The growing availability of new multislice computed tomographies (MSCTs) and software programs for post-processing perfusion measurements have allowed additional functional informations regarding flow quantification of cross section areas. As far as we know, there are no published reports about the use of pCT in monitoring of cryoablated RCC. Cryoablation technique is a thermal minimally invasive treatment, developed as an alternative to conventional surgical resection in patients with selected case of RCC, especially for whom the risk of surgery is too great [9, 22–28]. The area of necrosis resulting from cryoablation is directed by cytotoxic effect from intracellular ice crystallization during the active freezing cycles and micro-occlusive tissue ischemia by the active or Emricasan passive thaw cycle [29]. With time fibrosis occurs and the ablated area decreases in size. Although cryoablation of select renal masses is an effective technique in local tumor control [28, 30], the ablated renal tumor area is not excised.

A loss of LuxS function impacts on motility-associated genes in a range of different bacteria. For enterohemorrhagicE. coli(EHEC),H. pylori, andC. jejunia role of AI-2 in the regulation of motility associated genes has been proposed [35,44,60,61]. At least forC. jejuni, this view is not supported by the data contained

within the present study. The defect in motility caused by deletion ofluxSinH. pyloriwas shown to be restored by addition of cell free medium containing AI-2 [62], but this could not be demonstrated for theC. jejuni luxSmutant in this study. The flagella regulatorflhAwas also shown to be induced by addition of AI-2 in aluxSmutant background Selleck Fludarabine providing further evidence for the role of AI-2 in the global regulation of flagella gene transcription [62]. In contrast, transcription offlhAwas not altered in aluxSmutant ofC. jejuni(this study and [37]). A phylogenetic tree of the LuxS PRIMA-1MET mouse protein revealed that the LuxS ofC. jejuniis phylogenetically distant to that ofH. pyloriwhich could, in part, explain differences in function between the LuxS protein inC. jejuniandH. pylori[63]. Since it was probably acquired independently in the two species, the primary role taken on byluxS(gene regulation versus metabolic) would differ depending on what other pathways were already established. AI-2 production and degradation Virtually no AI-2 activity was detectable whenC. jejuniNCTC 11168 was grown in

MEM-α. This could be due to a lack of AI-2 export, selleck screening library rapid intracellular turnover of DPD or AI-2 or lack ofluxSorpfsexpression and thus DPD synthesis. The latter possibility could not be ruled out, as it was not possible to detect Pfs and LuxS enzyme activity

in cell extracts obtained from strain NCTC 11168 growing in MEM-α or in MHB. The reason for Etofibrate this remains unclear, as SAH and SRH conversion could be detected in similarly preparedE. colicell extracts. It could be that inC. jejuni, enzyme activity levels are below those detectable in the assay. There is unlikely to be an absence ofpfsexpression in MEM-α, as previous studies have indicated modulatedpfsexpression [58] rather than an on/off control. Moreover,pfsmutations cause severe growth defects [64]. Given the absence of a growth defect in MEM-α, Pfs is likely to be present. In support of this, although the differential expression was not significant (confidence level was 18%, based on two separate P-values; slope and intercept), theluxSmutant had 1.9 fold morepfsexpression than the WT in MEM-α. The overall differential gene expression detected in MEM-α suggests that the WT, but not the mutant produces LuxS. Exogenous AI-2 activity gradually diminished when added to MHB or MEM-α grownC. jejunicultures suggesting either uptake or degradation. However,C. jejunidoes not seem to possess an AI-2 uptake system homologous to that found inS. Typhimurium andE. coli.

plantarum Selleckchem SIS 3 strains investigated in this study including strain S1 and S2 corresponded with the size of the amplicon obtained for the Lb. plantarum DSM 20174T which was used as the reference strain

and were therefore identified as such. Similarly, unambiguous differentiation of W. confusa and W. cibaria strains could not be achieved based on 16S rRNA gene sequencing due to the close relatedness of the two species. However, using a species specific PCR method BMS907351 reported by Fuscos et al. [39], we were able to distinguish these two closely related species. DNA from all the Weissella strains generated a PCR product with a size of 225 bp similar to that of W. confusa LMG 11983T which was used as the reference strain and no amplified product was obtained in any of the negative control

strains (Ped. acidilactici DSM20284T, Ped. pentosaceus DSM20336T, Lb. fermentum DSM20052T, Lb. pentosus DSM20314T, Lb. paraplantarum LTH5200, Lb. delbrueckii subsp. lactis DSM20073, Lb. delbrueckii subsp. bulgaricus DSM20080). The strains were therefore identified as W. confusa. The reproducibility of the broth micro-dilution method used in this study for determining the antibiotics MIC values has been confirmed in previous studies and is one of National Committee for Clinical Laboratory Standards (NCCLS) recommended methods for determining antibiotic MIC values [41, 46]. Our results showed that the investigated buy PR-171 strains were resistant to high concentration of vancomycin. In a previous study, Danielsen and Wind [47] shown that Lb. Doxorubicin nmr plantarum/pentosus strains were resistant to higher concentrations of vancomycin (MIC ≥ 256 μg/ml). Furthermore, Lb. plantarum, Lb. rhamnosus, and Lb. brevis strains resistant to high concentrations of vancomycin (MICs ≥256 μg/ml) was also reported by Delgado et al. [48]. According to Ammor et al. [49], the resistance of Lactobacillus, Pediococcus and Leuconostoc species to vancomycin is due to the absence of D-Ala-D-lactate in their cell wall which is the target of vancomycin. Thus the resistance mechanisms observed among these strains is inherent or intrinsic to Lactobacillus, Leuconostoc and Pediococcus species and could

therefore not be attributed to acquisition of resistance genes. The SCAN report which was adopted on 3rd July 2001 and revised on 18 April 2002 has also indicated that certain species of Lactobacillus are inherently resistant to vancomycin [35]. The bacteria were highly sensitive to erythromycin. This same observation for lactic acid bacteria was reported by others [47, 50]. It was reported by Rojo-Bezares et al. [50] that Lb. plantarum, Leuc. pseudomesenteroides, Ped. pentosaceus and Ped. acidilactici strains were highly sensitive to erythromycin which is in agreement with our findings. In this study, it was observed that the majority of the bacteria (24 out of 31 strains) were resistant to gentamicin (MIC > 16 mg/L). Ouoba et al. [34] reported a gentamicin MIC value 16–32 mg/L for Lb.

smegmatis cell wall proteome. see more Other studies have previously used this approach to resolve mycobacterial

membrane proteins [9–12]. The goal of this study was to improve the identification of mybacterial cell wall and cell wall-associated proteins in Mycobacteria by analyzing the model organism Mycobacterium smegmatis. Results & discussion High-throughput identification of cell wall proteins with SDS-PAGE + LC-MS/MS Traditionally, proteomic analyses of cell wall samples involve the https://www.selleckchem.com/products/LY2603618-IC-83.html resolution of proteins using 2-DE followed by the identification of resolved proteins by MS [13]. However, a big proportion of cell wall proteins are membrane bound, and it is generally agreed that membrane proteins are highly underrepresented in 2 dimensional electrophoresis (2-DE) [14].

In view of the poor performance of the 2-DE technique for membrane proteins and because the electrophoretic resolution of 2-DE by contaminating mycolates and other cell wall components [15], an alternative approach for the analysis of the cell wall proteome, shotgun LC-MS/MS method, was conducted. Cell wall proteins were first separated by SDS-PAGE according to their molecular weight followed by in-gel digested with trypsin into complex peptide mixture, and then the mixture was analyzed directly by LC-MS/MS. Subsequently, protein identifications were determined by database searching selleck compound software [16]. Our experiments led to the identification of a much wider range of proteins in cell wall fraction than those identified using the conventional 2-DE based method and can therefore be used as a comprehensive reference for Mycobacterium spp. cell wall proteomic PTK6 studies. To avoid false-positive hits, we applied strict criteria for peptide and proteins identification. Additional file 1 shows the identified proteins in detail. In total, 390 unique proteins were identified, which

included 79 proteins previously annotated as hypothetical or conserved hypothetical, which is the largest number of cell wall and cell wall-associated proteins for mycobacteria reported in one study. Hydrophobicity analysis of the identified cell wall proteins Potential cell wall associated proteins with 1-15 TMHs (Transmembrane helix) were assigned using TMHMM 2.0 program against the Mycobacterial smegmatis MC2 155 protein sequence database (excluding the possible signal sequences). In our study, 64 proteins (16.41%) were identified to have at least 1 transmembrane domain. The predicted TMH numbers of these proteins ranged from 1 to 15, and 34 contained at least two TMHs. The profile of TMH in cell wall proteins of M. smegmatis is very similar to previous reports about TMH in M. tuberculosis cell wall proteome [17]. The distribution of these TMHs is shown in Figure 1.

The clinicopathological data including the histological type and grade of the tumor [17, 18], stage

of the disease [19], volume of ascites, time to progression, management of primary and recurrent disease, and time of death or last follow-up. Pathological diagnoses of recruited cases were reviewed by two JICR pathologists, namely, X. Xu and L. Hou. Definition of clinical response and surveillance The definition of CCR includes the absence of tumor-associated clinical symptoms and residual Bucladesine in vivo tumor on the physical examination, EOC-negative imaging study results and a serum CA-125 concentration below the upper limit of the normal range (ULN = 35U/mL) in the current study. Clinical recurrent was identified as the occurrence of any new measurable lesion through imaging studies or clinical examination

[15]. Patients underwent neoadjuvant chemotherapy followed by interval CRS. Platinum-sensitive recurrent was generally referring to the progression of the free interval at least 6 months from the completion of primary therapy. see more According to most of the gynecologists, secondary CRS is defined as an debulking procedure performed at some time remote (generally disease free interval of more than 6 months) from the completion of primary treatment with the intended purpose of tumor reduction. The criterion of optimal CRS was the threshold of residual tumor ≤ 1 cm or macroscopic free and suboptimal debulking was defined as more than 1 cm of nodules left. The overall survival (OS) duration was defined as the time from the disease diagnosis to death OSBPL9 or last follow-up. Proteasome inhibitor PFS was the length of time during and after initial therapy wherein the patient’s condition

does not worsen. Time to progression (TTP) was a measure of time from radiological defined relapse to the disease starts to get worse in present study. Statistical analysis Cox proportional hazards model was used to assess the relationship between the clinical characteristics and the OS and TTP. Step-wise regression was conducted to build the multivariate models. The log-rank test was used to assess this relationship. Logistic regression analysis was used to explore optimal secondary CRS related factors. The p values < 0.05 was considered statistically significant. All analyses were conducted using the SPSS statistical software program (version 18.0; SSPS Inc, Chicago, IL). Results Patient characteristics The clinicopathological characteristics of all patients included in the present study were given in Table 1. High-grade and low-grade primary EOC were 83 (86.5%) and 13 (13.5%), respectively, and serous carcinoma cases was 67 (69.8%). Median follow-up time was 37.6 months (interquartile range, 20.2 months to 69.0 months) in the living patients at the beginning of our analysis. The recurrent patients underwent secondary CRS were reported experiencing pain (2 patients), gastrointestinal dysfunction (8 cases), and/or mass effect (7 cases) and others (7 cases).

In the present study, hCG is associated with elevated VD in testicular tumors. hCG has been associated with angiogenesis in normal tissues; this has been confirmed in vivo and in

vitro by increasing capillary formation and endothelial cell migration [16, 18], and in regulation of placental angiogenesis [24]. Elevated hCG serum levels are present in pregnancy; thus, similarities between tumor invasion and its vascularization and blastocyst implantation and placental development have been described [25, 26]. In addition, it has been proposed that hCG could induce VEGF LY2874455 purchase production in tissues such as GDC-0941 chemical structure placenta [17] and granulosa cells [18, 19]. hCG administration to women undergoing in vitro fertilization increases urinary [27], serum, and follicular-fluid VEGF concentrations [28]. Furthermore, hCG exerts a direct angiogenic effect on hCG/LH receptor-expressing uterine endothelial cells, which respond with increased capillary formation in vitro [16, 29]. hCG receptors have been detected in breast carcinoma tissue, which indicates a probable link to a worse breast-cancer prognosis during pregnancy, which we previously hypothesized [30]. We found that predominantly in patients with hCG serum levels ≥ 25 mIU/mL there was increased tumoral

vascular neoformation, suggesting that hCG could be involved in angiogenic processes during tumor Mizoribine development. Intrinsic hCG activity is clinically relevant when serum concentrations are high, for instance, during pregnancy or under certain pathological conditions that might be associated to the carcinogenesis of testicular germ cells [6, 7]. In this study, a prominent VD (median, 19.0 ± 28.9) was observed in all tumors, especially non-seminomas, which would be expected as hCG is elevated in this subtype of germ tumors. Angiogenesis is essential for malignant Decitabine research buy neoplasm progression and is correlated with poor prognosis in numerous solid tumors [31], including germ cell testicular cancer [32, 33]. Particularly in normal testis, the endothelial cell proliferation rate is considerably higher than in other stationary

organs. It has been shown that this rate can be increased via hCG stimulation of Leydig cells [34]. In addition, a correlation between hCG and VEGF has been confirmed in rat models and transformed mouse Leydig cell lines (MA-10 cells) [35, 36]. In our results, VEGF expression was limited to 56% of the tumors studied, showing no clinical or histopathological association; nevertheless, tissue availability comprised a factor that could render the data less significant. VEGF expression in germ cell testicular tumors was previously found to be significantly higher than in normal testis and was correlated with microvessel density [11, 37]; it was also described as an indicator of metastatic disease [12].

Analysis of the polar bear faeces in this study showed a homogenous microbial flora dominated by Clostridia class. These bacteria are well characterized as they are dominant in the human gut and thereby in the interest of many scientists [34]. All 161 sequences obtained from polar bears were affiliated with the phylum Firmicutes (Table 1, Fig. 2). All except one sequence affiliated with the order Clostridiales, and

93% to the family Clostridiaceae. The low level of Selleckchem Torin 1 diversity observed in the polar bear clone library is in contrast to the diversity observed in colon content from another Arctic carnivorous animal belonging to the same order as polar bears, the hooded seal (Cystophora cristata) [35]. Sequences that affiliated with the phyla Bacteroides, Firmicutes, Fusobacteria, and Proteobacteria were identified in the colon content from the seals. The dominant phylum was the Bacteroides to which find more check details 68% of the sequences were affiliated, while 21% were affiliated to the Firmicutes

[35]. The same molecular methods were used to analyse both the polar bear and seal samples, indicating that the methods are not selective towards Firmicutes. Jores et al [36] found Clostridium in 44% of the samples when cultivating faeces from polar bears in Svalbard. In faeces from a herbivorous mammal, the wild gorilla, 71% of the phylogenetic ID-8 lineage was Firmicutes [37]. Ley et al [33] observed that the microbial faecal bacterial communities from bears on different diets cluster together, independent of the diet. However, these observations were made in animals kept in zoo’s and might not reflect the situation in the wild. Eight of the 673 sequences (GenBank/EMBL/DDBJ database, NCBI) from polar bear faeces collected in zoo’s [33] were compared to the sequences obtained in this study (Fig. 2). The eight zoo polar bear sequences included in Fig. 2 represent eight

out of 100 phylotypes (analysed by FastgroupII) and contain 59% of the 673 zoo polar bear sequences. Only two of the sequences, representing 10% of all the sequences, cluster together with sequences from our study, indicating a difference between the microbioma in faeces of wild and captive polar bears. We investigated the prevalence of bla TEM alleles in faeces from polar bears with little human impact in Svalbard, Norway. We have earlier investigated the prevalence of bla TEM alleles in Arctic soils and sediments, and in colon content of Arctic seals and found low prevalence of the alleles [15, 35]. This current cultivation study of faeces from polar bears did not give any growth on plates with ampicillin (Table 4). The bla TEM alleles are likely to be found in coliform bacteria, but the selective growth on MacConkey agar with ampicillin yielded < 0.3% ampr cfu (Table 4).

Chen MH designed research and supervised the writing and organization process. All authors read and approved the final manuscript.”
“Introduction Human gliomas represent the most common primary brain tumors in both children and adults. According to Bucladesine histopathological Duvelisib molecular weight and clinical criteria established by the World Health Organization (WHO), this dismal

disease can be classified as well-differentiated low grade astrocytomas [World Health Organization (WHO) grade I~II], anaplastic astrocytomas (WHO grade III) and glioblastoma multiforme (GBM, WHO grade IV) [1]. Despite recent therapeutic advances, the survival of patient with glioma is still poor. The median overall survival of patients with malignant gliomas is no more than one year and local recurrence occurs in more than 90% of patients [2]. Recent studies have indicated that patients’ age, Karnofsky performance status (KPS) score, histologic grade, and tumor necrosis are important

prognostic factors for gliomas [3]. However, the prognosis of both high- and low-grade tumors remains heterogeneous. The median survival time of patients with high-grade gliomas range from 5 to 59 months and some patients with low-grade tumors also present poor outcome [4]. Similar with other human solid tumors, the predominant features of gliomas are extensive local tumor invasion and metastasis, in which multiple molecular events are involved. Focusing CH5183284 cost on these genetic background and molecular pathogenic processes is necessary to identify novel diagnostic and prognostic markers for improving

the clinical outcome of patients with gliomas. In mammals, the chloride intracellular channel (CLIC) gene family has six members, including CLIC1, CLIC2, CLIC3, CLIC4, CLIC5, and CLIC6 [5]. This family is defined by a conserved, approximately 230 amino acid core sequence which comprises the C-termini of all known CLICs. CLIC1 is a newly discovered member Teicoplanin of the CLIC family [6]. In 1997, it was originally cloned from a human monocytic cell line activated by the phorbol ester, phorbol 12-myristate 13 acetate [7]. CLIC1 is expressed ubiquitously in human tissues and is usually localized in the cytoplasm and nucleoplasm with a soluble form. It has been demonstrated to be involved in the regulation of cell cycle, cell proliferation and differentiation [8]. In the G2/M phase, CLIC1 is detected on the plasma membranes of cells, and the inhibition of CLIC1 function prolongs the mean time of the cell cycle in cell culture [9]. Recent studies have found that CLIC1 is over-expressed in malignant tumors, such as hepatocellular carcinoma [10], gallbladder carcinoma [11], gastric carcinoma [12], and colorectal cancer [13, 14]. CLIC1 has been considered as a sensor and an effector during oxidative stress, which may lead cells through all the phases of the cell cycle [15].