MicroRNA-23b-3p targets non-SMC condensing I complex subunit G to promote proliferation and inhibit apoptosis of colorectal cancer cells via regulation of the PI3K/AKT signaling pathway.

Colorectal cancer (CRC) is one of the most common types of malignancy worldwide and has a poor prognosis. Non-SMC condensing I complex subunit G (NCAPG) has been reported to be upregulated in numerous types of malignant tumor. However, to the best of our knowledge, its clinicopathological and biological significance in CRC remain to be elucidated. The results of the present study revealed that NCAPG expression levels were upregulated in human CRC tissues and cell lines. The upregulated expression of NCAPG was positively associated with patient clinicopathological characteristics, such as differentiation and tumor size, and independently associated with poor survival. Consistent with the clinical observations, NCAPG was discovered to promote the proliferation and inhibit the apoptosis of CRC cells. Moreover, NCAPG-knockdown inhibited CRC cell proliferation by regulating the PI3K/AKT signaling pathway. Furthermore, NCAPG was identified as a potential target of microRNA (miR)-23b-3p, which was subsequently demonstrated to negatively regulate NCAPG expression. In conclusion, the findings of the current study indicated that the miR-23b-3p/NCAPG/PI3K/AKT signaling axis may play an important role in CRC carcinogenesis, and the status of the molecule may represent a promising prognostic marker for the disease.

Cytochrome C Oxidase Assembly Factor 1 Homolog Predicts Poor Prognosis and Promotes Cell Proliferation in Colorectal Cancer by Regulating PI3K/AKT Signaling.

PURPOSE: Colorectal cancer (CRC) is one of the most common malignancies in the world. The prognosis of advanced CRC is still poor. The purpose of this study was to identify a gene expression profile associated with CRC that may contribute to the early diagnosis of CRC and improve patient prognosis. PATIENTS AND METHODS: Five pairs of CRC tissues and paracancerous tissues were used to identify causative genes using microarray assays. The prognostic value of Cytochrome C Oxidase Assembly Factor 1 Homolog (COA1) in CRC was assessed in 90 CRC patients. Loss-of-function assays, cell proliferation assays using Celigo and MTT, colony formation assays, a subcutaneous xenograft mouse model, and apoptosis assays were used to define the effects of downregulation of COA1 in CRC cells in vitro and in vivo. The underlying molecular mechanisms of COA1 in CRC were also investigated. RESULTS: The causative gene COA1 was identified through microarray analysis. COA1 expression in CRC was notably associated with pathologic differentiation, tumor size, and tumor depth. COA1 expression may act as an independent prognostic factor for overall survival of CRC. Knockdown of COA1 inhibited the proliferation of CRC cells in vitro and the tumorigenicity of CRC cells in vivo. Decreased COA1 expression induced apoptosis of CRC cells. Based on the microarray assay results comparing HCT116 cells transfected with lentivirus encoding anti-COA1 shRNA or negative control shRNA, ingenuity pathway analysis (IPA) revealed that the PI3K/AKT signaling pathway was significantly enriched. Moreover, CCND1, mTOR, AKT1, and MDM2 were identified as the downstream genes of COA1. CONCLUSION: These findings demonstrate that COA1 promotes CRC cell proliferation and inhibits apoptosis by regulating the PI3K/AKT signaling pathway. Our results implicate COA1 as a potential oncogene involved in tumor growth and progression of CRC.

The prognostic value of proliferating cell nuclear antigen expression in colorectal cancer: A meta-analysis.

BACKGROUND: A number of studies have attempted to determine the prognostic significance of proliferating cell nuclear antigen (PCNA) in patients with colorectal cancer (CRC), but the reports are controversial and inconsistent. Thus, we conducted a meta-analysis to clarify the value of PCNA in CRC prognosis. METHODS: A systematic search of relevant studies was performed in 4 electronic databases including PubMed, Cochrane Library, Embase, and Web of Science until February 2018. Hazard ratios (HRs) combined with 95% confidence intervals (95% CIs) were used to evaluate the relationship of PCNA expression with overall survival (OS), cancer-specific survival (CSS), and disease-free survival (DFS). RESULTS: A total of 1372 CRC patients in 14 studies were identified eventually in our meta-analysis. The pooled HRs demonstrated that CRC patients with high PCNA expression was significantly correlated with poor OS (HR = 1.81; 95% CI: 1.51-2.17; P = .000), CSS (HR = 1.99; 95% CI: 1.04-3.79; P = .037); but not significantly with DFS (HR = 2.48; 95% CI: 0.98-6.26; P = .055). Sensitivity analysis showed the pooled HRs for OS, CSS, and DFS were stable when the included studies were removed one by one. CONCLUSION: Our meta-analysis suggested that high PCNA expression was associated with poor prognosis, and it could serve as a reliable and prognostic biomarker in CRC patients. More large-scale studies are needed to further support the conclusion.

MiR-92a promotes stem cell-like properties by activating Wnt/ß-catenin signaling in colorectal cancer.

We previously reported the oncogenic function of miR-92a in colorectal cancer. This study identified that miR-92a was upregulated in chemoresistant colorectal cancer cells and tissues. Ectopic expression of miR-92a conferred resistance to 5-fluorouracil-induced apoptosis in vitro, while antagomiR-92a significantly enhanced chemosensitivity in vivo. Moreover, Overexpression of miR-92a promoted the tumor sphere formation and the expression of stem cell markers. MiR-92a overexpression also displayed higher tumourigenesis in vivo. Furthermore, we demonstrated that miR-92a upregulates the Wnt/ß-catenin signaling activity via directly targeting KLF4, GSK3ß and DKK3, which are multiple level negative regulators of the Wnt/ß-catenin signaling cascade. In addition, our results indicate IL-6/STAT3 pathway increases miR-92a expression by directly targeting its promoter, resulting in Wnt/ß-catenin signaling activation and consequent promotion of stem-like phenotypes of colorectal cancer cells. Our present results suggest the essential role of IL-6/STAT3/miR-92a/Wnt/ß-catenin pathway in regulating the stem cell-like traits of colorectal cancer cells and provide a potential target for colorectal cancer therapy.

Adenoviral E4 34K protein interacts with virus packaging components and may serve as the putative portal.

Studies on dsDNA bacteriophages have revealed that a DNA packaging complex assembles at a special vertex called the 'portal vertex' and consists of a portal, a DNA packaging ATPase and other components. AdV protein IVa2 is presumed to function as a DNA packaging ATPase. However, a protein that functions as a portal is not yet identified in AdVs. To identify the AdV portal, we performed secondary structure analysis on a set of AdV proteins and compared them with the clip region of the portal proteins of bacteriophages phi29, SPP1 and T4. Our analysis revealed that the E4 34K protein of HAdV-C5 contains a region of strong similarity with the clip region of the known portal proteins. E4 34K was found to be present in empty as well as mature AdV particles. In addition, E4 34K co-immunoprecipitates and colocalizes with AdV packaging proteins. Immunogold electron microscopy demonstrated that E4 34K is located at a single site on the virus surface. Finally, tertiary structure prediction of E4 34K and its comparison with that of single subunits of Phi29, SPP1 and T4 portal proteins revealed remarkable similarity. In conclusion, our results suggest that E4 34K is the putative AdV portal protein.

Dual degradation signals destruct GLI1: AMPK inhibits GLI1 through ß-TrCP-mediated proteasome degradation.

Overexpression of the GLI1 gene has frequently been found in various cancer types, particularly in brain tumors, in which aberrant GLI1 induction promotes cancer cell growth. Therefore, identifying the molecular players controlling GLI1 expression is of clinical importance. Previously, we reported that AMPK directly phosphorylated and destabilized GLI1, resulting in the suppression of the Hedgehog signaling pathway. The current study not only demonstrates that AMPK inhibits GLI1 nuclear localization, but further reveals that ß-TrCP plays an essential role in AMPK-induced GLI1 degradation. We found that activation of AMPK promotes the interaction between ß-TrCP and GLI1, and induces ß-TrCP-mediated GLI1-ubiquitination and degradation. Inhibiting AMPK activity results in the dissociation of the ß-TrCP and GLI1 interaction, and diminishes ß-TrCP-mediated-GLI1 ubiquitination and degradation. On GLI1, substitution of AMPK phosphorylation sites to aspartic acid (GLI13E) results in stronger binding affinity of GLI1 with ß-TrCP, accompanied by enhanced GLI1 ubiquitination and later degradation. In contrast, the GLI1 alanine mutant (GLI13A) shows weaker binding with ß-TrCP, which is accompanied by reduced ß-TrCP-mediated ubiquitination and degradation. Together, these results demonstrate that AMPK regulates GLI1 interaction with ß-TrCP by phosphorylating GLI1 and thus both post-translational modifications by AMPK and ß-TrCP ultimately impact GLI1 degradation.

MicroRNA-22 suppresses the growth, migration and invasion of colorectal cancer cells through a Sp1 negative feedback loop.

MicroRNAs have recently emerged as regulators of many biological processes including cell proliferation, development and differentiation. This study identified that miR-22 was statistically decreased in colorectal cancer clinical specimens and highly metastatic cell lines. Moreover, low miR-22 expression was associated with tumor metastasis, advanced clinical stage and relapse. Consistent with clinical observations, miR-22 significantly suppressed the ability of colorectal cancer cells to growth and metastasize in vitro and in vivo. Sp1 was validated as a target of miR-22, and ectopic expression of Sp1 compromised the inhibitory effects of miR-22. In addition, Sp1 repressed miR-22 transcription by binding to the miR-22 promoter, hence forming a negative feedback loop. Further study has shown that miR-22 suppresses the activity of PTEN/AKT pathway by Sp1. Our present results implicate the newly indentified miR-22/Sp1/PTEN/AKT axis might represent a potential therapeutic target for colorectal cancer.

MicroRNA-106b promotes colorectal cancer cell migration and invasion by directly targeting DLC1.

BACKGROUND: Growing evidence suggests that microRNAs (miRNAs) play an important role in tumor development, progression and metastasis. Aberrant miR-106b expression has been reported in several cancers. However, the role and underlying mechanism of miR-106 in colorectal cancer (CRC) have not been addressed. METHODS: Quantitative RT-PCR(qRT-PCR) was performed to evaluate miR-106b levels in CRC cell lines and patient specimens. Cell proliferation was detected using MTT assay, and cell migration and invasion ability were evaluated by wound healing assay and transwell assay. The target gene of miR-106b was determined by qRT-PCR, western blot and luciferase assays. RESULTS: miR-106b was significantly up-regulated in metastatic CRC tissues and cell lines, and high miR-106b expression was associated with lymph node metastasis and advanced clinical stage. In addition, miR-106b overexpression enhances, whereas miR-106b depletion reduces CRC cell migration and invasion. Moreover, we identify DLC1 as a direct target of miR-106b, reveal its expression to be inversely correlated with miR-106b in CRC samples and show that its re-introduction reverses miR-106b-induced CRC cell migration and invasion. Furthermore, survival analyses showed the patients with high mi-106b/low DLC1 had shorter overall survival (OS) and disease-free survival (DFS) rates, and confirmed miR-106b may be an independent prognostic factor for OS and DFS in CRC patients. CONCLUSIONS: Our findings indicate that miR-106b promotes CRC cell migration and invasion by targeting DLC1. This miRNA may serve as a potential prognostic biomarker and therapeutic target for CRC.

Learning curve of endorectal ultrasonography in preoperative staging of rectal carcinoma.

Accurate preoperative staging of rectal carcinoma is essential for optimal treatment. This study was designed to evaluate the accuracy and learning curve of endorectal ultrasonography (ERUS) in the preoperative staging of rectal carcinoma. We retrospectively analyzed the records of patients with rectal carcinoma who underwent preoperative ERUS followed by curative surgery at the Shanxi Province Tumor Hospital between January, 2007 and March, 2010. The patients were divided into three groups, namely A, B and C, depending on whether the examination was performed between January and December, 2007, between January and December, 2008 or between January, 2009 and March, 2010, respectively. Five physicians with no prior experience in ERUS performed the examinations. We compared the ERUS staging with the pathological findings using the tumor-node-metastasis (TNM) classification. The accuracy of ERUS in T and N staging after each additional consecutive 20 patients was calculated for physicians D, E and F. A total of 319 patients underwent ERUS prior to surgery. There were 38 patients in group A, 135 in group B and 146 in group C. Two of the five physicians performed only 47 of the 319 examinations, whereas the remaining 272 patients were examined by physicians D (n=162), E (n=64) and F (n=46). The overall accuracy in assessing the extent of rectal wall invasion (T) was 67%, with 16% of the cases overstaged and 17% understaged and the accuracy in assessing nodal involvement (N) was 66%, with 11% of the cases overstaged and 23% understaged. The total T and N staging accuracy of physicians D, E and F was 75 and 72%; 59 and 59%; and 50 and 52%, respectively. For physicians D, E and F, the accuracy of T and N staging after each additional 20 patients was calculated and the curve of the accuracy reached a plateau after physician D completed 80 cases. Therefore, ERUS is a valuable tool for assessing the depth of tumor invasion and it appears that after ~80 cases a physician may be considered able to apply it efficiently.

[Calibration transfer without standards for spectral analysis based on stability competitive adaptive reweighted sampling].

A novel calibration transfer method based on stability competitive adaptive reweighted sampling (SCARS) was proposed in the present paper. An informative criterion, i. e. the stability index, defined as the absolute value of regression coefficient divided by its standard deviation was used. And the root mean squared error of prediction (RMSEP) after transfer was also used. The wavelength variables which were important and insensitive to influence of measurement parameters were selected. And then the differences in responses of different instruments or measurement conditions for a specific sample were eliminated or reduced to improve the calibration transfer results. Moreover, in the proposed method, the spectral variables were compressed, making calibration transfer more stable. The application of the proposed method to calibration transfer of NIR analysis was evaluated by analyzing the corn with different NIR spectrometers. The results showed that this method can well correct the difference between instruments and improve the analytical accuracy. The transfer results obtained by the proposed method, orthogonal signal correction (OSC), Monte Carlo uninformative variable elimination (MCUVE) and competitive adaptive reweighted sampling (CARS), respectively, for corn with different NIR spectrometers indicated that the former gave the best analytical accuracy, and was effective for the spectroscopic data compression which can simplify and optimize the transfer process.

miR­20a is an independent prognostic factor in colorectal cancer and is involved in cell metastasis.

Accumulating evidence indicates that dysregulated microRNAs (miRNAs) are involved in cancer development, progression and metastasis. miR­20a was found to be involved in invasion and epithelial­mesenchymal transition (EMT) programs, with its aberrant expression having been observed in a variety of malignant tumors. However, the molecular mechanisms underlying the role of miR­20a in colorectal cancer (CRC) development remain to be fully elucidated. In the present study, the expression of miR­20a was compared between CRC tissue samples and the normal adjacent mucosa using quantitative polymerase chain reaction. The association of miR­20a expression with clinicopathological characteristics was assessed using appropriate statistical analysis. The migration and invasion of SW480 cells was examined following transfection of the cells with either miR­20a precursor or a negative control miRNA precursor. The effect of miR­20a on the EMT in CRC cells in vitro was also analyzed. The regulatory effect of miR­20a on SMAD family member 4 (SMAD4) was evaluated using a dual­luciferase reporter assay. Relative expression levels of miR­20a were significantly higher in CRC tissue than those in the normal adjacent mucosa, and high expression of miR­20a correlated with lymph node metastases and distant metastases. Kaplan­Meier analysis indicated that patients with increased miR­20a levels exhibited unfavorable overall survival. Furthermore, multivariate analysis showed that miR­20a was an independent prognostic factor. The transfection of SW480 CRC cells with miR­20a promoted migration and invasion in vitro, and the upregulation of miR­20a induced EMT in CRC cells. An inverse correlation between the levels of miR­20a and SMAD4 was observed in patients with CRC. Overexpression of miR­20a in CRC cells decreased SMAD4 expression and decreased SMAD4­driven luciferase reporter activity. The present study revealed that miR­20a was an independent prognostic factor in CRC. Furthermore, miR­20a induced EMT and regulated migration and invasion of SW480 cells, at least in part via suppression of SMAD4 expression. The present study suggests that miR­20a may serve as a novel prognostic marker and therapeutic target for CRC.

MiR-378 is an independent prognostic factor and inhibits cell growth and invasion in colorectal cancer.

BACKGROUND: MicroRNAs(miRNAs) are small non-coding RNAs that participate in a variety of biologic processes, and dysregulation of miRNA is always associated with cancer development and progression. Aberrant expression of miR-378 has been found in some types of cancer. However, effects and potential mechanisms of miR-378 in colorectal cancer (CRC) have not been explored. METHODS: Quantitative RT-PCR was performed to evaluate miR-378 levels in CRC cell lines and 84 pairs of CRC cancer and normal adjacent mucosa. Kaplan-Meier and Cox proportional regression analyses were utilized to determine the association of miR-378 expression with survival of patients. MTT and invasion assays were used to determine the role of miR-378 in regulation of CRC cancer cell growth and invasion, respectively. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice. Luciferase assay was performed to assess miR-378 binding to vimentin gene. RESULTS: In this study, we confirmed that miR-378 significantly down-regulated in CRC cancer tissues and cell lines. Moreover, patients with low miR-378 expression had significantly poorer overall survival, and miR-378 expression was an independent prognostic factor in CRC. Over-expression of miR-378 inhibited SW620 cell growth and invasion, and resulted in down-regulation of vimentin expression. However, miR-378 knock-down promoted these processes and enhanced the expression of vimentin. In addition, we further identified vimentin as the functional downstream target of miR-378 by directly targeting the 3'-UTR of vimentin. CONCLUSIONS: In conclusion, miR-378 may function as a tumor suppressor and plays an important role in inhibiting tumor growth and invasion. Our present results implicate the potential effects of miR-378 on prognosis and treatment of CRC cancer.

Overexpression of microRNA-183 in human colorectal cancer and its clinical significance.

AIM: MicroRNA-183 (miR-183) has been shown to play a potential oncogenic role in colon cancer. The aim of this study was to evaluate the expression of miR-183 in colorectal cancer (CRC) and its potential relevance to clinicopathological characteristics and patient survival. MATERIALS AND METHODS: Surgical specimens of cancer tissue and adjacent normal mucosa were obtained from 94 patients with CRC. The relative expression levels of miR-183 in the cancer and the normal adjacent mucosa were measured by quantitative real-time PCR. We analyzed their correlation with clinicopathological parameters and prognostic value. RESULTS: The relative expression levels of miR-183 were significantly higher in CRC tissues than in the normal adjacent mucosa (P<0.001), and a high expression of miR-183 correlated with advanced clinical stage (P=0.030), lymph node metastasis (P=0.012), and distant metastasis (P=0.049). Kaplan-Meier analysis indicated that patients with high miR-183 expression had a poor overall survival (P=0.002). Moreover, multivariate analysis showed that increased expression of miR-183 was an independent predictor of overall survival. CONCLUSION: The increased expression of miR-183 is closely related to advanced clinical stage, lymph node and distant metastases, and poor prognosis of CRC, indicating that miR-183 may serve as a predictive biomarker for the prognosis or the aggressiveness of CRC.

Up-regulation of miR-224 promotes cancer cell proliferation and invasion and predicts relapse of colorectal cancer.

BACKGROUND: MicroRNAs (miRNAs) are small, non-coding RNAs that can function as oncogenes or tumor suppressors in human cancer. Abnormally expressed miR-224 was found to play a fundamental role in several types of cancer. The aim of this study was to investigate the prognostic and biological values of miR-224 in colorectal cancer (CRC). METHODS: Quantitative RT-PCR (qRT-PCR) was used to evaluate expression levels of miR-224. The postoperative survival rate was analyzed with Kaplan-Meier method. The roles of miR-224 in cell proliferation, migration and invasion were analyzed with pre-miR-224 transfected cells. In addition, the regulation of SMAD4 by miR-224 was evaluated by qRT-PCR, Western blotting and luciferase reporter assays. RESULTS: In the present study, we demonstrated that miR-224 was significantly up-regulated in CRC tissue samples and associated with disease relapse and a relative poorer disease-free survival rate. Moreover, ectopic expression of miR-224 potently promoted tumor cell proliferation, migration and invasion in vitro. Furthermore, the over-expression of miR-224 in CRC cell lines decreased SMAD4 expression at the translational level and decreased SMAD4-driven luciferase-reporter activity. CONCLUSIONS: Our data suggest that miR-224 could play an oncogenic role in the cellular processes of CRC and represent a novel biomarker for tumor relapse of CRC patients.

[Laparoscopic versus open intersphincteric resection for low rectal cancer: a clinical comparative study].

OBJECTIVE: To compare the clinical and oncological outcomes between laparoscopic and open intersphincteric resection in patients with low rectal cancer. METHODS: From January 2007 to January 2010, patients with low rectal cancer treated by laparoscopic or open intersphincteric resection were included in a retrospective comparative study. Patients were classified into laparoscopy group (n=27) and open group (n=41). The operative procedures, postoperative complications, anal function and clinicopathological data were compared. RESULTS: Compared to the open group, the laparoscopic group had longer operative time [(242.2±42.5) min vs. (199.1±44.3) min, P=0.000], less blood loss [(150.5±102.2) ml vs. (258.4±149.2) ml, P=0.002], faster recovery of bowel function [(2.9±1.1) d vs. (3.6±1.5) d, P=0.032] and resumption of regular diet [(6.6±1.2) d vs. [(7.5±1.7) d, P=0.012], and shorter postoperative hospital stay [(7.7±1.4) d vs. (9.1±2.4) d, P=0.006]. The postoperative complication rate between the laparoscopic and open groups was not significantly different [18.5% (5/27) vs. 19.5% (8/41), P=0.464]. Oncological parameters were comparable between the two groups including lymph node harvested [(14.1±4.1) vs. (16.4±6.8), P=0.113], distal resection margin [(1.4±0.7) cm vs. (1.6±0.8) cm, P=0.311], and circumferential margin [7.4% (2/27) vs. 2.4% (1/41), P=0.709]. Local recurrence rates in laparoscopic and open groups were 7.4% (2/27) and 2.4% (1/41), and distant metastasis rates were 0 and 4.9% (2/41) respectively, and the differences were not significant (both P>0.05). CONCLUSIONS: Laparoscopic intersphincteric resection possesses same efficacy of open intersphincteric resection with less blood loss, shorter recovery time and hospital stay, and similar oncological outcomes, and no increased postoperative morbidity and mortality.

Upregulation of microRNA-155 promotes the migration and invasion of colorectal cancer cells through the regulation of claudin-1 expression.

Human microRNA-155 (miR-155) has been demonstrated to regulate a variety of cellular functions, including epithelial-to-mesenchymal transition (EMT) by targeting multiple messenger RNAs (mRNAs). However, its role in colorectal cancer (CRC) remains unelucidated. Therefore, the aim of the present study was to investigate the effects of miR-155 on CRC cells. The expression level of miR-155 was quantified by quantitative real-time reverse transcriptase-PCR (qRT-PCR) in primary CRC tissues and normal adjacent mucosa. MTT, migration and invasion assays were used to examine the proliferation, migration and invasion of SW480 cells transfected with miR­155. The expression of miR-155 was significantly upregulated in the CRC tissues and the high expression of miR-155 correlated with an advanced clinical stage, lymph node and distant metastases. The ectopic expression of miR-155 enhanced the migration and invasive ability of the SW480 cells and altered their morphological appearance; however, cell proliferation was not affected. E-cadherin expression levels decreased, while ZEB1 expression levels increased in the SW480 cells overexpressing miR-155. Furthermore, the overexpression of miR-155 upregulated claudin-1 expression. Thus, our data suggest that miR-155 plays an important role in promoting CRC cell migration and invasion, at least in part through the regulation of claudin-1 expression and controlling metastasis in CRC.

High expression of ZEB1 correlates with liver metastasis and poor prognosis in colorectal cancer.

Zinc finger E-box binding homeobox 1 (ZEB1) has been shown to promote invasion and metastasis in several types of human cancer and to have a prognostic role in certain cancers. However, the clinical significance of ZEB1 in colorectal cancer (CRC) has not been sufficiently investigated. This study aimed to address this issue. In this study, we compared the expression of ZEB1 between CRC tissues and normal adjacent mucosa using quantitative real-time RT-PCR. The association of ZEB1 expression with clinicopathological characteristics was analyzed by appropriate statistical analyses. Kaplan-Meier analysis and Cox proportional hazards regression models were used to investigate the association of ZEB1 expression with survival of patients. The results showed that the relative expression levels of ZEB1 were significantly higher in CRC tissues compared to the normal adjacent mucosa and higher expression of ZEB1 correlated with liver metastasis. Kaplan-Meier analysis indicated that patients with high ZEB1 had a poor overall survival. Moreover, the multivariate analysis showed that high expression of ZEB1 was an independent predictor of overall survival. Our data indicate the potential of ZEB1 as a novel prognostic biomarker for CRC.

Plasma miR-200c and miR-18a as potential biomarkers for the detection of colorectal carcinoma.

It has been demonstrated that there are abundant stable microRNAs (miRNAs) in plasma/serum, which can be detected and are potentially disease-specific. The aim of this study was to investigate whether plasma miR-200c and miR-18a can be used as biomarkers for the detection of colorectal carcinoma (CRC). This study was divided into three parts: i) confirmation of higher miR-200c and miR-18a levels in primary CRC tissues compared to normal colorectal tissues; ii) evaluation of plasma miR-200c and miR-18a expression by comparing 78 patients with 86 healthy volunteers and iii) comparison of miR-200c and miR-18a levels in paired pre-and post-operative plasma in cancer patients who underwent curative CRC resection. Results showed that the expression of miR-200c and miR-18a was significantly higher in CRC compared to normal tissues. The plasma levels of miR-200c and miR-18a were significantly higher in CRC patients compared to controls. miR-200c yielded an area under the receiver-operating characteristics (ROC) curve (AUC) of 0.749 and miR-18a yielded an AUC of 0.804 when distinguishing CRC patients from the controls. Combined ROC analyses using the two miRNAs revealed an elevated AUC of 0.839 with 84.6% sensitivity and 75.6% specificity in discriminating CRC. Plasma levels of miR-200c and miR-18a were significantly lower in post-operative compared to pre-operative samples. The results of this study suggest that plasma miR-200c and miR-18a are significantly elevated in the plasma of CRC patients and that they may serve as non-invasive molecular markers for CRC screening.

Identification of colitis and cancer in colon biopsies by Fourier Transform Infrared spectroscopy and chemometrics.

Cancer is a disease that does great harms to the health of human beings. FT-IR spectroscopy could identify variability at the molecular level in biological specimens. It is a rapid and noninvasive method, which could be used intraoperatively to modify surgical procedures. The aim of this paper is to identify and separate cancer from colitis in endoscopic colon biopsies through the use of FT-IR spectroscopy. A total of 88 endoscopic colon samples, including 41 cases of colitis and 47 cases of colon cancer, were obtained. Specimens were placed on an ATR accessory linked to FT-IR spectrometer with a MCT detector for greater stability and sensitivity. Later, specimens were sent for the histological examination as the reference in the spectral analysis. 41 colitis and 47 cancer specimens were compared. Spectra preprocessed with smoothing and normalization were used for discrimination analysis. PCA was processed to simplify the spectrum data set. Naive Bayes classifier model was constructed for diagnostic classification. Leave-one-out cross-validation method was utilized to assess the discrimination results. The sensitivity of FT-IR detection for cancer achieves 97.6%. The results showed that colon cancer could be distinguished from colitis with high accuracy using FT-IR spectroscopy and chemometrics.

[Research on continuum power regression in noninvasive measurement of human blood glucose].

Accurate measurement of human blood glucose concentration is very significant for the treatment of diabetes. In the present paper, the method of continuum power regression can improve the predictive accuracy of noninvasive measurement of human blood glucose concentration with near infrared spectroscopy. This method is the expansion of the traditional method of partial least squares (PLS). It can achieve simpleness, and can significantly improve predictive accuracy when the power coefficient is fit. Using the method, quantitative analysis models of four ingredient experiment and noninvasive experiment of body were established, and these models can be used to predict the predictive samples. Experimental results show that compared with the PLS, the quantitative analysis models of this method not only can improve predictive accuracy, but also can set different power coefficient for different individuals to achieve the best results of models. According to different individuals, the power coefficient can be selected flexibly, which is of great value to the research on noninvasive measurement of human blood glucose concentration with near infrared spectroscopy.