Generation of an iPSC line (TSHSUi001-A) from a patient with Peutz-Jeghers syndrome due to STK11 mutation.

We established an iPSC line (TSHSUi001-A) from a patient with Peutz-Jeghers syndrome, carrying heterozygous c.290 + 1G > A mutation in STK11 gene. Peripheral blood mononuclear cells were reprogrammed using non-integrating delivery of OCT4, SOX2, KFL4, BCL-XL and c-MYC. The iPSC line expressed pluripotency markers, could differentiate into cells of three germ layers in vitro, and displayed a normal karyotype.

Predictors for Colorectal Polyps in an Asymptomatic Population Undergoing Medical Check-ups.

BACKGROUND: Colorectal cancer primarily arises from colorectal polyps. Early screening and removal is beneficial, especially in asymptomatic populations. This research aimed to reveal the risk factors detected in medical check-ups for colorectal polyps in asymptomatic people. MATERIALS AND METHODS: Clinical data of 933 asymptomatic people who underwent colonoscopies from May 2014 to December 2021 was analyzed retrospectively. Data included sex, age, colonoscopy findings, polyp pathology, polyp number, and blood test results. The distribution of colorectal lesions was analyzed. Participants were divided into control and polyp groups, adenomatous and non-adenomatous polyp groups, and single and multiple adenoma groups. RESULTS: Participants' age, proportion of males, carcinoembryonic antigen (CEA), uric acid and glycosylated hemoglobin levels were significantly higher ( P ≤0.05) in the polyp group. Age (>40 y), sex (male), and CEA level (>1.435 ng/mL) were independent risk factors for polyps. CEA, uric acid, carbohydrate antigen 19-9, triglyceride, and total cholesterol levels were significantly higher ( P <0.05) in the adenoma group than in the non-adenomatous group. CEA level (>1.435 ng/mL) was an independent predictor for adenomas ( P <0.05). Participants' age, proportion of males, CEA, glycosylated hemoglobin, and fasting blood glucose levels were significantly higher ( P <0.05) in the multiple adenoma group than in the single group; the high-density lipoprotein cholesterol level was lower ( P <0.05). No independent risk factors were found for the number of adenomas. CONCLUSIONS: Serum CEA level (>1.435 ng/mL) was independent risk factor for colorectal polyps. It may be conducive to improve discriminative ability of colorectal cancer risk stratification model.

Nanobubbles loaded with carbon quantum dots for ultrasonic fluorescence dual detection.

To increase the efficiency and accuracy of clinical tumor detection, we explored multiple imaging by preparing carbon quantum dot (CQD)-loaded nanobubbles for ultrasonic fluorescence dual detection. In this experiment, we prepared 1,2-dioleoyl3-trimethylammonium-propane chloride (DOTAP) cationic liposomes using the film dispersion method and chose perfluoropentane as the core gas material of the nanobubbles. The nanobubbles were coupled with the negatively charged CQDs through the charge effect to prepare the testing agent for two-way diagnosis with ultrasound contrast and fluorescence detection. The formulation and preparation of the loaded CQD liposome nanobubbles were screened. In vivo experiments showed that nanobubbles can be enriched to the tumor site within 5 min, which enables clearer ultrasound imaging and is conducive to tumor detection. We expect CQD-loaded liposome (Lip-CQD) nanobubbles to become a new ultrasonic contrast agent for clinical applications that can provide a basis for early tumor diagnosis and thus earlier treatment.

Betulinic acid targets drug-resistant human gastric cancer cells by inducing autophagic cell death, suppresses cell migration and invasion, and modulates the ERK/MEK signaling pathway.

The main purpose of this study was to examine the anticancer effects of betulinic acid - a plant triterpene, against gastric cancer, along with demonstrating its underlying mechanism. The MTT assay and clonogenic assays were executed to assess cellular viability in control and betulinic acid treated cells. Transmission electron microscopy and western blotting were implemented to study autophagy stimulation by betulinic acid. The ERK/MEK signaling pathway was monitored by western blotting. Migration and invasion of SGC-7901 cells was investigated via transwell chamber assay. Results of this investigation indicated that betulinic acid induced remarkable cytotoxicity against gastric cancer SGC-7901 cells, in contrast to normal gastric GES-1 cells. The cytotoxicity of betulinic acid was observed due to its autophagy stimulation tendency in target cells. Autophagic cell death was supported by the data attained from western blotting showing enhanced LC3-II, and lowered LC3-I and p62 expressions. Moreover, betulinic acid was observed to block the ERK/MEK signaling pathway in SGC-7901 cells, which was associated with declined levels of expressions of the phosphorylated ERK and MEK proteins. Finally, the transwell chamber assay revealed a potential lowering of migration and invasion by betulinic acid in the SGC-7901 cells. In conclusion, these results demonstrated that betulinic acid exhibited significant anti-gastric cancer effects mediated via autophagy induction, blocking of ERK/MEK signaling and suppression of migration and invasion. Therefore, betulinic acid may prove as a lead molecule in gastric cancer management and research.

SH3PXD2A-AS1/miR-330-5p/UBA2 ceRNA network mediates the progression of colorectal cancer through regulating the activity of the Wnt/ß-catenin signaling pathway.

Long non-coding RNAs have important roles in the occurrence and progression of various cancers. However, the molecular mechanism of lncRNAs in colorectal cancer (CRC) is not well illustrated. Thus, we used bioinformatics methods to find potential lncRNAs associated with CRC progression, and chose SH3PXD2A-AS1 as a candidate for further analysis. The roles of SH3PXD2A-AS1 in CRC cells were determined by CCK-8, transwell invasion, wound healing and flow cytometry assays. Besides, we established the CRC tumor models in nude mice to study the effect of SH3PXD2A-AS1 on the tumor growth. Based on the ceRNA hypothesis, we used miRDB and miRTarBase websites to identify the SH3PXD2A-AS1-related ceRNA regulatory network, and measured the roles of this network in CRC cells. The results revealed that the expression profiles of SH3PXD2A-AS1 from GEO and TCGA databases showed an aberrant high level in CRC tissues compared with colorectal normal tissues. SH3PXD2A-AS1 over-expression was also found in CRC cells. SH3PXD2A-AS1 knockdown inhibited the CRC cellular proliferation, invasion and migration but induced apoptosis. Besides, SH3PXD2A-AS1 knockdown also suppressed the growth of CRC tumors. Furthermore, SH3PXD2A-AS1 could function as a ceRNA of miR-330-5p. Additionally, UBA2 was proved to be a target gene of miR-330-5p. Moreover, SH3PXD2A-AS1 knockdown downregulated UBA2 expression through sponging miR-330-5p to inactivate the Wnt/ß-catenin signaling pathway, thereby inhibiting the cell growth and promoting apoptosis. Therefore, the SH3PXD2A-AS1/miR-330-5p/UBA2 network could regulate the progression of CRC through the Wnt/ß-catenin pathway. These findings offer new sights for understanding the pathogenesis of CRC and provide potential biomarkers for CRC treatment.

lncARSR sponges miR-34a-5p to promote colorectal cancer invasion and metastasis via hexokinase-1-mediated glycolysis.

Aerobic glycolysis metabolic reprogramming is one of the most important hallmarks of malignant tumors. Increasing evidence indicates that long non-coding RNAs (lncRNAs) are able to regulate glycolysis metabolic reprogramming and promote cancer progression by functioning as competing endogenous RNAs. lncARSR is a newly identified onco-lncRNA in renal cancer, but its potential role in metastatic colorectal cancer (CRC) remains unclear. Here, we analyzed specimens from 89 patients with CRC and demonstrated that lncARSR was highly expressed in CRC tissues and negatively associated with survival. Positron emission tomography-computed tomography imaging with fluoro-2-d-deoxyglucose F18 to evaluate glucose uptake showed that lncARSR expression was positively correlated with maximum standardized uptake values. Functionally, ectopic expression of lncARSR promoted the invasion, metastasis, and glycolysis metabolic reprogramming of CRC cells in vitro and in vivo, while these activities were inhibited by silencing lncARSR expression. Molecularly, lncARSR sponged miR-34a-5p and further mediated hexokinase 1 (HK1)-related aerobic glycolysis in vitro and in vivo. Clinically, high lncARSR and HK1 expression predicted poor survival of patients with CRC, especially when combined with low miR-34a-5p expression. Collectively, we identified lncARSR as an onco-lncRNA in CRC and demonstrated that the combination of lncARSR/miR-34a-5p/HK1 may be a potential prognostic biomarker of CRC.

LOC101060264 Silencing Suppresses Invasion and Metastasis of Human Colon Cancer.

BACKGROUND We explored the regulatory effects of long noncoding RNA (lncRNA) LOC101060264 silencing mediated by shRNA on invasion and metastasis of human colon cancer. MATERIAL AND METHODS Initially, 2 shRNA plasmids for LOC101060264 silencing - shRNA1 and shRNA2 - were introduced into LoVo cells. Following transfection, the expressions of LOC101060264, E-cadherin, and vimentin were determined. Next, to explore the regulatory effects of LOC101060264 silencing on cell growth, cell cycle, invasion, and migration abilities of LoVo cells, we performed MTT, flow cytometry, Transwell assay, and scratch assay, respectively. Furthermore, in nude mice with xenografted tumors, the tumor volume and weight were measured, and the expressions of PCNA, E-cadherin, vimentin, and MMP-9 in tumor tissues were determined by immunohistochemistry. RESULTS The level of E-cadherin increased and the level of vimentin decreased after LOC101060264 silencing mediated by shRNA1 and shRNA2 in LoVo cells. Silencing LOC101060264 repressed the migration, invasion, and proliferation of LoVo cells in vitro and inhibited tumor growth in nude mice in vivo. We also studied the expression of these proteins and found reduced expression of PCNA, vimentin, and MMP-9 protein, and found enhanced expression of E-cadherin protein. Moreover, the inhibitory effect of shRNA2 on the above cell behaviors was stronger than that of shRNA1. CONCLUSIONS In summary, LOC101060264 silencing decreased LoVo cell invasiveness via suppressing ETM and attenuated tumor metastasis, which provides a novel therapeutic target for patients with colon cancer.

Long non-coding RNA MBNL1-AS1 regulates proliferation, migration, and invasion of cancer stem cells in colon cancer by interacting with MYL9 via sponging microRNA-412-3p.

BACKGROUND/AIMS: Colon cancer is a common cancer that is a threat to human health. Some long non-coding RNAs (lncRNAs) have been observed to exert roles in colon cancer. Here, the current study is aimed to explore the potential mechanism of lncRNA MBNL1 antisense RNA 1 (MBNL1-AS1) in progression of colon cancer and the associated mechanisms. METHODS: Microarray analysis was performed to screen differentially expressed lncRNA and genes associated with colon cancer and its potential mechanism. The functional role of MBNL1-AS1 in colon cancer was analyzed, followed identification of the interaction among MBNL1-AS1, microRNA-412-3p (miR-412-3p), and MYL9. Subsequently, CSC viability, migration, invasion, and apoptosis were detected though a series of in vitro experiments. At last, in vivo experiments were performed to assess tumor formation of colon CSCs. RESULTS: MBNL1-AS1 and MYL9 were poorly expressed in colon cancer. MBNL1-AS1 could competitively bind to miR-412-3p so as to promote MYL9 expression. Enhancement of MBNL1-AS1 or inhibition of miR-412-3p was shown to decrease CSC proliferation, migration, and invasion but promote apoptosis. Moreover, MBNL1-AS1 reversed the CSC-like properties as well as xenograft tumor formation in vivo induced by miR-412-3p. CONCLUSION: Collectively, the present study suggests an inhibitory role of MBNL1-AS1 in colon cancer by upregulating miR-412-3p-targeted MYL9. Thus, this study provides an enhanced understanding of MBNL1-AS1 along with miR-412-3p and MYL9 as therapeutic targets for colon cancer.

Hsa_circ_0001546 acts as a miRNA-421 sponge to inhibit the chemoresistance of gastric cancer cells via ATM/Chk2/p53-dependent pathway.

Circular RNAs (circRNAs) are a new class of noncoding RNAs, play a crucial role in tumor initiation and development. Hsa_circ_0001546 is a novel circular RNA that was downregulated in gastric cancer (GC) tissues, however its function and mechanism in GC has not been studied. Our study verified that circ_0001546 was decreased in GC and correlated with the poor prognosis. Next, Pull-down assay and dual-luciferase reporter assay verified that miR-421 was a target of circ_0001546 while ATM (Ataxia telangiectasia mutated) was target by miR-421. Overexpression of circ_0001546 inhibited the proliferation and chemoresistance of HGC-27 cells, and increased the expression of ATM. In addition, circ_0001546 overexpression reversed the effect of miR-421 overexpression. What is more, circ_0001546 inhibits the chemoresistance of HGC-27 cells to L-OPH (Oxaliplatin) may through the activation of the ATM/checkpoint kinase 2 (Chk2)/p53-dependent signaling pathway. In summary, our study proved that circ_0001546 sponges miR-421 to upregulate the expression level of ATM and inhibit the proliferation and chemoresistance through the activation of the ATM/Chk2/p53-dependent pathway.

lncRNA MALAT1 overexpression promotes proliferation, migration and invasion of gastric cancer by activating the PI3K/AKT pathway.

Long non-coding RNA (lncRNA) has been implicated in various types of human cancer. However, the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in gastric cancer remains unclear. In the present study, MALAT1 expression was significantly upregulated in gastric tumors compared with adjacent healthy tissue in patients with gastric cancer. Furthermore, MALAT1 plasma expression was higher in patients with gastric cancer compared with healthy controls and was found to have prognostic and diagnostic value independent of patients' lifestyle choices. Cell proliferation assay and Transwell migration and invasion results indicated that the overexpression of MALAT1 resulted in increased proliferation, migration and invasion of gastric cancer cells in vitro, possibly through activation of the phosphoinositide 3-kinase/protein kinase B pathway.

Relationship between esophageal motility and severity of gastroesophageal reflux disease according to the Los Angeles classification.

The current study aimed to investigate the relationship between the severity of gastroesophageal reflux disease (GERD) according to the Los Angeles (LA) classification and esophageal motility using high-resolution manometry (HRM) and 24-hour esophageal pH monitoring.We examined 124 patients with GERD from January 2016 to June 2018. The LA classification of each patient was determined by endoscopy. HRM was performed by the intraluminal water infusion method. HRM and 24-hour esophageal pH monitoring parameters of the patients were studied and statistically compared.On HRM examination, GERD symptoms were found to be associated with worsened distal contractile integral (DCI), ineffective esophageal motility (IEM), peristalsis break (PB), lower esophageal sphincter (LES) pressure, and the 4-second integrated relaxation pressure (IRP4s) of LES pressure along with the grade of LA classification, especially in patients having grade C and D GERD who had transverse mucosal breaks. The 24-hour pH monitoring study revealed that patients classified as having grade C or D GERD had an esophageal pH < 4.0 for a longer time than those with grade O, A, or B GERD. Similar results were found regarding the duration of the longest reflux event, the number of reflux episodes longer than 5 minutes, and the number of reflux episodes. Patients with higher grade esophagitis had higher De Meester scores, which suggested greater esophageal acid exposure. Hiatal hernia (HH) was more closely related to LES pressure, IRP4s, and acid exposure, whereas DCI, IEM, and PB were not statistically different between patients with GERD with and without HH.Patients with severe esophagitis may have motor dysfunction not only in the LES but also in the esophageal body, with resulting increased esophageal acid exposure, which causes esophagitis. Low LES pressure might be the main reason that patients with HH develop esophagitis. GERD without HH may be due to a variety of motor dysfunctions.

Synchronous Neoplastic Lesions In Referred Patients With Colorectal Cancer: A Retrospective Cohort Study.

BACKGROUND: Synchronous neoplastic lesions are usually present in patients with colorectal cancer (CRC) at diagnosis or postoperative follow-up endoscopy. However, few studies have been published about the clinicopathological features of synchronous lesions, especially those of synchronous advanced neoplasia. This study aimed to describe synchronous lesions in patients with CRC because this knowledge may be useful for preventing the development of metachronous cancer. MATERIAL AND METHODS: We retrospectively reviewed 261 primary CRC cases with synchronous lesions referred to our hospital during a 4-year period. Personal history, habits, family history, characteristics of index cancer, and synchronous lesions were assessed. RESULTS: In total, the 261 patients with CRC had 812 synchronous adenomas and 146 advanced neoplasia. Diminutive, small, and large polyps made up 66.7%, 20.2%, and 13.1% of all lesions, respectively; 9.3% of diminutive and small adenomas were advanced neoplasia, and 45.2% of synchronous advanced lesions were subcentimeter polyps. Both synchronous non-advanced lesions and advanced lesions developed most frequently in the distal colon, followed by the proximal colon, and were least frequently found in the rectum (P < 0.001). Older age (P = 0.04) and male gender (P = 0.001) were associated with the presence of advanced neoplasia in CRC cases with synchronous neoplastic lesions. Meanwhile, the use of aspirin may be associated with a lower incidence of advanced neoplasia (P = 0.04). CONCLUSION: Patients diagnosed with CRC require detailed clearing of the remainder of the colon at baseline coloscopy or postoperative follow-up examination, and we should take a more cautious approach to synchronous subcentimeter polyps in this group of patients.

Overexpression of miR-21-5p promotes proliferation and invasion of colon adenocarcinoma cells through targeting CHL1.

BACKGROUND: This study aims to investigate the effect of miR-21-5p on process of colon adenocarcinoma (COAD) cells and its connection with neural cell adhesion molecule L1 (CHL1). METHODS: Different expressions of mRNAs and miRNAs were calculated with microarray analysis. QRT-PCR and western blot were performed to quantify miR-21-5p and CHL1 expression. Flow Cytometry, MTT assay, colony formation assay, transwell assay and ELISA were performed to evaluate propagation and invasiveness of COAD cells. Dual luciferase reporter assay was employed to scrutinize the relationship between miR-21-5P and CHL1. We performed in vivo experiment to detect the impact of miR-21-5p and CHL1 on COAD tumor growth. RESULTS: Expression level of miR-21-5p increased in both COAD tissues and cells. MTT and Cell cycle assay showed that overexpression of miR-21-5p accelerated proliferation of COAD cells. Transwell assay indicated that miR-21-5p promoted cell invasion. The result of dual luciferase reporter assay indicated that miR-21-5p targeted CHL1 directly and inhibited its expression. The result of in vivo experiments showed that down-regulation of miR-21-5p decreased the volume and weight of tumor, while knockdown of CHLI stimulated tumor growth. CONCLUSIONS: The overexpression of miR-21-5p can promote propagation and invasiveness of COAD cells through inhibiting the expression of CHL1.

Comparison of Esophageal Function Tests to Investigate the Effect of Helicobacter Pylori Infection on Gastroesophageal Reflux Disease (GERD).

BACKGROUND The effects of Helicobacter pylori (H. pylori) infection on gastroesophageal reflux disease (GERD) remain unclear. The aim of this study was to compare the results of clinical esophageal function tests and the effect of H. pylori infection on GERD. MATERIAL AND METHODS A prospective clinical study included 124 patients diagnosed with GERD (four grades). H. pylori infection was determined by gastroscopy and a rapid urease test (RUT) to divide patients into an HP-positive and an HP-negative group. Esophageal function tests included high-resolution manometry (HRM), peristalsis break (PB), and 24-hour pH monitoring (composite pH DeMeester score). Different grades of GERD, with and without H. pylori infection, esophageal function test results were analyzed. RESULTS The HP-positive group, compared with the HP-negative group with GERD, showed a significantly reduced median PB value (3.41±3.65 vs. 6.18±5.27), reduced PBs >5 cm per ten swallows (2.23±3.05 vs. 4.04±3.70) indicating that that H. pylori infection improved esophageal peristalsis. During 24-hour esophageal pH monitoring, the HP-positive group showed a significantly reduced percentage of time for esophageal pH <4.0, number of reflux events >5 min, and number of reflux episodes in 24 hours, compared with the HP-negative group. The DeMeester score was significantly increased in the HP-negative group, indicating a higher esophageal acid exposure (9.11±8.15 vs. 24.30±30.27). CONCLUSIONS H. pylori infection improved esophageal peristalsis, enhanced lower esophageal sphincter (LES) pressure, and reduced esophageal acid exposure, which might be protective factors for GERD.

WITHDRAWN: Serum miR-106b upregulation predicts poor prognosis in patients with colorectal cancer.

Ahead of Print article withdrawn by publisher.

Serum miR-106b upregulation predicts poor prognosis in patients with colorectal cancer.

Colorectal cancer (CRC) is one of most common cancers and a leading cause of cancer-related death around the world. Identification of reliable biomarkers contributes to facilitate disease detection of this malignancy. This study aimed to explore the serum miR-106b expression in CRC and its potential clinical significance. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure the miR-106b expression levels in the serum from 122 CRC patients, 40 advanced adenomas and 50 healthy individuals. Serum miR-106b levels were significantly increased in CRC patients compared to healthy controls. Elevated serum miR-106b expression occurred more frequently in CRC patients with lymph node metastasis and distant metastasis. Moreover, receiver operating characteristic (ROC) curve analysis revealed that serum miR-106b could well discriminate CRC patients from healthy controls. In addition, miR-106b levels were greatly reduced in post-operative samples from CRC cases with early clinical stage. Furthermore, increased miR-106b expression was positively correlated with aggressive clinical variables and poor prognosis. Finally, serum miR-106b was identified as an independent prognostic predictor for CRC. Collectively, our findings suggest serum miR-106b might potentially serve as a promising biomarker in the diagnosis and prognosis of CRC.

MiR-181b regulates steatosis in nonalcoholic fatty liver disease via targeting SIRT1.

Non-alcoholic fatty liver diseases (NAFLD) is one of the leading cause of chronic liver diseases in the world. However, the pathogenesis of NAFLD is still unclear. Emerging studies have demonstrated that microRNAs (miRs) are profoundly involved in NAFLD and related metabolic diseases. Here, we investigated the mechanisms by which miR-181b influences NAFLD via direct targeting SIRT1. The expression of miR181b was up-regulated while SIRT1 was down-regulated in both human NAFLD patients and high fat diet (HFD) induced NAFDL mice model. And palmitic acid (PA) treatment increased the miR-181b expression while decreased SIRT1 expression in HepG2 cells. Further, we identified that SIRT1 is a direct downstream target of miR-181b. Ectopic expression of miR-181b significantly repressed the 3'-UTR reporter activities of SIRT1 in a dose-dependent manner, while the effect of miR-181b was interrupted when the binding site of miR-181b within the SIRT1 3'-UTR was mutated. And overexpression of miR-181b reduced both the mRNA and protein levels of SIRT1 in HepG2 cells. We also found that inhibition of miR-181b expression alleviates hepatic steatosis both in vitro and in vivo. And the effect of miR-181b on steatosis was blocked by SIRT1 overexpression. Taken together, our data indicated that increased expression of miR-181b potentially contributes to altered lipid metabolism in NAFLD. Downregulation of miR-34a may be a therapeutic strategy against NAFLD by regulating its target SIRT1.

Detection Rate, Anatomic Sites, and Pathologic Types of Colorectal Cancer During Colonoscopy Procedures.

PURPOSE: This study aims to help physicians obtain the detection rate and colonoscopic information of colorectal cancer (CRC) among patients in a city in China. METHODS: A total of 15,189 participants who underwent total colonoscopy between January 2000 and December 2015 were studied. A total of 1022 CRCs were diagnosed. We analyzed the detection rate, anatomic sites, and pathologic types among different sex, age, and decade groups. Moreover, we investigated the corresponding relationships between the anatomic sites and the pathologic types. RESULTS: Colonoscopic examinations revealed that the risk for CRC between men and women showed no significant difference (6.97% vs. 6.42%). The detection rate of CRC significantly increased with age (2.08% vs. 5.95% vs. 15.09%). The proportion of poorly differentiated adenocarcinoma among the youth group was significantly higher than that in the other age groups (25.0% vs. 11.54% vs. 8.33%). However, the numbers of cases with well-differentiated and moderately differentiated adenocarcinoma observed in the old-aged group were higher than other age groups. This finding demonstrated that the differentiation degree of adenocarcinoma increased with the age. Neuroendocrine tumor was mainly located in the rectum (95.0%), and appeared more frequently among the youth group (7.5% vs. 1.48% vs. 1.06%). CONCLUSIONS: We found the detection rate of CRC varied in terms of sex and decade. The CRC cases in the youth group exhibited a high malignant degree. The most common anatomic site was rectum, so we should focus more on digital rectal examination.

Outcome Analyses of 15,189 Screenings Via Colonoscopy.

PURPOSE: This study investigated the detection rates of common colorectal diseases during colonoscopy procedures to provide reference for clinical diagnoses in China. METHODS: A total of 15,189 participants, who underwent total colonoscopy, were studied. We analyzed the detection rates of common colorectal diseases in different sex, age, and decade groups. RESULTS: The most common indication for colonoscopy is abdominal pain followed by change in bowel habits. Among the 15,189 participants, 5658 cases (37.25%) were normal. The most common positive finding was colorectal polyp (27.32%) followed by nonspecific colitis (12.06%), colorectal cancer (CRC) (7.71%), and ulcerative colitis (4.64%). The frequencies of polyp (31.56% vs. 21.99%; P=0.000) and CRC (8.28% vs. 7.00%; P=0.004) were higher in males than in females. By contrast, ischemic colitis (0.08% vs. 0.31%; P=0.001) and melanosis coli (1.15% vs. 1.87%; P=0.000) were more seen in females than in males. In addition, the detection rates for CRC (2.42% vs. 7.18% vs. 16.67%; P=0.000), colorectal polyp (17.65% vs. 32.27% vs. 34.73%; P=0.000), ischemic colitis (0.09% vs. 0.19% vs. 0.32%; P=0.033), and melanosis coli (0.71% vs. 1.09% vs. 3.21%; P=0.000) increased with age. CONCLUSIONS: The frequent positive findings were colorectal polyp, nonspecific colitis, and CRC. Patients showing alarming symptoms definitely require colonoscopy. The detection rates for colorectal polyp and melanosis coli were significantly higher in the later decade, so we should focus on these deseases.

FRAT1 expression regulates proliferation in colon cancer cells.

Colorectal cancer is one of the most common gastric malignancies worldwide. However, the underlying mechanism of colon cancer development and valuable indicators of the disease remain unclear. In this study, the expression of frequently rearranged in advanced T-cell lymphomas 1 (FRAT1) in colon cancer was investigated and the association between FRAT1 expression and biological properties of tumors was analyzed. A total of 147 colon cancer tissue samples and adjacent normal tissues were collected between January 2013 and June 2014. The FRAT1 gene and protein expression levels were analyzed in tissues with different TNM and pathological stages. Small hairpin RNAs (shRNAs) containing the human FRAT1 gene were constructed and transfected into colon cancer HT-29 cells. The proliferation and migration of the cells was also analyzed in relation to a reduction in FRAT1 expression. In colon cancer tissues, the expression of FRAT1 was significantly higher when compared with adjacent tissues. In addition, FRAT1 expression was found to positively correlate with the degree of tumor malignancy, and this difference was determined to be statistically significant (P<0.05). Following shRNA transfection in HT-29 cells to decrease the expression of FRAT1, the proliferation and migration of the HT-29 cells decreased (due to conversion of the shRNA into small interfering RNA). These results indicate that in colon cancer, FRAT1 may present a novel tool for analyzing the tumor progression and may be a novel therapeutic target for the treatment of colon cancer.