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Background Protective loop ileostomy is commonly performed in laparoscopic low anterior rectal resection to prevent the serious complications of anastomotic fistula. It is usually created at the right lower quadrant of the abdomen and another wound is required for stoma. The study aimed to evaluate the outcomes of ileostomy at the specimen extraction site (SES) and another site (AS) beside the auxiliary incision. Methods A retrospective analysis was conducted on 101 eligible patients with pathologically diagnosed adenocarcinoma of the rectum from January 2020 to December 2021 in the study center. According to whether the ileostomy was at the specimen extraction site, patients were divided into SES group (40 patients) and AS group (61 patients). Clinicopathological characteristics, the intraoperative details, and postoperative outcomes of the two groups were measured. Results Univariate analysis showed that the operative time was significantly shorter and the blood loss was significantly less in the SES group than in the AS group during laparoscopic low anterior rectal resection, the time to first flatus was significantly shorter, and the pain was significantly less in the SES group than in the AS group during ileostomy closure. The postoperative complications were similar in both groups. Multivariable analysis showed that ileostomy at the specimen extraction site was a significant factor influencing the operative time and blood loss of rectal resection, and influencing the pain and the time to first flatus during ileostomy closure. Conclusion Compared to ileostomy at AS, protective loop ileostomy at SES was time-saving and less bleeding during laparoscopic low anterior rectal resection, and more quick to first flatus and less pain during stoma closure, and did not lead to more postoperative complications. The median incision of the lower abdomen and the left lower abdominal incision were both good sites for ileostomy.

The treatment of gastric cancer (GC) is extremely challenging; however, the specific pathogenesis of GC remains unclear. Circular RNAs (CircRNAs) are non-coding RNAs that can regulate gene expression both transcriptionally and post-transcriptionally. However, little is known about the circRNAs that are important in the progression of GC. This study identified significantly dysregulated circRNAs by analyzing gastric cancer patients and normal control tissues. The target gene was predicted using online bioinformatics tools and verified using RNA pull-down and luciferase reporter assays. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to evaluate gene and protein expression. The malignant behavior of GC cells was determined using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, wound healing assay, Transwell invasion assay, and flow cytometry. CircPFKP is downregulated in GC tissues, and overexpression of circPFKP inhibits malignant behavior in GC cells. Bioinformatics predicted that circPFKP could bind to miR-644, and miR-644 could target disintegrin-like and metalloprotease domain-containing thrombospondin type 1 motif-like 5 (ADAMTSL5). Overexpression of circPFKP enhances the expression of ADAMTSL5 by decreasing the expression of miR-644 to suppress the growth of xenograft GC tumors in vivo and in vitro. In conclusion, the circPFKP/miR-644/ADAMTSL5 regulatory pathway inhibited the malignant progression of GC. These findings may extend our understanding of the effects of circRNAs on cancer development and provide novel targets for the diagnosis of GC.

Insulin resistance (IR) is the most common pathophysiological change in patients with type 2 diabetes mellitus (T2DM). Several recent studies have suggested that the gut microbiome and microbial metabolites are involved in the pathogenesis of IR. Bariatric surgery, as an effective treatment for T2DM, can markedly alleviate IR through mechanisms that have not been elucidated. In this review, we summarize the current evidence on the changes in the gut microbiome and microbial metabolites (including lipopolysaccharide, short-chain fatty acids, branched-chain amino acids, aromatic amino acids, bile acids, methylamines, and indole derivatives) after bariatric surgery. Additionally, we discuss the mechanisms that correlate the changes in microbial metabolites with the postoperative alleviation of IR. Furthermore, we discuss the prospect of bariatric surgery as a treatment for T2DM.

Protective loop ileostomy is widely performed during rectal resection surgery. The study aimed to introduce the one-stitch method (OM) of protective loop ileostomy in laparoscopic low anterior resection and compare this new method with the traditional method (TM).A retrospective analysis was conducted on 109 patients with pathologically diagnosed adenocarcinoma of the rectum from January 2017 to December 2018 in the study centre, and the intraoperative details and postoperative outcomes of the two groups were measured.A total of 95 patients were included: 54 underwent protective loop ileostomy with the TM, while 41 underwent surgery utilizing the OM. Univariate analysis demonstrated that the operative times of resection and closure were significantly shorter (resection, 200.0 vs. 227.5 min, P = 0.028; closure, 70.0 vs. 92.5 min, P = 0.018) and the peristomal adhesions during closure were milder (P = 0.007) in the OM group than in the TM group. The postoperative complications were similar in both groups. In multivariate analysis, the OM (OR 0.352, 95% CI = 0.155-0.799, P = 0.013) was a significant factor influencing the operative time of resection. The peristomal adhesion extent was the only independent risk factor for the stoma closure time (mild, OR 0.036, 95% CI = 0.010-0.129, P 0.001; moderate, OR 0.128, 95% CI = 0.033-0.494, P = 0.003). No significant predictive factor of peristomal adhesion extent was identified in multivariable analysis.The OM of protective loop ileostomy in laparoscopic low anterior resection was time-saving, simple and easy to popularize and did not lead to more postoperative complications than the TM.

Genome-wide association studies of colorectal cancer (CRC) have identified two risk SNPs. The characterization of these risk regions in diverse racial groups with different linkage disequilibrium structure would aid in localizing the causal variants. Herein, fine mapping of the established CRC loci was carried out in 1,508 cases and 1,482 controls obtained from the Han Chinese population. One distinct association signal was identified at these loci, where fine mapping implicated rs1010208 as a functional locus. Next, the candidate target genes of functional SNP rs1010208 were analyzed using data from TCGA databases by expression quantitative trait loci analysis method; the data from Peking University People's Hospital were utilized for verification. The dual-luciferase reporter system analysis confirmed that rs1010208 is a regulatory region that can be mutated to decrease the expression of HINT1, resulting in proliferation and invasiveness of CRC.

Integrative expression Quantitative Trait Loci (eQTL) analysis found that rs8180040 was significantly associated with Coiled-coil domain containing 12 (CCDC12) in colon adenocarcinoma (COAD) patients. Immunohistochemical staining and western blotting confirmed CCDC12 was highly expressed in COAD tissues, which was consistent with RNA-Seq data from the TCGA database. Knockdown of CCDC12 could significantly reduce proliferation, migration, invasion, and tumorigenicity of colon cancer cells, while exogenous overexpression of CCDC12 had the opposite effect. Four plex Isobaric Tags for Relative and Absolute Quantitation assays were performed to determine its function and potential regulatory mechanism and demonstrated that overexpression of CCDC12 would change proteins on the adherens junction pathway. Overexpressed Snail and knocked down CCDC12 subsequently in SW480 cells, and we found that overexpression of Snail did not significantly change CCDC12 levels in SW480 cells, while knockdown of CCDC12 reduced that of Snail. CCDC12 plays a significant role in tumorigenesis, development, and invasion of COAD and may affect the epithelial to mesenchymal transformation process of colon cancer cells by regulating the Snail pathway.

Background: To determine the role of Coiled-coil domain containing 12 (CCDC12) in colon adenocarcinoma (COAD).Methods: We used integrative expression Quantitative Trait Loci (eQTL) analysis to identify risk single nucleotide polymorphisms (SNPs) and associated genes. Immunohistochemical staining (IHC) and western blotting (WB) were used to detect CCDC12 expression. We selected SW480 and LOVO cell lines to knock down CCDC12, while HCT116 and SW480-KD cell lines were up-regulated. Then performed functional studies and established a xenograft tumor model in BALB/c mice. Four plex Isobaric Tags for Relative and Absolute Quantitation (iTRAQ) assays were performed to determine its function and potential regulatory mechanism. Overexpressed Snail and knocked down CCDC12 subsequently in SW480 cells to find them association.Results: Integrative eQTL analysis found that rs8180040 was significantly associated with CCDC12 in COAD patients. IHC and WB confirmed CCDC12 was highly expressed in COAD tissues (IHC 51/75 vs 8/75, WB 10/12 vs 2/12). This was consistent with RNA-Seq data from TCGA database (P value < 0.001). Knockdown of CCDC12 could significantly reduce proliferation, migration, invasion and tumorigenicity of colon cancer cells, while exogenous overexpression of CCDC12 had the opposite effect. iTRAQ assays demonstrated that overexpression of CCDC12 would change proteins on adherens junction pathway. Overexpression of Snail did not significantly change CCDC12 levels in SW480 cells, while knock down of CCDC12 reduced that of Snail.Conclusions: CCDC12 plays a significant role in tumorigenesis, development and invasion of COAD and may affect the epithelial to mesenchymal transformation process of colon cancer cells by regulating the Snail pathway.

Background: Many complications are frequently reported in the carbon dioxide pneumoperitoneum surgery, except hyperamylasemia occurring in pancreas.Methods: Using data from 380 patients with colorectal cancer registered for a prospective cohort study comparing postoperative serum amylase level, risk factors for postoperative hyperamylasemia and surgical complications were identified by multivariate logistic regression analysis.Results: Hyperamylasemia occurred in 140 patients, and a total of 52 patients in 380 patients had short-term postoperative complications, including 25 patients with hyperamylasemia in which 2 patients with acute pancreatitis. The method of operation, injury of pancreas during operation, the duration of pneumoperitoneum and intraoperative blood loss were significant predictors of hyperamylasemia. However, the economic significance of this phenomenon is not certain.Conclusion: High incidence of hyperamylasemia in laparoscopy-assisted surgery for colorectal cancer, the incidence of postoperative infectious complications will increase significantly. Surgical treatment of rectal cancer, operation around the pancreas, intraoperative blood loss, duration of pneumoperitoneum should be considered when planning surgery. Although patient’s hospital cost and postoperative hospital stay were well documented, it is unclear whether this is of any economic significance.Trial registration: The study was registered with the China Clinical Trial Registry with registration number ChiCTR1800015311 and was registered on March 22, 2018.

Colorectal cancer (CRC) is the third most common cancer worldwide and its treatment remains a challenge. Effective control of cell survival and proliferation is critical in the prevention of oncogenesis and successful treatment of cancer. Long non-coding RNAs (lncRNAs) have emerged as primary regulators of carcinogenesis. Growth arrest specific 5 (GAS5), a lncRNA, is known to be aberrantly expressed in several types of cancer, however, the role of GAS5 in CRC remains unclear. In the present study, GAS5 mRNA expression was measured in CRC and adjacent normal mucosa tissue samples from 53 patients using reverse transcription-quantitative polymerase chain reaction analysis, in addition to seven CRC cell lines. GAS5 mRNA expression was observed to be markedly downregulated in human CRC tissues and cell lines. Decreased GAS5 expression was associated with an increase in tumor diameter [odds ratio (OR), 0.176 (95% CI, 0.053–0.586); P=0.003] and later tumor-node-metastasis stage [OR, 0.261 (95% CI, 0.083–0.819); P=0.019]. Patients with decreased GAS5 expression exhibited decreased overall survival rates compared with patients with increased GAS5 expression (P=0.015). The Cox proportional hazards model demonstrated that downregulated GAS5 expression was an independent prognostic factor for CRC (hazard ratio, 0.236; 95% confidence interval, 0.067–0.827; P=0.024). Functional assays demonstrated that overexpression of GAS5 inhibited cell proliferation and survival, and induced G0/G1 cell cycle arrest and apoptosis; however, knockdown of GAS5 expression enhanced cell proliferation, and reduced G0/G1 arrest and apoptosis. In conclusion, the results of the present study suggest that GAS5 is essential in the control of apoptosis and cell growth in CRC. Therefore, GAS5 may represent a novel prognostic and diagnostic marker of CRC, in addition to being a potential therapeutic target.

The progression of distant metastasis cascade is a multistep and complicated process, frequently leading to a poor prognosis in cancer patients. Recently, growing evidence has indicated that deregulation of microRNAs (miRNAs) contributes to tumorigenesis and tumor progression in colorectal cancer (CRC). In the present study, by comparing the miRNA expression profiles of CRC tissues and corresponding hepatic metastasis tissues, we established the downregulation of miR-199b in CRC metastasis tissues. The decrease in miR-199b expression was significantly correlated to late TNM stage and distant metastasis. Moreover, Kaplan-Meier curves showed that CRC patients with high expression level of miR-199b had a longer median survival. Functional assays results indicated that the restoration of miR-199b considerably reduced cell invasion and migration in vitro and in vivo, and increased the sensitivity to 5-FU and oxaliplatin. Further dual-luciferase reporter gene assays revealed that SIRT1 was the direct target of miR-199b in CRC. The expression of miR-199b was inversely correlated with SIRT1 in CRC specimens. SIRT1 knockdown produced effects on biological behavior that were similar to those of miR-199b overexpression. Furthermore, through Human Tumor Metastasis PCR Array we discovered KISS1 was one of the downstream targets of SIRT1. Silencing of SIRT1 upregulated KISS1 expression by enhancing the acetylation of the transcription factor CREB. The latter was further activated via binding to the promoter of KISS1 to induce transcription. Thus, we concluded that miR-199b regulates SIRT1/CREB/KISS1 signaling pathway and might serve as a prognosis marker or a novel therapeutic target for patients with CRC.

It is not known whether low-dose radioiodine is as effective as high-dose radioiodine for treating patients with differentiated thyroid cancer after surgery. This study compared ablation success rates of different doses of radioiodine in patients with differentiated thyroid cancer after thyroidectomy. Fifteen randomized controlled trials were obtained from PubMed, Embase, and Cochrane Library (1966 to February 2013). Stata version 12.0 was used to pool the outcomes. Mantel-Haenszel (MH) and inverse variance (IV) methods were used in a fixed-effects and random-effects model, respectively. The relative risk (RR) with 95% confidence interval (CI) was used to compare the success rates of different doses of radioiodine. There were a total of 3,046 patients. The pooled RR for comparing ablation success with low- and high-dose radioiodine was 0.90 (95% CI 0.83-0.98, IV). Excluding a study with a distinctive outcome, sensitivity analysis showed that the pooled RR was 0.95 (95% CI 0.92-0.99, MH). In subgroup analysis, the pooled RR of three studies that only administrated radioiodine to patients with pT2-4 cancer was 0.93 (95% CI 0.83-1.04, MH); the pooled RR of five studies with total thyroidectomy for all patients was 0.96 (95% CI 0.92-1.00, MH); and the pooled RR of four studies that used thyrotropin α to stimulate serum thyrotropin was 0.96 (95% CI 0.90-1.02, MH). The pooled RRs for comparing ablation success for moderate-dose versus high-dose and low-dose radioiodine were 0.94 (95% CI 0.85-1.04, IV) and 0.87 (95% CI 0.73-1.04, IV), respectively. Low-dose radioiodine can be used in patients undergoing total thyroidectomy. For those who receive insufficient surgical treatment, high-dose radioiodine is more appropriate.

The AJCC seventh edition TNM classification for gastric cancer was released in 2010 and included major revision. Large-volume gastric cancer centers have evaluated the prognostic significance of the new system and obtained paradoxical results. The authors performed a meta-analysis of these studies to evaluate the new classification. Fifteen eligible studies with 38,972 patients were included in the analysis. Hazard ratios (HRs) and associated 95 % confidence intervals were extracted from identified studies. The primary outcome was overall survival. The HRs for the seventh edition T classification and N classification were found to increase steadily and reasonably. The cumulative survival rates of the seventh edition subgroups of T classifications demonstrated obvious differences; meanwhile, the differences between subgroups of N classifications including N3a and N3b categories were also significant. The 5-year survival rates according to the seventh edition TNM staging system were 94.71 % (stage IA), 88.72 % (stage IB), 80.45 % (stage IIA), 67.24 % (stage IIB), 53.68 % (stage IIIA), 37.56 % (stage IIIB), and 21.26 % (stage IIIC), respectively. The results of this study indicate that the seventh edition of the TNM classification was considered valid, although further evaluation was needed for N3a and N3b categories.

To evaluate the prognostic value and staging accuracy of the metastatic lymph node ratio (rN) staging system for colorectal cancer. A total of 1,127 patients with colorectal cancer who underwent curative surgery between 2000 and 2011 at our institute were analyzed. Lymph nodes status was assigned according to American Joint Committee on Cancer (AJCC) pN system and rN system. Patients with colon cancer (group 1, n = 652) and rectal cancer (group 2, n = 475) were analyzed separately. The rN staging system was generated using 0.2 and 0.6 as the cutoff values of lymph node ratio and then compared with AJCC pN stages. Linear regression model revealed that the number of retrieved lymph node was related to number of metastatic lymph nodes. After a median follow-up of 46 months, the 5-year survival rates of patients with more than 12 lymph nodes (LNs) retrieved were better than cases with fewer than 12 LNs, while the differences were not obvious in rN classification. The rN category is a better prognostic tool than the AJCC pN category for colorectal cancer patients after curative surgery.

To evaluate the prognostic significance of the seventh edition TNM staging classification for gastric cancer.The seventh edition TNM staging system for gastric cancer was adopted by the American Joint Committee on Cancer/International Union Against Cancer on January 1, 2010, and included major revisions.The authors analyzed data retrospectively collected on patients with gastric cancer who underwent surgery at the Affiliated Hospital of Qingdao University Medical College between 2000 and 2008. A total of 964 patients with gastric cancer who underwent R0 surgical resection were included.The relative risk (RR) for the seventh edition T classification was found to increase steadily and reasonably compared with the sixth edition. However, the RR for the sixth edition N classification was found to increase steadily and reasonably compared with the seventh edition classification. Cox regression multivariate analysis showed that the sixth edition N classification was superior to the seventh edition N classification as an independent prognostic factor. In survival analysis, the seventh edition TNM classification provided a more detailed classification; however, some subgroups of the seventh edition TNM classification did not demonstrate significantly different survival rates. The combination of the seventh edition T classification and the sixth edition N classification, with ideal RR results, showed significantly different survival rates except for IA and IB.The combination of the seventh edition T classification and the sixth edition N classification seems to provide the optimal prognosis.

To evaluate the prognostic value and staging accuracy of the metastatic lymph node ratio (rN) staging system for gastric cancer.A total of 1,075 patients with gastric cancer who underwent curative surgery between 2000 and 2009 at our institute were analyzed. Lymph node status was assigned according to the American Joint Committee on Cancer (AJCC) pN system and rN system. Patients with15 (group 1, n = 691) and ≤15 lymph nodes (group 2, n = 384) retrieved were analyzed separately.The rN staging system was generated using 0.2 and 0.5 as the cutoff values of lymph node ratio and then compared with AJCC pN stages. A linear regression model revealed that the number of retrieved lymph nodes was related to the number of metastatic lymph nodes, but not with rN. After a median follow-up of 47.66 months, the 5-year survival rates of N0, N1, N2, and N3 patients of group 1 were significantly better than group 2, whereas the differences were not obvious in the rN classification.The rN category is a better prognostic tool than the AJCC pN category for gastric cancer patients after curative surgery regardless of the number of lymph node examined.

Tumor growth cascade is a complicated and multistep process with numerous obstacles. Until recently, evidences have shown the involvement of microRNAs (miRNAs) in tumorigenesis and tumor progression of various cancers, including colorectal cancer (CRC). In this study, we explored the role of miR-194 and its downstream pathway in CRC. We acquired data through miRNA microarray profiles, showing that the expression of miR-194 was significantly suppressed in CRC tissues compared with corresponding noncancerous tissues. Decreased miR-194 expression was obviously associated with tumor size and tumor differentiation, as well as TNM stage. Both Kaplan–Meier and multivariate survival analysis showed that downregulated miR-194 was associated with overall survival. Moreover, functional assays indicated that overexpression of miR-194 in CRC cell lines inhibited cell proliferation both in vitro and in vivo. In addition, using dual-luciferase reporter gene assay, we found MAP4K4 was the direct target of miR-194. Silencing of MAP4K4 resulted in similar biological behavior changes to that of overexpression of miR-194. We also observed through Human Gene Expression Array that MDM2 was one of the downstream targets of MAP4K4. Knockdown of MAP4K4 downregulated MDM2 expression through transcription factor c-Jun binding to the −1063 to -1057 bp of the promoter. These results suggest that miR-194, regulating the MAP4K4/c-Jun/MDM2 signaling pathway, might act as a tumor suppressor and serve as a novel target for CRC prevention and therapy.

Although genome-wide association studies have identified many risk loci associated with colorectal cancer, the molecular basis of these associations are still unclear. We aimed to infer biological insights and highlight candidate genes of interest within GWAS risk loci. We used an in silico pipeline based on functional annotation, quantitative trait loci mapping of cis-acting gene, PubMed text-mining, protein-protein interaction studies, genetic overlaps with cancer somatic mutations and knockout mouse phenotypes, and functional enrichment analysis to prioritize the candidate genes at the colorectal cancer risk loci. Based on these analyses, we observed that these genes were the targets of approved therapies for colorectal cancer, and suggested that drugs approved for other indications may be repurposed for the treatment of colorectal cancer. This study highlights the use of publicly available data as a cost effective solution to derive biological insights, and provides an empirical evidence that the molecular basis of colorectal cancer can provide important leads for the discovery of new drugs.

The aim of this study was to identify the best cutoff points for lymph node classification to improve the prognostic prediction of gastric cancer in China. Patients who had undergone surgery for gastric cancer were retrospectively evaluated in two high-volume institutions from Peking University People’s Hospital (PKUPH, N = 503) and Affiliated Hospital of Qingdao University (AHQU, N = 1,003). The prognosis of these patients was assessed according to the number of metastatic lymph nodes with an increment of one node at one time. A new lymph node classification was proposed based on the relation between prognosis and the number of metastatic lymph nodes. According to the prognostic value, the proposed node (N) stage was categorized as N0 (no regional LNs metastasis), N1 (1–3 involved regional LNs), N2 (4–6 involved regional LNs), and N3 (≥7 involved regional LNs). The hazard ratio for the proposed N classification increased steadily and reasonably compared with the 7th edition. Moreover, the Cox regression multivariate analysis showed that the proposed N classification was superior to the 7th N classification as an independent prognostic factor. The proposed N category was superior to 7th edition N category of the American Joint Committee on Cancer (AJCC) for assessing the prognosis for gastric cancer patients in China.

Genome-wide association studies have identified many risk loci associated with colorectal cancer. Strategies integrating biological data sets with GWAS results will provide insights into the roles of risk single-nucleotide polymorphisms. We performed expression quantitative trait locus-based analyses using the information provided in The Cancer Genome Atlas. Analysis of the cis-expression quantitative trait loci (eQTLs) of 18 previously reported colorectal cancer risk loci resulted in the discovery of five variants that were significantly associated with gene expressions. Analysis of the trans-eQTLs identified three risk loci that affect the expression levels of a neighboring transcription factor, MYC. These findings provide a more comprehensive picture of gene expression determinants in colorectal cancer and insights into the underlying biology of risk loci.

Sirtuin 1 (SIRT1) has been reported to have diverse roles in various biological processes through deacetylation of histone and nonhistone proteins. However, the correlations among SIRT1 protein expression, clinicopathological parameters, and survival of colorectal cancer patients remain unclear.SIRT1 protein expression was measured by immunohistochemistry in a paraffin-embedded tissue microarray, including 120 paired colorectal cancer and normal mucosa tissues. The correlations among SIRT1 protein expression, clinicopathological features, and prognosis were analyzed.All samples (100%) were positive for SIRT1, with variable staining in the cytoplasm rather than in the nucleus. There was significant difference in SIRT1 overexpression between adenocarcinomas and normal mucosal tissue (P0.01, χ(2) test). SIRT1 overexpression was more frequently observed in advanced-stage tumors (P = 0.046, 0.002, χ(2) test). SIRT1 overexpression was significantly correlated with poor overall survival (P = 0.013, log-rank test) and diseasefree survival (P = 0.012, log-rank test).SIRT1 overexpression correlated with advanced stage and poor prognosis. SIRT1 may play an important role in the progression of colorectal cancer.

Sirtuin 1 (SIRT1) has been reported to have diverse roles in various biological processes through deacetylation of histone and nonhistone proteins. However, the correlations between SIRT1 protein expression, clinicopathological parameters, and survival of colorectal cancer patients remain unclear. SIRT1 protein expression in a paraffin-embedded tissue microarray, including 13 benign adenomas, nine liver metastasis tissues, and 120 paired colorectal cancer and normal mucosa tissues, was measured by immunohistochemistry. SIRT1 mRNA and protein expression in colon cancer cell lines with different metastatic potential and normal colon cells were detected by real-time reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. The correlations between SIRT1 protein expression, clinicopathological features, and prognosis were analyzed. All samples (100 %) were positive for SIRT1, with variable staining in the cytoplasm rather than the nucleus. There was significant difference in SIRT1 overexpression between adenocarcinomas and normal mucosal tissues (P < 0.01, χ(2) test). SIRT1 overexpression was more frequently observed in advanced-stage tumors and lymph node or liver metastases (P = 0.046, 0.002, and 0.004, respectively, χ(2) test). SIRT1 expression was also significantly elevated in the more aggressive colon cancer cell line SW620. SIRT1 overexpression was significantly correlated with poor overall survival (P = 0.013, log-rank test) and disease-free survival (P = 0.012, log-rank test). SIRT1 overexpression was correlated with advanced-stage and poor prognosis. SIRT1 may play an important role in the progression of colorectal cancer.

Summary Diffuse cutaneous mastocytosis (DCM) is an extremely rare disease characterized by massive proliferation of mast cells infiltrating the entire skin. We report a Chinese family with indolent DCM, and detection of a new germline KIT mutation located in the fifth immunoglobulin-like loop of the KIT protein, which probably results in a gain-of-function effect and consequent overactivation of mast cells. Our report expands the knowledge of correlations between the genotype of KIT mutations and the phenotype of DCM.

Background Recent studies have indicated the possible function of miR-217 in tumorigenesis. However, the roles of miR-217 in colorectal cancer (CRC) are still largely unknown. Methods We examined the expression of miR-217 and AEG-1 in 50 CRC tissues and the corresponding noncancerous tissues by qRT-PCR. The clinical significance of miR-217 was analyzed. CRC cell lines with miR-217 upregulation and AEG-1 silencing were established and the effects on tumor growth in vitro and in vivo were assessed. Dual-luciferase reporter gene assays were also performed to investigate the interaction between miR-217 and AEG-1. Results Our data demonstrated that miR-217 was significantly downregulated in 50 pairs of colorectal cancer tissues. MiR-217 expression levels were closely correlated with tumor differentiation. Moreover, decreased miR-217 expression was also associated with shorter overall survival of CRC patients. MiR-217 overexpression significantly inhibited proliferation, colony formation and invasiveness of CRC cells by promoting apoptosis and G0/G1 phase arrest. Interestingly, ectopic miR-217 expression decreased AEG-1 expression and repressed luciferase reporter activity associated with the AEG-1 3′-untranslated region (UTR). AEG-1 silencing resulted in similar biological behavior changes to those associated with miR-217 overexpression. Finally, in a nude mouse xenografted tumor model, miR-217 overexpression significantly suppressed CRC cell growth. Conclusions Our findings suggest that miR-217 has considerable value as a prognostic marker and potential therapeutic target in CRC. Electronic supplementary material The online version of this article (doi:10.1186/s12885-015-1438-z) contains supplementary material, which is available to authorized users.