Xi Tao Xu

Meta-analysis: circulating adiponectin levels and risk of colorectal cancer and adenoma.

OBJECTIVE:  To provide a systematic review with a meta‐analysis for addressing the association between circulating adiponectin levels and the risk of colorectal cancer and adenoma.

Comparison of immunochemical and guaiac-based fecal occult blood test in screening and surveillance for advanced colorectal neoplasms: a meta-analysis.

OBJECTIVE:  To systematically evaluate whether immunochemical fecal occult blood tests (iFOBT) could improve clinical performance and test accuracy in screening and surveillance for advanced colorectal neoplasms.

MicroRNA 506 regulates expression of PPAR alpha in hydroxycamptothecin-resistant human colon cancer cells

Chemotherapeutic drug resistance remains a major obstacle to the successful treatment of colon cancer. Here, we show that 77 differentially expressed miRNAs were identified in SW1116/HCPT versus SW1116, and over‐expressed miR‐506 in SW1116/HCPT cells was validated. Then it was indicated that PPARα is a common target of miR‐506 by using a luciferase reporter assay. Our results also demonstrated that cytotoxic ability of HCPT requires the concomitant presence of PPARα, and that loss of PPARα expression imparts resistance to HCPTs anti‐tumor effects. All together, our studies indicate that miR‐506 over‐expression in established HCPT‐resistant colon cancer cell line confers resistance to HCPT by inhibiting PPARα expression, then providing a rationale for the development of miRNA‐based strategies for reversing resistance in HCPT‐resistant colon cancer cells.

Predictive and prognostic roles of BRAF mutation in patients with metastatic colorectal cancer treated with anti-epidermal growth factor receptor monoclonal antibodies: A meta-analysis

This study aimed to evaluate the predictive and prognostic roles of BRAF mutation in patients with metastatic colorectal cancer (mCRC) treated with anti‐epidermal growth factor receptor (EGFR) monoclonal antibodies (MoAbs).

Increased JNK1 signaling pathway is responsible for ABCG2-mediated multidrug resistance in human colon cancer.

Multidrug resistance remains a major obstacle to effective chemotherapy of colon cancer. ABCG2, as a half-transporter of the G subfamily of ATP-binding cassette transporter genes (ABC transporters), is known to play a crucial role in multidrug resistance. However, the molecular mechanism of controlling ABCG2 expression in drug resistance of colon cancer is unclear and scarcely reported. In the present study, we systematically investigate the potential role of the c-Jun NH2-terminal kinase (JNK) signal pathway in ABCG2-induced multidrug resistance in colon cancer. In the hydroxycamptothecin (HCPT) resistant cell line SW1116/HCPT from human colon cancer cell line SW1116, ABCG2 is the major factor for multidrug resistance, other than well-studied ABCB1 or ABCC1. Our findings indicate that blocking the JNK pathway by pathway inhibitor SP600125 reduces the expression level and transport function of ABCG2 in drug-resistant cells SW116/HCPT. Notably, the experiments of small interfering RNA directed against JNK1 and JNK2 show that only silence of JNK1 gene has the equal effect as SP600125 on dephosphorylation of transcription factor c-Jun and the expression of ABCG2 protein, while the corresponding phenomena were not observed after silence of JNK2 gene. Meanwhile, SP600125 induces the apoptosis of SW116/HCPT cells by promoting the cleavage of PARP and suppressing the anti-apoptotic protein survivin and bcl-2, and increases the sensitivity of SW1116/HCPT to HCPT. Taken together, our work demonstrated that JNK1/c-jun signaling pathway was involved in ABCG2-mediated multidrug resistance in colon cancer cells. Definitely, inhibition of the JNK1/c-jun pathway is useful for reversing ABCG2-mediated drug resistance in HCPT-resistant colon cancer cells.

Meta‐analysis: The efficacy and safety of monoclonal antibody targeted to epidermal growth factor receptor in the treatment of patients with metastatic colorectal cancer

OBJECTIVE:  To evaluate systematically the efficacy and safety of anti‐epidermal growth factor receptor (EGFR) monoclonal antibody added to a chemotherapeutic regimen in the treatment of patients with metastatic colorectal cancer (mCRC).

High suppressor of cytokine signaling-3 expression impairs STAT3-dependent protective effects of interleukin-22 in ulcerative colitis in remission.

Background:High SOCS3 expression in intestinal epithelial cells (IECs) of patients with ulcerative colitis (UC) in remission reflects the shorter time to relapse. We investigated whether high SOCS3 increased risk for relapse through violating STAT3-dependent protective effects of interleukin (IL)-22 during UC remission. Methods:Expression of IL-22 and c-Myc in UC remission mucosa was analyzed by immunohistochemistry. Effects of IL-22 on migration and proliferation of IEC cell lines with enforced SOCS3 expression were assessed with wounding assay and CCK-8 assay, respectively. Influence of STAT3 interference and SOCS3 overexpression on IL-22–regulated expression of antimicrobial peptide and proliferation-related molecules, including DMBT1, c-Myc, Survivin, Bcl-2, and Bcl-xL, were performed with quantitative real-time polymerase chain reaction or Western blot. Results:Patients with UC in remission showed significantly more IL-22–positive immune cells, but no difference of epithelial c-Myc levels, in mucosa compared with healthy controls. Overexpression of SOCS3 nearly abolished IL-22–induced activation of STAT3. By inhibiting STAT3 signaling, SOCS3 influenced IL-22–induced expression of DMBT1, c-Myc, Survivin, and Bcl-2 as well as proliferation and migration processes in cultured IEC cell line. Conclusions:SOCS3 overexpression impairs IL-22–mediated epithelial homeostasis and mucosal wound healing, which could be the mechanism for high SOCS3 IEC expression contributed early relapse of mucosal inflammation. Prevention of SOCS3 expression or enhancement of IL-22/STAT3 signaling in IEC seems to be rational therapeutic strategies for UC remission maintenance.

Prevalence and factors related to hepatitis B and C infection in inflammatory bowel disease patients in China: A retrospective study

OBJECTIVES The objectives of this retrospective study were to assess the prevalence of HBV and HCV infection in Chinese IBD patients, identify potential risk factors of the infection in this population, and discuss the prevalence of HBV and HCV in the general Chinese population. METHODS A total of 714 IBD patients who had been investigated for HBV and/or HCV infection were consecutively enrolled in the study. Clinical and laboratory data on IBD and hepatitis infection were collected. A control group of 22,373 healthy individuals was also included in the study. RESULTS Present and past HBV infection was found in 40.62% of IBD patients (ulcerative colitis: HBsAg+, 5.68%; anti-HBc+, 41.64%; Crohns disease: HBsAg+, 5.29%; anti-HBc+, 39.80%;), and 27.58% of the non-IBD group (HBsAg+, 5.52%; anti-HBc+, 27.58% [P = 0.00]). HCV infection was found in 0.42% of IBD patients and 0.36% of the non-IBD group (P=0.80). One hundred and fifty-four of the IBD patients (21.57%) had been effectively vaccinated for HBV. In a multivariate analysis, age, family history of hepatitis B, and IBD-related admission were significantly related to HBV infection in IBD patients. Potential risk factors for HCV were not analyzed due to the limited number of HCV-positive patients in the study. CONCLUSIONS Prevalence of HBV infection in IBD patients was higher than that in the non-IBD patients, whereas prevalence of HCV infection was similar to that of the non-IBD group. Effective vaccination for HBV was present in only a small proportion of IBD patients.

Gene expression of tumor necrosis factor receptor associated-factor (TRAF)-1 and TRAF-2 in inflammatory bowel disease

This study aimed to investigate the expression of tumor necrosis factor receptor‐associated factor (TRAF)‐1 and TRAF‐2 in patients with inflammatory bowel disease (IBD).

Chemopreventive effect of epigallocatechin-3-gallate (EGCG) and folic acid on the N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastrointestinal cancer in rat model.

OBJECTIVE:  To investigate the chemopreventive effect and mechanisms of epigallocatechin‐3‐gallate (EGCG) and folic acid on N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG)‐induced gastrointestinal cancer in rats, and to investigate and compare the combinatorial effects of EGCG and folic acid on the chemoprevention of gastrointestinal carcinogenesis.