Interleukin-22 promotes PD-L1 expression via STAT3 in colon cancer cells.

Blocking the expression of programmed cell death ligand 1 (PD-L1) is a promising approach for the treatment of colon cancer. The binding of PD-L1 to its receptor programmed cell death 1 (PD-1) on immune cells leads to the apoptosis of activated T cells and causes immune escape. However, there is a limited number of patients with colon cancer that can benefit from the inhibition of PD-L1, and the regulation of PD-L1 expression is poorly understood in colon cancer. The present study demonstrated that interleukin-22 (IL-22) and PD-L1 were upregulated in colon cancer tissues and there was a positive correlation between IL-22 expression and PD-L1 expression. In the present study, exogenous IL-22 was found to upregulate PD-L1 expression via the signal transducer and activator of transcription 3 signaling pathway in human colon cancer cells (DLD-1 and primary colon cancer cells). The results of the present study revealed a novel regulatory mechanism of PD-L1 expression in colon cancer, which provides a theoretical basis for decreasing the immune tolerance of colon cancer via IL-22 overexpression.

MicroRNA-204-3p represses colon cancer cells proliferation, migration, and invasion by targeting HMGA2.

Colon cancer is a detrimental neoplasm of the digestive tract. MicroRNAs (miRNAs) as central regulators have been discovered in colon cancer. Nonetheless, the impact of miR-204-3p on colon cancer remains indistinct. The research attempted to uncover the impacts of miR-204-3p on colon cancer cells growth, migration, and invasion. miR-204-3p expression level in colon cancer tissues and diverse colon cancer cell lines were testified by the quantitative real-time polymerase chain reaction. Exploration of the impacts of miR-204-3p on cell growth, migration, invasion, and their associated factors through assessment of CCK-8, flow cytometry, Transwell, and western blot, respectively. High mobility group AT-hook 2 (HMGA2) expression was then detected in Caco-2 cells after miR-204-3p mimic and inhibitor transfection, additionally dual-luciferase activity was implemented to further uncover the correlation between HMGA2 and miR-204-3p. The impact of HMGA2 on Caco-2 cell growth, migration, and invasion was finally assessed. We found that repression of miR-204-3p was discovered in colon cancer tissues and HCT116, SW480, Caco-2, HT29 and SW620 cell lines. MiR-204-3p overexpression mitigated Coca-2 cell viability, facilitated apoptosis, simultaneously adjusted CyclinD1 and cleaved caspase-3 expression. Cell migration, invasion, and the associated factors were all suppressed by miR-204-3p overexpression. Reduction of HMGA2 was presented in Caco-2 cells with miR-204-3p mimic transfection, and HMGA2 was predicated to be a target gene of miR-204-3p. Besides, HMGA2 silence showed the inhibitory effect on Caco-2 cells growth, migration, and invasion. In conclusion, miR-204-3p repressed colon cancer cell growth, migration, and invasion through targeting HMGA2.

Clinical Values of Preoperative Use of Antibiotics in Transanal Endoscopic Microsurgery.

OBJECTIVE: To investigate the clinical values of preoperative use of antibiotics in transanal endoscopic microsurgery (TEM). METHODS: Thirty patients undergoing TEM surgery to treat rectal neoplasms in our hospital were selected in this study. All patients were randomly divided into two groups: antibiotic group that antibiotics were used before and after surgery, and control group that antibiotics were only used after surgery. Several markers were evaluated before and after surgery in all patients, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), changes procalcitonin (PCT), white blood cell count (WBC), neutrophils (NE%) and temperature (T). RESULTS: The patients in the antibiotic group at the first and third days after surgery showed lower values of ESR, CRP, WBC, NE% and T than the control group (p < 0.05), furthermore, the WBC and NE% were significantly decreased at the third day after surgery compared with the first day after surgery. For the PCT, there was a significant difference in the first day after surgery between the two groups (p < 0.05), but no significant difference was observed between them at the third day after surgery (p > 0.05). CONCLUSION: The preoperative use of antibiotics in TEM surgery to treat rectal neoplasms may become an effective method to reduce inflammation and prevent infecting after surgery, which will be verified by an amount of studies on large sample.

MicroRNA-17 induces epithelial-mesenchymal transition consistent with the cancer stem cell phenotype by regulating CYP7B1 expression in colon cancer.

MicroRNA-17 (miRNA-17/miR­17) expression has been confirmed to be significantly higher in colorectal cancer tissues than in normal tissues. However, its exact role in colorectal cancer has not yet been fully elucidated. In this study, we found that miR-17 not only promoted epithelial-mesenchymal transition (EMT), but also promoted the formation of a stem cell-like population in colon cancer DLD1 cells. We also wished to determine the role of cytochrome P450, family 7, subfamily B, polypeptide 1 (CYP7B1) in CRC. miR-17 was overexpressed using a recombinant plasmid and CYP7B1 was silenced by transfection with shRNA. Western blot analysis was used to determine protein expression in the DLD1 cells and in tumor tissues obtained from patients with colon cancer. Our results revealed that miR­17 overexpression led to the degradation of CYP7B1 mRNA expression in DLD1 cells. In addition, we found that the silencing of CYB7B1 promoted EMT and the formation of a stem cell-like population in the cells. Thus, our findings demonstrate that miR­17 induces EMT consistent with the cancer stem cell phenotype by regulating CYP7B1 expression in colon cancer.

Serum pentraxin 3 is a novel marker in Crohn's disease.

In Crohn's disease (CD), clinical symptoms correspond poorly to inflammatory disease activity. Biomarkers, which reflect the level of intestinal inflammation are considered to enable effective monitoring of disease activity. The present study evaluated the role of serum pentraxin 3 (PTX3) as a marker of disease activity in patients with CD. Serum PTX3 levels were determined using an enzyme-linked immunosorbent assay in patients with CD (n=240), ulcerative colitis (UC; n=240) and healthy controls (HC; n=80). The expression levels of PTX3 were also evaluated in 35 fresh colonic tissue samples by western blot analysis. The association between levels of serum PTX3 with disease activity and its diagnostic role were analyzed. The levels of serum PTX3 were significantly increased in patients with active CD compared with patients in remission (UC and HC; P<0.01). A significant increase in the expression levels of PTX3 was identified at a protein level in inflamed colonic tissues compared with uninflamed colonic tissues. The levels of serum PTX3 were also positively correlated with disease activity in CD. These results indicated that serum and colonic expression of PTX3 were upregulated in patients with active CD, suggesting serum PTX3 is superior to CRP in predicting CD activity.

Nemo­like kinase expression predicts poor survival in colorectal cancer.

Nemo­like kinase (NLK), a serine/threonine protein kinase, was previously reported to be associated with tumor proliferation and invasion. The present study aimed to evaluate whether NLK participates in the tumorigenesis and progression of colorectal cancer (CRC). NLK expression was examined using reverse transcription quantitative polymerase chain reaction (RT­qPCR) and western blot analysis in 50 paired CRC tissues as well as immunohistochemical analysis of 406 cases of primary CRC tissues and paired non­cancerous tissues. Correlations between NLK expression, the clinicopathological features of CRC patients and clinical outcome were then analyzed. NLK expression was found to be significantly higher in CRC tissues as well as associated with the depth of tumor invasion, lymph node metastasis, distant metastasis, histological differentiation, vascular invasion and advanced tumor stage. Patients with NLK­positive tumors demonstrated higher rates of recurrence and mortality than patients with NLK­negative tumors. Multivariate analyses revealed that NLK expression was an independent factor for overall survival [hazard ratio (HR)=0.035; 95% confidence interval (CI)=0.02­0.19; P<0.001] and disease­free survival (HR=0.033; 95% CI=0.007­0.09; P<0.001) in CRC patients. In conclusion, the results of the present study indicated that NLK may serve as a novel biomarker for tumor recurrence and survival for CRC patients.