MiR-31 is a potential biomarker for diagnosis of head and neck squamous cell carcinoma.

MicroRNAs (miRNAs) play important roles in the development of head and neck squamous cell carcinoma (HNSCC). However, their potential clinical value as biomarkers remains poorly known. The aim of this study was to assess the association between tissue/serum miR-31 expression levels and prognosis of HNSCC. In this clinical study, tumor samples were obtained from 118 patients with HNSCC and 48 patients with oral epithelial dysplasia, and blood samples were collected from all the HNSCC cases and 60 normal controls. The expression levels of tissue/serum miR-31 were measured by real-time PCR. Chi-square test was used to evaluate the correlation between tissue/serum miR-31 and clinical parameters of HNSCC. Survival curves were constructed using the Kaplan-Meier method and log-rank test. Multivariate Cox regression analyses were used to estimate independent predictors of survival for HNSCC. Our findings showed that tissue miR-31 levels in HNSCC tumor specimens exhibited higher than that in oral epithelial dysplasia samples and normal tissues. Oral epithelial dysplasia with higher expression of miR-31 was more prone to progress into HNSCC. Likewise, serum miR-31 expression in HNSCC patients was markedly increased in compared to normal controls. Moreover, serum miR-31 performed well to distinguish HNSCC subjects from controls. In addition, increased tissue/serum miR-31 expression was positively correlated with poor clinical variables and dismal prognosis. Finally, tissue miR-31 was confirmed to be an independent prognostic factor for HNSCC. Taken together, miR-31 had strong potential as a promising biomarker in HNSCC detection.

Astragaloside IV inhibits pathological functions of gastric cancer-associated fibroblasts.

AIM: To investigate the inhibitory effect of astragaloside IV on the pathological functions of cancer-associated fibroblasts, and to explore the underlying mechanism. METHODS: Paired gastric normal fibroblast (GNF) and gastric cancer-associated fibroblast (GCAF) cultures were established from resected tissues. GCAFs were treated with vehicle control or different concentrations of astragaloside IV. Conditioned media were prepared from GNFs, GCAFs, control-treated GCAFs, and astragaloside IV-treated GCAFs, and used to culture BGC-823 human gastric cancer cells. Proliferation, migration and invasion capacities of BGC-823 cells were determined by MTT, wound healing, and Transwell invasion assays, respectively. The action mechanism of astragaloside IV was investigated by detecting the expression of microRNAs and the expression and secretion of the oncogenic factor, macrophage colony-stimulating factor (M-CSF), and the tumor suppressive factor, tissue inhibitor of metalloproteinase 2 (TIMP2), in different groups of GCAFs. The expression of the oncogenic pluripotency factors SOX2 and NANOG in BGC-823 cells cultured with different conditioned media was also examined. RESULTS: GCAFs displayed higher capacities to induce BGC-823 cell proliferation, migration, and invasion than GNFs (P < 0.01). Astragaloside IV treatment strongly inhibited the proliferation-, migration- and invasion-promoting capacities of GCAFs (P < 0.05 for 10 µmol/L, P < 0.01 for 20 µmol/L and 40 µmol/L). Compared with GNFs, GCAFs expressed a lower level of microRNA-214 (P < 0.01) and a higher level of microRNA-301a (P < 0.01). Astragaloside IV treatment significantly up-regulated microRNA-214 expression (P < 0.01) and down-regulated microRNA-301a expression (P < 0.01) in GCAFs. Reestablishing the microRNA expression balance subsequently suppressed M-CSF production (P < 0.01) and secretion (P < 0.05), and elevated TIMP2 production (P < 0.01) and secretion (P < 0.05). Consequently, the ability of GCAFs to increase SOX2 and NANOG expression in BGC-823 cells was abolished by astragaloside IV. CONCLUSION: Astragaloside IV can inhibit the pathological functions of GCAFs by correcting their dysregulation of microRNA expression, and it is promisingly a potent therapeutic agent regulating tumor microenvironment.

Correlation study of Bcl-2, B7-H1, EGFR, VEGF and colorectal cancer.

OBJECTIVE: To analyze the expressions of Bcl-2, B7-H1, EGFR and VEGF in colorectal cancer for the further investigation of their correlations with the clinical pathological features of colorectal cancer. METHOD: Fresh colorectal cancer tissues and the expressions of Bcl-2, B7-H1, VEGF and EGFR in paraneoplastic normal mucosal tissues of 57 cases were tested by immunohistochemisty method, and the results were analyzed by SPSS10.0. RESULTS: 1. Compared with paraneoplastic normal tissues, the expressions of Bcl-2 and B7-H1 in colorectal cancer tissues increased significantly with significant difference (P<0.05), while the expression of EGFR and VEGF in colorectal cancer tissues showed no significant difference with those in paraneoplastic normal tissue (P>0.05); 2. The correlation with clinical pathological features: there was significant difference of expression rates of EGFR between different genders (P<0.05); the expressions of BCL-2 and B7-H1 in colorectal cancer of the high- and medium- differentiated groups were significantly higher than those of the low-differentiated group, and the difference was significant (P<0.01); compared with the colorectal cancer patients without lymph node metastasis (Dukes stage A+B), the expression of B7-H1 in patients with lymph node metastasis (Dukes stage C+D) was significantly higher (P<0.05); 3. Within the high- and medium- differentiated colorectal cancer tissues, Bcl-2 expression rate in B7-H1 negative group was higher than the positive group with significant difference (P<0.01). CONCLUSIONS: In colorectal carcinoma, Bcl-2, B7-H1, EGFR and VEGF were all expressed, independent from age and depth of invasion. However, the expression level of Bcl-2 and B7-H1 correlated with tissue differentiation, and the latter also had correlation with tumor staging. Meanwhile, the short-term follow-up showed that high expression of Bcl-2/B7-H1 existed in death cases. Therefore, the expression detection of Bcl-2, B7-H1 might provide a clear understanding of the biological behavior of colorectal cancer, and was important for the diagnosis, treatment and prognosis judgment of colorectal cancer.

Effect of CXCR4 and CD133 co-expression on the prognosis of patients with stage II~III colon cancer.

BACKGROUND: To explore the relationship between CXCR4, CD133 co-expression and clinicopathological features as well as prognosis of patients with phase II~III colon cancer. MATERIALS AND METHODS: Forty-nine paraffin-embedded samples of tumor tissue and epithelial tissue adjacent to cancer were collected from patients with colon cancer undergoing radical surgery in Baotou Cancer Hospital from January, 2010 to June, 2011. CXCR4 and CD133 expression was detected using immunohistochemistry and its relationship with clinicopathological features and the 3-year survival rate was analyzed. RESULTS: In the tumor tissue and colonic epithelial tissue adjacent to cancer, the positive expression rates of CXCR4 were respectively 61.2% (30/49) and 8.16% (4/49), while those of CD133 being 36.7% (18/49) and 6.12% (3/49). CXCR4 and CD133 expression in tumor tissue was not related to patient age, gender, primary focal sites, tumor size, TNM staging, histological type, tumor infiltration depth and presence or absence of lymphatic metastasis, but CXCR4 and CD133 co-expression was associated with TNM staging and lymphatic metastasis. The 3-year survival rate of patients with CXCR4 and CD133 co-expression was 27.3% (3/11), and that of the remainderwas 76.3% (29/38), the difference being significant (χ2=7.0206, p=0.0081). CONCLUSIONS: CXCR4 and CD133 co-expression may be a risk factor for poor prognosis of patients with stage II~III colon cancer.

[Expression of Bcl-2, PD-L1 and its clinical significance in colorectal cancer].

OBJECTIVE: To study the expression of Bcl-2 and PD-L1 in colon cancer and its relationship with metastasis. METHODS: Tumor samples were collected from 57 cases of colon cancer, and tumor adjacent normal mucous tissue were obtained as normal control. The expressions of Bcl-2 and PD-L1 were assayed by immunohistochemical staining, and its correlations with patients' clinical pathological indexes were analyzed. RESULTS: The positive rate of Bcl-2 protein was 75.43% and 52.63% in colon cancer tissues and tumor adjacent colon mucous tissue respectively, with statistically significant difference (P<0.05). While the positive rate of PD-L1 was 45.61% and 15.79% in colon cancer tissues and tumor adjacent colon mucous tissue respectively, also with signficant difference (P<0.01). The positive rate of Bcl-2 was correlated with cellular differentiation, and the positive rate of PD-L1 protein was correlated with lymph node metastasis (P<0.05). CONCLUSION: The expression of Bcl-2 may be associated with colon cancer pathologic differentiation, and the expression of PD-L1 may be associated with colon cancer metastasis.