ABSTRACT. This study aimed to determine the expression of integrin β1 and vascular endothelial growth factor (VEGF) and microvascular density (MVD) by CD105 staining in hypopharyngeal squamous cell carcinoma to determine their association with clinicopathologic characteristics, and to determine their role and the effects of their interactions in the development and progression of hypopharyngeal squamous cell carcinomas. The expression of integrin β1 and VEGF and MVD in hypopharyngeal squamous cell carcinomas and normal hypopharyngeal tissues were evaluated using immunohistochemistry. The Image-Pro Plus software was used to determine the mean optical density of the immunohistochemical images. Integrin β1 expression was significantly higher in hypopharyngeal squamous cell carcinoma tissues (78.00%) than in normal hypopharyngeal tissues (35.00%; P = 0.001) and significantly differed across pathologic grades and different T stages, and regarding the presence of cervical lymph node metastasis (P < 0.05). VEGF expression was significantly higher in hypopharyngeal squamous cell carcinoma tissues (74.00%) than in normal hypopharyngeal tissues (30.00%; P = 0.002), VEGF overexpression differed significantly across different pathologic grades and different T stages, and regarding the presence of cervical lymph node metastasis (P < 0.05). The MVD count was significantly higher in hypopharyngeal squamous cell carcinoma tissues (37.10 ± 5.95) than in normal hypopharyngeal tissues (8.70 ± 3.34; P = 0.000). MVD differed significantly across different pathologic grades and different T stages, and regarding the presence of cervical lymph node metastasis (P < 0.05). The expression of integrin β1 and VEGF and the MVD count exhibited no significant differences in terms of age, gender, history of smoking, and clinical stages (P > 0.05). VEGF expression was positively associated with the MVD count of hypopharyngeal squamous cell carcinomas (r = 0.582, P = 0.000); however, integrin β1 was not associated with VEGF or MVD (P > 0.05). Integrin β1 and VEGF are overexpressed and MVD increased in hypopharyngeal squamous cell carcinomas. VEGF is positively correlated with MVD.

Background: Colorectal cancer (CRC), the most commonly diagnosed cancer in the world, has a high mortality rate. In recent decades, long non-coding RNAs (lncRNAs) have been proven to exert an important effect on CRC growth. However, the CTBP1-AS2 expression and function in CRC are largely unknown.Materials and Methods: The CTBP1-AS2 and miR-93-5p expression in CRC and para-cancerous tissues was detected by reverse transcription-PCR. The expression of CTBP1-AS2, miR-93-5p and the transforming growth factor-beta (TGF-β)/small mothers against decapentaplegic 2/3 (SMAD2/3) pathway was selectively regulated to study the correlation between CTBP1-AS2 expression and prognosis of patients with CRC. CRC cell proliferation, apoptosis, and invasion were measured in vivo and in vitro. In addition, bioinformatics was applied to explore the targeting relationship between CTBP1-AS2 and miR-93-5p. The targeting binding sites between CTBP1-AS2 and miR-93-5p, as well as between miR-93-5p and TGF-β, were verified by the dual-luciferase reporter assay and the RNA immunoprecipitation experiment.Results: Compared with normal para-cancerous tissues, CTBP1-AS2 was considerably overexpressed in CRC tissues and was closely associated with worse survival of patients with CRC. Functionally, gain and loss in experiments illustrated that CTBP1-AS2 accelerated CRC cell proliferation and invasion and inhibited cell apoptosis. Mechanistically, CTBP1-AS2 regulated the malignant phenotype of tumor cells through the TGF-β/SMAD2/3 pathway. Moreover, miR-93-5p, as an endogenous competitive RNA of CTBP1-AS2, attenuated the oncogenic effects mediated by CTBP1-AS2.Conclusion: CTBP1-AS2 promotes the TGF-β/SMAD2/3 pathway activation by inhibiting miR-93-5p, thereby accelerating CRC development.

Colorectal cancer (CRC) is a malignancy with high metastatic rates. The mechanism of miR-128 on the regulation of Ribophorin-II (RPN2) in CRC cells was explored in the present study. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) or western blot analyses were conducted to detect miR-128 and RPN2 levels in tissues and cell lines. AmiR-128 overexpression model was constructed using miR-128 mimic transfection in HT29 CRC cells. Then, cell proliferation was detected using a Cell Counting Kit-8 assay, and the migratory and invasive abilities were measured by Transwell assay. RT-qPCR and western blot analysis were used to detect expression levels of protein kinase-B (Akt)-tumor protein 53 (p53)-cyclin pathway and metastasis-associated factors. In the present study, it was identified that aberrant decreased miR-128 was negatively correlated with RPN2 in CRC tissues. The increased RPN2 levels were significantly associated with poorly-differentiated histology, advanced stages and lymph nodes metastasis in patients with CRC. The survival rate of patients with CRC was also closely associated with RPN2 levels. In HT29 cells, miR-128 upregulation downregulated mRNA and protein levels of RPN2, and significantly inhibited cell proliferative, migratory and invasive abilities. Markedly decreased Akt phosphorylation and cyclin D1 levels and increased p53 levels were detected when cells were transfected with miR-128 mimics. Concurrently, decreased levels of matrix metalloproteinase (MMP)-2, MMP-9 and metastasis-associated protein 1, and increased levels of epithelial-cadherin and tissue inhibitor of metalloproteinases 2, were revealed in miR-128 mimic-transfected cells. Subsequent to screening with miRNA target prediction databases, the specificity of miR-128-targeted RPN2 was validated by a luciferase reporter assay. In conclusion, the results suggested that miR-128 was a specific negative regulator of RPN2, which regulated colorectal cancer cell proliferation and migration by affecting the Akt-p53-cyclin pathway. These data may provide novel evidence for the therapeutic potential of miR-128-based treatments for colorectal cancer.

Background: Colon adenocarcinoma (CA) is the most common one with poor survival in colon cancer.This study aims to investigate the effect of miR-1245a on the process of CA cells and its target gene BRCA2. Methods:The expression of CA tissues and cells were evaluated by q RT-PCR. Then we explore the association between expression of miR-1245a and prognosis in the CA patients from the TCGA database. CCK8 assays, colony formation assays were performed to explore the effect of miR-1245a in CA cell proliferation. The invasion ability of CA cells was evaluated by Transwell assays. Western blot was performed to assess the BRCA2 expression. Luciferase reporter assay was employed to scrutinize the relationship between miR-1245a and BRCA2. Finally, rescue experiments were performed through BRCA2 downregulation and miR-1245a inhibitors by using colony formation assay and Transwell invasion assay.Results: miR-1245a is upregulated in CA cells and tissues. Additionally, the high expression of miR-1245a was related to poor survival. CCK8 assays, colony formation assays and Transwell assays showed that miR-1245a promotes the proliferation and invasion of CA cells. The luciferase reporter assay indicated that miR-1245a targeted BRCA2 and inhibited its expression. The rescue experiment further showed that miR-1245a could restore the effect of BRCA2 on CA.Conclusions: miR-1245a promotes the proliferation and invasion of CA by targeting BRCA2.Our results suggested that miR-1245a could be a potential biomarker for CA progression.

Purpose: Preoperative progressive pneumoperitoneum (PPP) has not been reported in the management of parastomal hernias; therefore, the present study evaluated its effectiveness in the surgical management of large parastomal hernias. Patients and Methods: This prospective, observational study included 23 consecutive patients with large parastomal hernias who underwent PPP between January 2016 and September 2018. The volume of parastomal hernia (VPH), volume of the abdominal cavity (VAC), and the VPH/VAC ratio were measured before and after PPP using abdominal computed tomography scan data. All the hernias were repaired by a laparoscopic or laparoscopic-open-laparoscopic approach using the intraperitoneal Sugarbaker technique. Results: Before and after PPP, the mean VPH was 1442 and 1581 mL (P<0.01), and the mean VAC was 5667 and 9194 mL (P<0.01). The VAC increased by 3527 mL (P<0.01) and was greater than the mean VPH before PPP. The VPH/VAC ratio after PPP was reduced at an average of 8.1% (P<0.01). Fascial closure was achieved in all patients, with no clinical evidence of elevated intra-abdominal pressures. The mean follow-up was 24 months (13 to 40 mo), and, to date, no hernia recurrences have been reported in these patients. Conclusions: PPP is a feasible and useful tool in the surgical management of large parastomal hernias. It passively expands the abdominal volumes, thereby resulting in respiratory adaptation to elevated intra-abdominal pressures.