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Abstract Background To investigate the relationship between cyclin D2 (CCND2) and miR-206 expression in fine-needle aspiration cytology of thyroid carcinoma. Methods A total of 65 patients with thyroid carcinoma were selected as the subjects and 65 patients with benign thyroid nodules were in control group. The fine-needle aspiration cytology of thyroid nodules was performed. CCND2 and miR-206 levels were detected by PCR. Results Compared with the patients with benign thyroid nodules, the expression level of miR-206 in fine-needle aspiration cytology of thyroid cancer patients decreased significantly and the expression level of CCND2 increased significantly. CCND2 and miR-206 expression was negatively correlated in thyroid cancer tissues. Area under curve (AUC) of miR-206 level in the diagnosis of thyroid cancer was 0.889, and the sensitivity and specificity were 92.3% and 81.5%, respectively. AUC of CCND2 level in the diagnosis of thyroid cancer was 0.837, and the sensitivity and specificity were 67.7% and 89.2%, respectively. The AUC of combined detection of CCND2 and miR-206 in the diagnosis of thyroid cancer was 0.959, and the sensitivity and specificity were 93.8% and 87.7%, respectively. The levels of miR-206 and CCND2 were significantly correlated with TNM staging and lymph node metastasis. Conclusions miR-206 and CCND2 may become new biomarkers for clinical diagnosis of thyroid cancer based on the fine-needle aspiration cytology of thyroid nodules.

This study aimed to investigate the expression and function of substance P in cervical squamous cell carcinoma. Cancer tissues and adjacent tissues of 20 patients with cervical squamous cell carcinoma in our hospital were collected. The expression of substance P was detected by immunohistochemistry and Western blot analysis. Cervical squamous cell carcinoma line SiHa was treated with different concentrations of substance P. The proliferation of SiHa cells was detected by EdU assay, and the invasion ability of SiHa cells was detected by transwell assay. The phosphorylation of ERK1/2 and the expression of MMP9 were detected by Western blot analysis. The results showed that substance P was expressed in the cytoplasm and some cell membranes of cervical squamous cell carcinoma cells. The expression of substance P in cervical cancer tissues was significantly higher than that in the adjacent tissues. Compared with the control group, substance P significantly promoted the proliferation and invasion of SiHa cells in a concentration dependent manner and activated the phosphorylation of ERK1/2 and upregulated the expression of MMP9 in SiHa cells. In conclusion, substance P is highly expressed in cervical squamous cell carcinoma and can promote cervical cancer cell proliferation and invasion. The mechanism is related to the activation of ERK1/2 pathway to upregulate MMP9.

Neurokinin-1 receptor (NK1R) belongs to tachykinin receptor family. Recent studies have suggested that NK1R was upregulated in cancer tissues including breast cancer, glioma and melanoma. Furthermore, NK1R antagonists have been employed to exert anti-tumor effect and promote cancer cell apoptosis. However, the role of NK1R in cervical cancer remains largely unknown. In this study, we aimed to detect the expression of NK1R in cervical cancer and evaluate the anti-tumor effects of NK1R antagonist on cervical cancer cells. We found that NK1R was highly expressed in cervical cancer tissues than in adjacent normal cervical tissues. Furthermore, by using NK1R antagonist we demonstrated that NK1R antagonist inhibited the viability and induced the apoptosis of cervical cancer cells in a dose-dependent manner, and the mechanism may be related to the inhibition of ERK activation and the regulation of apoptosis proteins Bcl-2 and BAX. In conclusion, these findings suggest that NK1R plays an oncogenic role in cervical cancer and is a promising target for cervical cancer therapy.

Objectives: It has been demonstrated that substance P (SP) promotes while neurokinin-1 receptor (NK-1R) antagonist inhibits the proliferation of several human cancer cells. Currently, it is still unknown whether such actions exist in human endometrial carcinoma. This study aimed to explore the role of SP/NK-1R signaling in the progression of endometrial adenocarcinoma. Materials and Methods: The expression levels of SP and NK-1R in endometrial adenocarcinoma tissues and Ishikawa cell line were detected by real-time quantitative PCR and Western blot analysis. The effects of SP on Ishikawa cells proliferation and invasion were analyzed usingMTTassay and transwell matrigel invasion assay, respectively. The expression levels of matrix metalloproteinase 9 (MMP-9) and vascular endothelial growth factor C (VEGF-C) in Ishikawa cells after administration of SP were detected by real-time quantitative RCR and Western blot analysis. Results: The expression levels of SP and NK-1R were significantly higher in endometrial adenocarcinoma tissues and Ishikawa cells than in normal endometrium. Substance P significantly enhanced the proliferation and invasion of Ishikawa cells. In addition, SP induced the expression of MMP-9 and VEGF-C in Ishikawa cells, whereas NK-1R antagonist inhibited these effects. Conclusions: Substance P plays an important role in the development of endometrial carcinoma by inducing the expression of MMP-9 and VEGF-C and promoting cancer cell proliferation and metastasis, which can be blocked by NK-1R antagonist. [ABSTRACT FROM AUTHOR]

Purpose: To determine the effect of paclitaxel octreotide conjugate (POC) on human ovarian paclitaxelresistant cell xenograft tumor model and the mechanism underlying reversal of paclitaxel resistance. Methods: Forty female BALB/c-nu/nu mice were subcutaneously inoculated with 106 paclitaxel-resistant cells (a2780/taxol) per mouse during the logarithmic growth phase of ovarian cancer. They were randomly divided into four groups (control, octreotide, paclitaxel and POC). Immunohistochemical streptavidin-peroxidase (SP) method was used to determine expression of nuclear proliferation antigen (PCNA) while TUNEL method was used to assess apoptosis of human ovarian cancer metastasis. Realtime polymerase chain reaction (PCR) was used to assay mRNA expression levels of somatostatin receptor 2 (SSTR2), multidrug-resistant gene (MDR1), vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), and acetylated tubulin (a-tubulin and ß-III-tubulin), while the corresponding protein expressions were assayed using western blotting. Results: Immunohistochemical SP showed significantly lower PCNA levels in octreotide, paclitaxel and POC groups than in control mice, but that of POC mice was significantly reduced, relative to those of octreotide and paclitaxel groups (p < 0.05). There were significantly higher expression levels of SSTR2 mRNA and protein in octreotide, paclitaxel and POC groups than in control mice, but they were significantly higher in POC group than in octreotide and paclitaxel groups (p < 0.05). The mRNA and protein expressions of other factors in POC mice were significantly lower than those in both octreotide and paclitaxel groups (p < 0.05). Conclusion: Paclitaxel-octreotide conjugate effectively inhibits the growth of a2780/taxol xenografts in nude mice, induces tumor cell apoptosis, and suppresses tumor cell growth via mechanism involving enhancement of SSTR2 expression, and decreases in levels of acetylated tubulin, matrix metalloproteinase-9, and vascular endothelial growth factor. [ABSTRACT FROM AUTHOR]