Abstract. The increasing expression of microRNA-155 (miR-155) and decreasing expression of RNA-binding protein quaking (QKI) in colon cells have been observed previously. In this study, we attempted to establish the correlation between miR-155 and QKI. In addition, we assessed whether the expression of miR-155 and QKI is linked to the proliferation and invasion capabilities of colon cells. Firstly, nineteen tumor samples, divided into two groups according to the presence or absence of lymphatic metastasis, were obtained from colon cancer patients at the First Affiliated Hospital of Wenzhou Medical University, China. The expression level of miR-155 and QKI was measured by quantitative polymerase chain reaction (qPCR). Secondly, the GES-1, SW480 and COLO205 cell lines were cultured and the expression level of QKI and miR-155 was also assessed by qPCR. Thirdly, a luciferase reporter gene assay was performed to detect the association between miR-155 and QKI, and qPCR and western blot analysis were performed to confirm the effects of miR-155 on the expression of QKI at the mRNA and protein level. Subsequently, the SW480 cells were used in the following experiments. Following treatment with miR-155 inhibitor and QKI overexpression vector, western blot analysis, propidium iodide (PI) staining and a cell scratch assay were carried out to assess the effects of miR-155 on the proliferation and invasion potential of colon cancer cells. qPCR findings revealed higher miR-155 expression and lower QKI expression in colon cancer tissues as well as the colon cancer cell lines SW480 and COLO205. The relative luciferase activity of the 3' untranslated region (3'UTR) was decreased by approximately 45% when SW480 cells stimulated by mimic-miR-155 were combined with the wild-type 3'UTR constructs. In addition, when the cells were treated with mimic-miR-155, QKI expression was significantly decreased at the mRNA and protein level. These outcomes revealed that miR-155 decreased the production of QKI by acting on the 3'UTR of the QKI gene. Furthermore, PI staining and the cell scratch assay revealed that miR-155 influenced the cell cycle and invasion abilities of colon cancer cells by directly targeting QKI and decreased the production of QKI by acting on the 3'UTR of the QKI gene. This study has demonstrated the correlation between miR-155 and QKI, in which miR-155 regulates the cell cycle and invasion ability of colon cancer cells via the modulation of QKI expression. Our study provides novel therapeutic strategies for colon cancer therapy.
The objective of this study was to explore the clinical significance of perioperative CTCs (circulating tumor cells) counts and EMT-CTCs (epithelial-mesenchymal transition-CTCs) in rectal cancer patients. A total of 30 patients with rectal cancer who underwent radical resection of rectal cancer at the Guangxi Zhuang Autonomous Region People's hospital were enrolled. Five ml peripheral blood was withdrawn from 30 patients with rectal cancer before the operation and seven days after the operation and at the corresponding time also from 20 healthy volunteers. CanPatrol™ CTC detection technique was used to enrich and identify CTCs and IER3 expression simultaneously. We found out that the preoperative total CTCs were correlated with lymph node metastasis (p=0.008) and tumor size, and mixed CTCs were closely correlated with lymph node metastasis (p=0.009). The number of IER3-positive total CTCs and mesenchymal CTCs were statistically associated with tumor size, p=0.034 and 0.043, respectively. The number of CTCs varied significantly before and after the operation in all patients (p=0.049). There were significant differences in CTCs variations between the open operation group and the laparoscopic operation group. In the laparoscopic operation group, the average number of single-cell CTCs was 6.9 before operation and 3.5 after the operation (p=0.013). In the open operation group, the average number of single-cell CTCs was 5.9 before operation and 4.2 after the operation. To conclude, surgery is associated with a decrease of CTCs in rectal cancer patients, especially in patients receiving laparoscopic surgery. The number of CTCs before the operation in rectal cancer patients is related to the size of tumors and regional lymph node metastasis. CTCs detection and characterization may be useful for clinical staging and lymph node dissection during operation.
CIITA (class II transactivator) is a coactivator essential for transcription of MHC class II genes. In this study, a construct with a mutated CIITA gene with N-terminal domains depleted was constructed. This mutated CIITA (mCIITA) was able to repress DR and DQ expression in 45.0-60.0% of the mCIITA-transfected clones of swine endothelial cell line PIEC and in B cell line L23, as well as in human cell lines HeLa and Raji. Similarly, 30.0-46.7% of swine cell clones containing the human CIITA antisense RNA also failed to express DR molecules. However, the persistence of the DR repression on the cell lines is quite different. Transfection with mCIITA was persistent for at least 120 days, while with the CIITA antisense RNA, persistence existed for only 35-45 days. To explore the underlying mechanism, Raji cells were transfected with pUHD10-3-mCIITA, a mCIITA-containing, doxycycline-dependent plasmid. The intensity of DR repression is correlated quite well with the efficiencies of the mCIITA expression within the cells in a doxycycline dose-dependent manner. This implicates a competition between the mCIITA and its endogenous full-length counterpart. In addition, we were able to show that purified human CD4 T cells did not respond to the mCIITA-transfected PIECs in xenogeneic mixed lymphocyte endothelial reaction (MLER). The stimulating indices (SI) were only 1.0-1.5, compared with 15.2-18.2 for those transfected with empty vector or an initiation codon-depleted mCIITA that is dysfunctional for protein translation. The results we obtained, especially those for persistent suppression of class II genes, show promise for the possible development of mCIITA-transgenic swine for organ/tissue xenotransplantation.
The current study reports a case of an extremely rare tumor that presented in an uncommon location, which was successfully treated via radical resection and reconstruction. A 37-year-old female, with no notable medical history, with the exception of a cesarean delivery, was admitted to The First Affiliated Hospital of Wenzhou Medical University (Wenzhou, China) due to pain and a lump of the anterior chest wall. The mass was identified on the manubrium sterni and was not tender on palpation. A chest computed tomography (CT) scan reconstruction identified the abnormal mass on the manubrium sterni (size, 5×4 cm in diameter) and positron emission tomography-CT interpretation strongly indicated a type of well-differentiated malignant tumor, such as a giant cell tumor. An aspiration needle biopsy was not conducted, however, the patient underwent tumor radical resection and sternal reconstruction using steel wire and titanium mesh. Histopathological examination of the surgical specimen determined the diagnosis of chondrosarcoma. A postoperative chest X-ray revealed that the sternal defect had repaired well, therefore, this procedure may be highly beneficial in future for repairing defects in the sternum.
#2057 Purpose: Bone metastases are commonly observed in patients with advanced breast cancer. Tumor cells interact with the bone microenvironment to induce osteoclastogenesis via local bone stromal expression of receptor activator of NF-kB ligand (RANKL), leading to bone destruction and release of growth factors. In addition to its critical role in tumor-induced osteolysis, RANKL has been demonstrated to enhance the invasive behavior of epithelial tumor cells that express RANK, and RANK over-expression in transgenic mice using the breast-specific MMTV promoter results in increased mammary carcinoma. This study assessed the expression of human RANK and its ligand (RANKL) in invasive ductal carcinoma (IDC).
 Methods: We studied a total of 57 IDC specimens. Antibodies against human RANK (AF683) and human RANKL (M366; Amgen) were used for immunohistochemistry (IHC) cell staining along with an isotype control. The specificity of the 2 antibodies was substantiated by IHC, flow cytometry and Western blot analysis of positive and negative control cells. In addition, for RANK, mass spectrometry/protein sequencing of immunoprecipitated proteins was performed. The intensity of IHC staining was scored on a semiquantitative scale (1=weak, 2=moderate, 3=intense) or a complex scale (sum of percentages of stained tumor cells x staining intensity (0-3)).
 Results: Using a complex score with a threshold of 10, 20/57 IDC (35%) expressed minimal level of RANK (range 0 to <10, median 1) while 37/57 IDC (65%) expressed RANK protein with a score ranging from 10 to 100 (median 50). The expression in the tumor was heterogeneous, with cells having no expression and cells having intense expression. In addition, RANK was intensely expressed in the basal layer of all normal ducts and lobules. RANKL was observed in rare tumors (7/57; 11%), in rare lymphocytes of most tumor stroma (42/62; 68%), and in rare fibroblast-like cells in the stroma of rare tumors (3/62; 4.8%).
 Conclusion: In this study, RANK expression was observed by IHC in the majority (65%) of IDC. RANKL expression was observed in the epithelial carcinoma element of some tumors (11%) and was detected in 68% of tumors in rare lymphocytes infiltrating the tumor stroma. Correlation studies between prognosis markers ER, PR, Her2, and CK5/6 expression and RANK or RANKL expression in those IDC have been initiated. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2057.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.