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Clay Asmussen posted an update 6 months, 1 week ago
y modulating KDM5D.OBJECTIVE Gastric cancer (GC) remains a serious disease to human health with high mortality worldwide. Evolving evidence implied that long non-coding RNA Opa interacting protein 5-antisense RNA1 (OIP5-AS1) went in for the pathological progress of GC. Nevertheless, the potential molecular mechanism of OIP5-AS1 needed to be further investigated. MATERIALS AND METHODS Levels of OIP5-AS1, microRNA (miR)-153-3p, and zinc finger and BTB domain containing 2 (ZBTB2) were assessed using quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assays. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) was implemented to detect cell proliferation in vitro. Cell apoptosis was evaluated by flow cytometry. Besides, transwell assay was conducted to examine cell migration and invasion in AGS and MKN45 cells. The interaction between miR-153-3p and OIP5-AS1 or ZBTB2 was validated utilizing dual-luciferase reporter assay. Lastly, the role of OIP5-AS1 in tumor growth was researched through adopting xenograft tumor model. RESULTS OIP5-AS1 and ZBTB2 were strongly higher in GC tissues than noncancerous samples. OIP5-AS1 silencing remarkably curbed cell proliferation, migration and invasion, and elevated cell apoptosis in both AGS and MKN45 cells. Functional analysis indicated that OIP5-AS1 regulated ZBTB2 expression via binding to miR-153-3p. Moreover, the role of miR-153-3p in cell growth and metastasis was abrogated by ZBTB2 overexpression. Above all, OIP5-AS1 could reduce the growth of xenograft tumor in vivo. CONCLUSIONS OIP5-AS1 exerted its role via miR-153-3p/ZBTB2 axis in the progression of GC cells. These findings might supply a biomarker for the diagnosis and therapy of GC clinically.OBJECTIVE To explore the expression of pyrroline-5-carboxylate reductase 1 (P5CR1) and its clinical significance and function in gastric cancer (GC). PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) and Western blot (WB) were performed to detect the expression of P5CR1 in GC tissues and normal cells. The correlation between the expression level of P5CR1 and the clinicopathological characteristics of GC patients was analyzed by the Chi-square test. Moreover, the potential of P5CR1 in predicting the postoperative prognosis of GC was assessed by Kaplan-Meier method and Log-rank test model. Clone formation, flow cytometry, scratch wound healing, and transwell assay were performed to explore the effects of P5CR1 on cell function of GC. RESULTS The expression of P5CR1 significantly increased in GC tissues and cell lines. Its expression was significantly correlated with tumor differentiation and TNM stage of GC patients. Moreover, the GC patients with lower expression of P5CR1 had a better overall survival (OS). In univariate analyses and multivariate analyses, the expression of P5CR1 was an independent prognosis index of GC. Knockdown of P5CR1 significantly attenuated clone formation, migration, and invasion abilities, while the apoptotic rate of GC cells increased. CONCLUSIONS P5CR1 was a novel factor involved in GC progression and constituted a potential biomarker and therapeutic target of GC.OBJECTIVE To determine expression characteristics of XTP8 and TGIF1 in gastric carcinoma (GC), and the potential roles of XTP8/TGIF1 axis in influencing the progression of GC. MATERIALS AND METHODS The expression levels of XTP8 and TGIF1 in GC tissues and cells were detected. Their functions in prognosis in GC patients were evaluated by the Kaplan-Meier method. The correlation between the XTP8 level and the pathological indexes of the GC patients were analyzed. The changes in the proliferation, migration, and invasion capacities of MKN-45 and SGC-7901 cells affected by XTP8 and TGIF1 were assessed. The interaction between XTP8 and TGIF1 was determined through Dual-Luciferase reporter gene assay and rescue experiments. RESULTS XTP8 was upregulated in GC tissues and cells. XTP8 level was positively correlated with lymphatic and distant metastasis, as well as poor prognosis of GC patients. The silence of XTP8 attenuated proliferation, migration, and invasion capacities of MKN-45 and SGC-7901 cells. TGIF1 was the downstream gene binding to XTP8, which was downregulated in GC, and XTP8 negatively regulated the TGIF1 level in GC tissues. MYCi975 Myc inhibitor Importantly, the knockdown of TGIF1 could abolish the regulatory effect of XTP8 on GC cell behaviors. CONCLUSIONS XTP8 is upregulated in GC and is closely linked to lymphatic metastasis, distant metastasis, and poor prognosis of GC patients. Besides, it accelerates the malignant progression via negatively regulating TGIF1.OBJECTIVE Colorectal cancer is one of the most common cancers in the world. LncRNA ROR, is a tumor oncogene associated with various human cancers. However, the role of ROR in colorectal cancer cells still remains unknown. The aim of this study was to measure the expression level of ROR and clarify its biological functions in colorectal cancer cells. MATERIALS AND METHODS The expression level of ROR in colorectal cancer cells was detected using qRT-PCR. We performed CCK8 assay, colony formation assay, cell migration and invasion assays to evaluate the effects of ROR on cell proliferation, migration and invasion of colorectal cancer cells. Then, transfection of ROR, ROR inhibitor, miRNA-223-3p-mimics and miRNA-223-3p-inhibitor, qRT-PCR, and luciferase reporter assay were used to explore the molecular mechanisms. RESULTS In the present study, Lnc-ROR was highly expressed in colorectal cancers compared with adjacent non-cancerous normal tissues. And the expression level of ROR was also increased in colorectal cancer cells (p less then 0.05). CCK8 assay and invasion assay suggested that ROR can promote cell proliferation and invasion. The luciferase reporter assay showed ROR acted as sponge and directly competed with miRNA-223-3p, then decreasing the expression of tumor suppressor gene NF2. CONCLUSIONS The findings of this study first revealed that ROR was upregulated in colorectal cancer cells and can promote cell proliferation and invasion by inhibiting tumor suppressor gene NF2 through interacting with miR-223-3p.