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Early diagnosis is important to improve the prognosis of pancreatic cancer (PC). Identifying potential biomarkers is essential for the monitoring and treatment of PC. The long noncoding RNA (lncRNA) UFC1 has been identified as an oncogenic factor in many cancers. However, the expression of UFC1 and its potential role in diagnosis and prognosis of PC remain largely unknown. The present study aimed to investigate the role of serum UFC1 in diagnosis and prognosis. The results indicated that serum UFC1 expression was relatively higher in PC patients than that in healthy volunteers. ROC curve analysis revealed that the serum UFC1 levels could distinguish PC patients from healthy controls, with an AUC value of 0.810. In addition, the serum UFC1 expression level was associated with lymph nodes metastasis, distant metastasis, and clinical stage. Kaplan-Meier analysis indicated that patients with high UFC1 expression exhibited shorter progression-free survival (PFS) and overall survival (OS) than those with low UFC1 expression. Multivariate analysis demonstrated that clinical stage and UFC1 expression level were significant, independent prognostic factors in PC patients. Our data demonstrate that serum UFC1 might serve as a potential biomarker for diagnosis and prognosis of PC.

Purpose: The aim of this study was to investigate effects of adipose-derived mesenchymal stem cells (AMSCs) on radioresistance of breast cancer cells. Materials and Methods: MTT assays were used to detect any influence of AMSC supernatants on proliferation of breast cancer cells; cell migration assays were used to determine the effect of breast cancer cells on the recruitment of AMSCs; the cell survival fraction post-irradiation was assessed by clonogenic survival assay; γ-H2AX foci number post-irradiation was determined via fluorescence microscopy; and expression of IGF-1R was detected by Western blotting. Results: AMSC supernatants promoted proliferation and radioresistance of breast cancer cells. Breast cancer cells could recruit AMSCs, especially after irradiation. IGF-1 derived from AMSCs might be responsible for the radioresistance of breast cancer cells. Conclusions: Our results suggest that AMSCs in the tumor microenvironment may affect the outcome of radiotherapy for breast cancer in vitro.

To evaluate the effect of gemcitabine in enhancing the radiosensitivity of hepatoma cell line HepG2 and explore its mechanisms.Clonogenic survival assay is employed to calculate the ratios of L-Q model radiation biology parameters and radiosensitization after different doses of irradiation. Flow cytometry was used to detect the changes in HepG2 cell cycle and apoptosis rate after gemcitabine treatment and radiation exposure.The survival fraction at 2 Gy of HepG2 cells treated with gemcitabine was significantly lower, and the value of alpha was significantly higher than those of untreated cells. GEM treatment increased the percentage of radiation-induced G0/G1 phase cells and cell apoptosis.Gemcitabine can significantly enhance the radiosensitivity of HepG2 cells by enhancing radiation-induced cell cycle arrest in G0/G1 phase and cell apoptosis.

To evaluate the effect of COX-2 silencing on the radiosensitivity of a nasopharyngeal carcinoma (NPC) cell line C666-1.Anti-COX-2 C666-1 cell line with COX-2 gene silencing mediated by shRNAmir lentiviral vector and the control cell line Anti-GL-2 C666-1 were exposed to various radiation doses. The clonogenic survival assay and curve fitting was used to calculate the radiobiological parameters and the sensitization enhancement ratio after the radiation. Cell cycle changes were assessed after the exposure by flow cytometric analysis. In a BALB/c nude mouse model, the growth curve of the xenografts was generated and the tumor growth inhibition rate was calculated.Compared with the control cells, Anti-COX-2 C666-1 cells showed obviously lowered values of SF2, D0 and Dq but significantly increased α/β with a sensitivity enhancement ratio of 1.4014. COX-2 gene silencing increased the inhibition rate of the tumor xenografts after the radiation, and caused also decreased percentage of G2/M arrest resulting from the exposure.Stable COX-2 silencing in NPC cells can improve the effect of radiotherapy both in vitro and in vivo. By changing the radiobiological parameters, genetically based COX-2 inhibitor may be a potentially promising radiosensitizer of NPC.

To investigate radiation-induced cell cycle changes of human breast cancer stem cells enriched by suspension culture.The tumorigenicity of human breast cancer stem cell line MCF-7 cultured in serum-free media was confirmed in NOD/SCID mice, and the radiosensitivity of the cells was tested by clone formation assay following radiation exposure. Flow cytometry was performed to evaluate radiation-induced cell cycle changes, and the protein expression of pCDC25C (ser216) was measured by Western blotting.After the exposure to 2 Gy radiation, the survived fraction of the cells in suspension culture and those in adherent culture was 0.856 ∓ 0.061 and 0.783 ∓ 0.097, respectively, and the cells in suspension culture showed an obviously greater capacity of tumorigenicity in NOD/SCID mice. The radiation exposure resulted in an obvious increase in the proportion of G2 phase cells from (22.03 ∓ 2.12)% to (45.83 ∓ 2.25)% and significantly increased the expression of pCDC25C (ser216).Radiation- induced G2 phase arrest may contribute to the resistance of the breast cancer stem cells to radiotherapy.