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To explore the most predictive lymph node (LN) scheme for stage IIIC endometrial cancer (EC) patients after hysterectomy and develop a scheme-based nomogram.Data from 2626 stage IIIC EC patients, diagnosed between 2010 and 2014, were extracted from the Surveillance, Epidemiology, and End Results (SEER) registry. The predictive ability of four LN schemes was assessed using C-index and Akaike information criterion (AIC). A nomogram based on the most predictive LN scheme was constructed and validated. The comparison of the predictive ability between nomogram and FIGO stage was conducted using the area under the receiver operating characteristic curve (AUC) and decision curve analysis (DCA).FIGO stage (stage IIIC1/stage IIIC2) was not an independent risk factor for OS in stage IIIC EC patients (P = 0.672) and log odds of positive lymph nodes (LODDS) had the best predictive ability (C-index: 0.742; AIC: 8228.95). A nomogram based on LODDS was constructed and validated, which had a decent C-index of 0.742 (0.723-0.762). The nomogram showed a better predictive ability than that of the FIGO staging system.FIGO IIIC1/FIGO IIIC2 could not differentiate the prognosis for stage IIIC EC patients. We developed and validated a nomogram based on LODDS to predict OS for post-operative patients with stage IIIC EC.

Many of the current methods for enzyme purification and immobilization suffer from several drawbacks, such as requiring tedious multistep procedures or long preparation, and being environmentally unfriendly, due to the chemicals and conditions involved. Thus, a simple technique for direct purification and immobilization of target enzymes from cell lysates was proposed. The elastin-like polypeptides (ELPs)-SpyCatcher chimera could mediate the formation of silica carriers within seconds and the target enzymes were then covalently immobilized on silica carriers via SpyCatcher/SpyTag spontaneous reaction. These tailor-made carriers were easily prepared, with precisely controlled morphology and size, as well as none-consuming surface modification needed, which could specifically immobilize the SpyTag-fused target enzymes from the cell lysate without pre-purification.

Tumor angiogenesis plays a critical role in hepatocellular carcinoma (HCC) development and progression, but its mechanism is unclear. Krüppel-like factor 8 (KLF8) is a transcription factor that plays an important role in HCC progression. Here, we investigated the role of KLF8 in angiogenesis in HCC and its possible mechanism. Immunohistochemistry, quantitative RT-PCR, western blotting, promoter reporter assays, chromatin immunoprecipitation (ChIP), and chicken chorioallantoic membrane (CAM) and nude mouse tumor models were used to show that the mRNA and protein expression levels of KLF8 and VEGFA are highly correlated in HCC tissue samples. The up-regulation of KLF8 increased VEGFA protein levels and induced VEGFA promoter activity by binding to the CACCC region of the VEGFA promoter. In addition, KLF8 regulated HIF-1α and Focal adhesion kinase (FAK) expression. The PI3K/AKT inhibitor LY294002 inhibited KLF8-induced VEGFA expression, whereas PI3K/AKT signaling pathway proteins, such as P-PDK1(Ser241) and P-AKT(Thr308), were decreased significantly. KLF8-overexpressing HCC cells had a higher potential for inducing angiogenesis. Thus, our results indicate that KLF8 may induce angiogenesis in HCC by binding to the CACCC region of the VEGFA promoter to induce VEGFA promoter activity and through FAK to activate PI3K/AKT signaling to regulate HIF-1α expression levels.

Radiotherapy is the principal therapy for nasopharyngeal carcinoma (NPC) at early stages. A number of chemotherapeutic methods have been used to inhibit the progression of NPC at elevated stages. Suramin has been reported to inhibit the growth of certain tumor cells via various pathways. In the present study, we aimed to analyze the effects of suramin on the proliferation of NPC cells (CNE-2). Suramin was proved to demonstrate NPC cell growth-inhibiting effects both in a dose- and time-dependent manner. To determine the potential mechanisms of these effects, western blotting and flow cytometric analysis were performed. Suramin was found to have the potential to induce cell cycle arrest in S-phase CNE-2 cells. Additionally, we found that the OPN level may decrease in suramin-treated CNE-2 cells. The changes of certain apoptosis- and p-AKT-associated proteins possibly regulating the OPN expression were measured by western blotting. In conclusion, suramin may function as a potential agent for the adjunctive therapy of NPC.

Objective To investigate the effects of Id1 on proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells in vitroand its mechanism. Methods Human nasopharyngeal carcinoma cell NP69 and CNE1 were cultured in vitro. Small interfering RNA and expression vector of Id1 were transfected into NP69 and CNE1 cells respectively. NP69 cells transfected with Id1 siRNA or control plasmid Scramble for 72h (named NP69si-Id1 and NP69-NC respectively), and CNE1 cells transfected with pcDNA3.1-Id1 and control pcDNA3.1 for 48h (named CNE1-Id1 and CNE1-Vector respectively) were collected. The effect of siRNA or pcDNA3.1-Id1 on the expression level of Id1 was evaluated by reverse transcriptase-PCR and Western blotting. MTT assay was performed to compare the effects of DDP on proliferation of both CNE1-Id1 and CNE1-Vector and both NP69si-Id1 and NP69-NC. CalcuSyn software was used to calculate the IC50 values of cells to cisplatin (DDP). After the 1μg/ml DDP and nasopharyngeal carcinoma cells were coincubated for 24 hours, the expressions of cell apoptotic protein caspase-3, Bax, Bad, and the Thr308 and Ser473 phosphorylation of protein kinase B (Akt) were analyzed by Western blotting. Results Obviously lower Id1 mRNA and protein levels were detected in NP69si-Id1 cells as compared with NP69-NC cells and obviously higher Id1 mRNA and protein levels in CNE1-Id1 cells than in CNE1-Vector were found. The IC50 value of the NP69si-Id1 cells for DDP (0.207±0.008μg/ ml) was significantly lower than the NP69-NC cells (0.405±0.009μg/ml, P < 0.05), and the IC50 value of CNE1-d1 cells for DDP (0.671±0.012μg/ml) was significantly higher than that of CNE1-Vector (0.445±0.008/ml, P < 0.05). Western blotting results indicated that the fault zone of caspase-3 increased, and Akt phosphorylation at Thr308 and Ser473 decreased in NP69si-Id1 than in NP69-NC, while the fault zone decreased, and Akt phosphorylation at Thr308 and Ser473 increased more significantly in CNE1-Id1 than in CNE1-Vector. Conclusion Id1 can promote the proliferation of nasopharyngeal carcinoma cells and resist the apoptosis induced by DDP, and the mechanism may be related to the up-regulation of p-Akt.

Purpose: Repair of radiation-induced DNA damage plays a critical role for both the susceptibility of patients to side effects after radiotherapy and their subsequent cancer risk. The study objective was to evaluate whether DNA repair data determined in vitro are correlated with the occurrence of acute side effects during radiotherapy. Experimental Design: Nasopharyngeal cancer patients receiving radiation therapy were recruited in a prospective epidemiologic study. As an indicator for clinical radiosensitivity, adverse reactions of the skin were recorded. Cryopreserved lymphocytes from 100 study participants were γ-irradiated with 5 Gy in vitro and analyzed using the alkaline comet assay. Reproducibility of the assay was determined by repeated analysis (n = 22) of cells from a healthy donor. A coefficient of variation of 0.24 was calculated. Results: The various parameters determined to characterize the individual DNA repair capacity showed large differences between patients. Twenty-one patients were identified with considerably enhanced DNA damage induction, and 19 patients exhibited severely reduced DNA repair capacity after 15 and 30 minutes. Eight patients were considered as clinically radiosensitive, indicated by moist desquamation of the skin after a total radiation dose of 70 Gy. Conclusions: Using the alkaline comet assay as described here, nasopharyngeal cancer patients were identified showing abnormal cellular radiation effects, but this repair deficiency corresponded only at a very limited extent to the acute radiation sensitivity of the skin.

To investigate the relationship between the radiosensitivity of hepatic carcinoma cells and their survivin expression levels.Hepatic carcinoma cell lines HepG2 and SMMC-7721 were irradiated with various doses of 60Co gamma-rays. The cell survival rate, expression of survivin, cell cycle profile and activity of caspase-3 were respectively detected by clonogenic assay, immunocytochemistry, flow cytometry and chromatometry.The surviving fraction at 2Gy (SF2) of HepG2 and SMMC-7721 were 0.43+/-0.01 vs 0.70+/-0.02, and HepG2 had higher radiosensitivity than SMMC-7721. gamma-rays radiation up-regulated the expression of survivin. SMMC-7721 had a significantly higher expression of survivin than HepG2 (t = 2.81-5.20, P0.05). The activity of caspase-3 was more powerful in HepG2 than in SMMC-7721 (t = 6.05-6.72, P0.01).Survivin may play a critical role in mediating radiation resistance in SMMC-7721 through its up-regulation and caspase-3 dependent manner.

Purpose The purpose of this study was to determine whether the distribution of radiosensitivities in normal tissues of head and neck cancer patients, measured using a DNA damage assay on lymphocytes, is likely to provide sufficient discrimination to enable reliable identification of patients with abnormal sensitivities. Material and methods Radiosensitivity was assessed in 307 lymphocyte samples from unselected head and neck cancer patients and was quantified as the initial number of DNA double-strand breaks (dsb) induced per Gray and per DNA unit (200 Mbp). Results The existence of an inter-individual variation in the radiosensitivity parameter is described by the range (0.41--9.38 dsb/Gy/DNA unit) of the values found. We detected 37 patients who developed severe skin reactions during radiotherapy treatment and we compared their radiosensitivity values with the remaining patients treated. Radiosensitivity values of >7.20 dsb/Gy/DNA unit should theoretically correspond to highly radiosensitive patients. Conclusions Our results suggest that initial DNA damage measured on lymphocytes offers an approach to predict the acute response of human normal tissues prior to radiotherapy. .

To investigate the inhibition effects of c-erbB-2 and c-raf-1 antisense oligodeoxynucleotides (ASODN) combined transfection on the human ovarian epithelial cancer transplanted subcutaneously in nude mice.There were 7 groups: normal control group, c-erbB-2 sense observed group, c-raf-1 sense observed group, c-erbB-2 antisense observed group, c-raf-1 antisense observed group, whole dose combined group, half dose combined group. Human ovarian epithelial cancer cells SKOV3 were treated by different oligodeoxynucleotides, then transplanted subcutaneously in nude mice, respectively. The changes of tumor volume were observed and the tumor growth inhibitory rate was calculated.There was no difference between sense observed group and normal control group. There was a larger growth inhibitory rate in whole -dose combined group and half -dose combined group, the first time that can be detected was 13.7 days and 15.2 days, and the maximum tumor growth inhibitory rates were 61.1% and 71.3%, respectively.The results suggested that ASODN combined transfection can inhibit the tumorigenesis of ovarian epithelial cancer cells in nude mice, it may be a more useful gene therapy for the ovarian epithelial carcinoma.