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OBJECTIVE: To investigate clinical effects of hepatic artery interventional embolization chemotherapy (TACE) for primary hepatocellular carcinoma (PHC). METHODS: 73 patients with PHC in our hospital from January 2017 to January 2018 were selected and divided into 37 cases in study group and 36 cases in control group by random number table method. The control group received only ultrasound-guided microwave ablation treatment, and the study group received TACE treatment again before surgery based on control group. The expression levels of cancer antigen 125 (CA125), alpha-fetoprotein (AFP), multiple tumor suppressors 1 (P16) proteins, and cancer antigen 19-9 (CA19-9) were compared between the two groups at different time periods after treatment, and the remission rate (ORR), control rate (DCR), complication rate at 3 months after treatment and survival rate at 3 years after treatment were compared. RESULTS: After 1 year of treatment, ORR, DCR, and P16 protein levels in the study group were higher than those in the control group (P < 0.05), and differences were statistically significant; CA125, CA19-9, and AFP levels in study group were lower than those in the control group (P < 0.05), and differences were statistically significant. The regression equation showed that long-term survival rate of both groups showed decreasing trend over time, while long-term survival rate of study group was always higher than that of the control group. CONCLUSION: Comprehensive intervention for hepatic artery interventional chemoembolization in patients with primary hepatocellular carcinoma is more effective, which can effectively reduce incidence of complications and adverse effects in patients and help shorten treatment time of hepatic artery interventional chemoembolization in patients.

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INTRODUCTION: FENDRR is a long non-coding RNA (lncRNA) that mediates the modification of the epigenetic landscape of target promoters by binding to polycomb repressive complex 2. However, the role of FENDRR in breast cancer remains unknown. MATERIALS AND METHODS: We detected the expression of FENDRR in 52 breast cancer patients' tissues and five breast cancer cell lines. The association between FENDRR expression and clinicopathological features and prognosis of breast cancer patients was also analyzed. Moreover, cell proliferation assays, flow cytometry analysis, wound-healing assays, and transwell migration assays were performed to detect the biological effects of FENDRR in the breast cancer cells. A xenograft model was used to explore the role of FENDRR expression on tumor growth. RESULTS: We found that FENDRR expression was lower in breast cancer cell lines and cancerous tissues than in the adjacent normal tissues. Low expression of FENDRR was associated with a shorter overall survival and a shorter progression-free survival in breast cancer patients (p<0.001, p<0.001, respectively). We found that FENDRR inhibits breast cancer cell proliferation and migration and promotes cell apoptosis, while FENDRR knockdown promotes breast cancer cell proliferation and migration and suppresses cell apoptosis. Finally, we also detected that FENDRR overexpression could inhibit tumor growth in a xenograft model. CONCLUSION: Our data suggested that FENDRR inhibits breast cancer cell proliferation, promotes cell apoptosis, and is associated with good prognosis in breast cancer. Thus, FENDRR plays an important role in the growth and progression of breast cancer.

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A reversible Schiff's base fluorescence probe for Al3+, (3,5-dichloro-2- hydroxybenzylidene) quinoline-2-carbohydrazide (QC), based on quinoline derivative has been designed, synthesized and evaluated. The QC exhibited a high sensitivity and selectivity toward Al3+ in EtOH-H2O (v/v=1:9, pH=6) by forming a 1:1 complex with Al3+ and the detection limit of QC for Al3+ was as low as 0.012µM. Furthermore, these results displayed that the binding of QCAl3+ was broken by F-, so this system could be used to monitor F- in the future. The enhancement fluorescence of the QC could be attributed to the inhibition of PET and ESIPT and the emergency of CHEF process induced by Al3+. More importantly, QC was not only successfully used for the determination of trace Al3+ in the tap water and the human blood serum, but was valid for fluorescence imaging of Al3+ in the Hela cells.

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Prohibitin (PHB) is an evolutionarily conserved protein with multiple functions in both normal and cancer cells. Androgen receptor (AR) was reported to act as a different role in the ER-positive and ER-negative breast cancer. However, little is known about the role of PHB and whether PHB could regulate AR expression in the ER-positive breast cancer. Here, we determined the expression and clinical outcomes of PHB in breast cancer samples using 121 breast cancer tissues and published databases, and investigated the role of PHB in breast cancer cell growth, apoptosis and cell cycle arrest in the ER-positive breast cancer cells. We obtained the expression of PHB is significantly low in breast cancer samples, and low PHB expression positively correlated with poor prognosis of breast cancer. We detected that PHB could inhibit breast cancer cell proliferation, change cell cycle distribution and promote cell apoptosis in the ER-positive breast cancer cells. Moreover, we found PHB could significantly increase AR expression in both mRNA and protein levels in the ER-positive breast cancer cells. Additionally, a significant positive correlation between PHB and AR expression was identified in the 121 breast cancer tissues. PHB and AR expression are associated with prognosis in the ER-positive breast cancer patients. Our results indicate that PHB promotes AR activation in ER-positive breast cancer, making PHB and AR potential molecular targets for ER-positive breast cancer therapy.

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PURPOSE: Although existing evidence from clinical trials has demonstrated manifestation of gastrointestinal perforation with the use of ramucirumab, overall risks have yet to be reported. Therefore, we performed a meta-analysis of published randomized controlled trials (RCTs) to get a better understanding of the overall incidence and risk of gastrointestinal perforation associated with ramucirumab. METHODS: The PubMed and Web of Science databases as well as abstracts presented at American Society of Clinical Oncology conferences were searched to identify relevant studies published up to 01 May 2015. Eligible studies included randomized trials of ramucirumab either alone or in combination with another agent compared with the control arm without ramucirumab and that reported gastrointestinal perforation event. Overall incidence, relative risk (RR) and 95% confidence intervals (CI) were computed using fixed- or random-effects models depending on the heterogeneity of the included studies. RESULTS: A total of 4579 patients with a variety of solid malignancies from six RCTs were included in our meta-analysis. The incidence of gastrointestinal perforation related to ramucirumab was 1.5% (95% CI 1.1-2.1%) with a mortality of 29.8% (95% CI 14.9-50.7%). The RR of gastrointestinal perforation associated with ramucirumab was 2.56 (95% CI 1.29-5.09; P = 0.007). CONCLUSIONS: Treatment with the ramucirumab is associated with a significant increase in risk of gastrointestinal perforation in cancer patients.

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Gracillin, a kind of steroidal saponin isolated from the root bark of wild yam Dioscorea nipponica has been reported to exert antitumor activity. In the present study, we investigated the anticancer activity of gracillin against HL60 cells, and evaluated the possible mechanism involved in its antineoplastic action. The cell proliferation was evaluated by cell counting Kit-8 (CCK-8) assay, gracillin inhibited the growth of HL60 cells in a time- and concentration-dependent manner. Flow cytometry was used to analyze the cell cycle distribution whereas Annexin V-FITC/PI flow cytometry analysis was carried out to confirm apoptosis induced by gracillin, Our results demonstrated that gracillin could induce cell cycle arrest of G1 and apoptosis in HL60 cells. Furthermore, based on the biochemical methods, induction of oxidative stress by gracillin was indicated by increased the content of malondialdehyde (MDA), and decreased superoxide dismutase (SOD) activity. In addition, real time-PCR verified the expression of apoptosis-related genes, the mRNA level of Bcl-2 was decreased dramatically, while Bax was remarkably increased by gracillin. Taken together, gracillin could induce cell cycle arrest, oxidative stress, and apoptosis in HL60 cells, and has the potential to be developed as an antitumor agent.

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OBJECTIVE: The aim of this study was to investigate the inhibitory effects of cytokine-induced killer (CIK) cells combined with docetaxel (DTX) on the growth of drug-resistant lung adenocarcinoma cell line SPC-A1/DTX in vitro and in vivo. METHODS: The MTT assay was employed to evaluate the cytotoxic activity of DTX, CIK cells, and DTX plused CIK cells against SPC-A1/DTX cells in vitro. For the in vivo assay, SPC-A1/DTX cells were injected into nude mice subcutaneously to establish a tumor-bearing mice model. On the day 14, normal saline, docetaxel, CIK cells, and CIK cells combined with docetaxel were administered intraperitoneally, respectively. All the nude mice were sacrificed at day 15 after treatment and the tumors were weighed out. RESULTS: The MTT assay showed that CIK cells possessed a higher antitumor cytotoxic activity against SPC-A1/DTX cells than SPC-A1 cells in vitro (p < 0.05). The synergetic antitumor activity positively correlated with the E:T ratio and the concentration of docetaxel. The animal data also suggested that CIK cells combined with DTX had a stronger suppressive effect on tumor growth in vivo. CONCLUSION: CIK cells plused with docetaxel demonstrated a prominent augmentation of antitumor activity against multidrug resistance lung adenocarcinoma cell lines both in vitro and in vivo.

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