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    Different doses of radiation on agar colony forming development in C6 glioma cells
    (Ortadogu Ad Pres & Publ Co, 2007) Ozmen, Tolga; Oktem, Gulperi; Tuna, Sevilcan; Biltekin, Burcu; Denir, Secnur; Bilir, Ayhan
    Objective: Gliomas are relatively frequent in adults, and are among the most malignant primary brain tumors. Glioblastoma. multiforme, like many other tumors that exhibit radiation sensitivity in vitro, seems to be very resistant to radiation in vivo, thus suggesting that irradiation may not be a rate-limiting factor for malignant glioma tumor growth. In this study, we aimed to determine the optimal dose of radiation in C6 glioma colony forming assay, which is a valuable tool for antitumor treatment screening. Material and Methods: 10(5) cell/lamella colony forming cells were radiated with 200 cGy, 400 cGy, 800 cGy and 1600 cGy for 10 minutes. Radiosensitivity was measured systematically 24, 48, 72 and 96 hours after the radiation by three methods: soft-agar bilayer assay, thymidinE incorporation, and bromodeoxyuridine (BrdU) incorporation. Results: The soft-agar bilayer assay, which assessed the colony-forming units, showed that the number of colonies in the control group (609, 3 +/- 86.8) were decreased after 200 cGy (8.3 +/- 3.6) and 400 cGy (7.2 +/- 4.3). No colony was detected in 800 cGy and 1600 cGy irradiated cells [3H] Thymidine incorporation was more prominent with higher doses of radiation. BrdU incorporation revealed that even at low doses (200 cGy) of radiation there was a significant decrease of cell proliferation. On higher doses like 1600 cGy it was more prominent. Conclusion: Cell survival, doubling time, and cell phases are parameters of growth kinetics, and the results suggest that C6 glioma cells are radiosensitive and are virtually affected by all radiation doses in our experiment even 200 cGy at 24 hours. Besides, colony forming assay with thymidine labeling index, and BrdU labeling index may be used as new methods for determining radiotherapy doses in clinical applications.
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    Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway
    (Elsevier France-Editions Scientifiques Medicales Elsevier, 2018) Erdogan, Suat; Turkekul, Kader; Dibirdik, Ilker; Doganlar, Oguzhan; Doganlar, Zeynep B.; Bilir, Ayhan; Oktem, Gulperi
    Aims: To examine the functions of growth factor midkine (MK) and a flavonoid quercetin on survival, apoptosis and migration of prostate cancer (PCa) stem cells (CSCs). Main methods: CD44(+)/CD133(+) and CD44(+) stem cells were isolated from PC3 and LNCaP cells, respectively by magnetic-activated cell sorting system. 3D cell culture was used to evaluate the ability of quercetin, MK siRNA, and the combination of both to inhibit spheroid formation, apoptosis and cell cycle arrest. Image-based cytometer, RT-qPCR, Western blotting and transwell migration assays were performed. Key findings: Quercetin treatment for 24-72 h inhibited PC3 and CD44+/CD133+ stem cell proliferation in a time-and dose-dependent manner. Knockdown of endogenous MK expression significantly suppressed proliferation of CD44(+)/CD133(+) and CD44(+) cells as well as their parent cells. Co-administration of MK siRNA and quercetin reduced the cell survival, induced apoptosis and caused G1 phase cell cycle arrest more effectively than the individual therapy. Knockdown of MK significantly enhanced the inhibitory effect of quercetin on CD44(+)/CD133(+) migration and spheroid formation. In addition, the combined therapy inhibited the phosphorylation of PI3K, AKT and ERK1/2, and reduced the protein expression of p38, ABCG2 and NF-kappa B. Significance: Quercetin alone exhibited significant cytotoxic effects on CD44(+)/CD133(+). MK plays an important role in the proliferation of CD44(+)/CD133(+) and CD44(+) cells in particular, and quercetin and MK-silencing therapy may be an important strategy in targeting CSCs that play a role in relapse, migration and drug resistance.