roniciclib (Bayer AG)
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Roniciclib, supplied by Bayer AG, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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1) Product Images from "Potent effects of roniciclib alone and with sorafenib against well-differentiated thyroid cancer"
Article Title: Potent effects of roniciclib alone and with sorafenib against well-differentiated thyroid cancer
Journal: Endocrine-related cancer
doi: 10.1530/ERC-18-0150
Figure Legend Snippet: Roniciclib induces cytotoxicity in well-differentiated thyroid cancer cells. Cytotoxicity was evaluated in cells treated with a series of six two-fold dilutions of roniciclib starting from 100 nmol/L. Dose-response curves were obtained on day 4 using LDH assays. The median-effect dose (IC50) of roniciclib on day 4 was calculated for each cell line using CompuSyn software.
Techniques Used: Software
Figure Legend Snippet: Roniciclib stimulates caspase-3 activity and induces apoptosis in well-differentiated thyroid cancer cells. (A) Caspase-3 activity was evaluated using a fluorometric assay kit in BHP7–13, K1, WRO82–1 and FTC-133 cells treated with roniciclib (25 nmol/L) or vehicle for 24 h. (B) BHP7–13 cells were treated with roniciclib (25 nmol/L) or placebo for 24 h and stained with DAPI (blue) and fluorescent antibodies against cleaved caspase-3 (red) and α-tubulin (green). A cell with cleaved caspase-3 expression is shown (arrow). (C) The percentages of cells with cleaved caspase-3 expression were assessed after treatment with placebo or roniciclib (25 nmol/L) for 24 h. Cells were stained with fluorescent antibodies against cleaved caspase-3, and its expression was evaluated using immunofluorescence confocal microscopy. A minimum of 861 cells from at least 12 different fields was counted for each condition. Roniciclib significantly increased the proportion of BHP7–13, K1, WRO82–1 and FTC-133 cells with cleaved caspase-3 expression. (D) Sub-G1 apoptotic cells were detected by measuring the DNA content using flow cytometry in cells treated with roniciclib (25 nmol/L) or vehicle for 24 h. Roniciclib increased the proportion of sub-G1 cells in four well-differentiated thyroid cancer cell lines. Scale bar, 20 μm.
Techniques Used: Activity Assay, Staining, Expressing, Immunofluorescence, Confocal Microscopy, Flow Cytometry
Figure Legend Snippet: Roniciclib decreases the protein levels of aurora A and cyclin B1 and induces G2/M phase accumulation in well-differentiated thyroid cancer cells. (A) Cell cycle distribution was analyzed by evaluating the DNA content in BHP7–13 cells treated with placebo or roniciclib (25 nmol/L) for 24 h using flow cytometry. (B) Statistical analyses revealed that roniciclib treatment (25 nmol/L) significantly arrested BHP7–13, K1, WRO82–1 and FTC-133 cells in the G2/M phase at 24 h. (C) The proportion of well-differentiated thyroid cancer cells in mitosis was assessed after treatment with roniciclib (25 nmol/L) or placebo for 24 h. Cells were stained with DAPI, and chromosome characteristics were evaluated using immunofluorescence confocal microscopy. The mitotic index was assessed with a minimum of 420 cells counted from at least 10 different fields for each condition. Roniciclib significantly decreased the proportion of BHP7–13, K1, WRO82–1 and FTC-133 cells in mitosis. (D) The expression of aurora A and cyclin B1 was evaluated by Western blotting in BHP7–13, K1, WRO82–1 and FTC-133 cells treated with roniciclib (25 nmol/L) or placebo for the indicated periods.
Techniques Used: Flow Cytometry, Staining, Immunofluorescence, Confocal Microscopy, Expressing, Western Blot
Figure Legend Snippet: Roniciclib inhibits subcutaneous xenograft growth of two well-differentiated thyroid cancer models. (A) The therapeutic efficacy of roniciclib for papillary thyroid cancer was evaluated in mice bearing K1 flank tumors. Serial oral gavage of low-dose (1.0 mg/kg) and high-dose (1.3 mg/kg) roniciclib significantly repressed K1 tumor growth by day 3 when compared with control mice, and the effect persisted through day 14. (B) Serial treatment of low-dose (1.0 mg/kg) and high-dose (1.3 mg/kg) roniciclib did not significantly decrease body weight when compared with control mice. (C) The therapeutic efficacy of roniciclib for follicular thyroid cancer was evaluated in mice bearing FTC-133 flank tumors. Serial oral gavage of low-dose (1.0 mg/kg) and high-dose (1.3 mg/kg) roniciclib significantly repressed FTC-133 tumor growth by day 3 when compared with control mice, and the effect persisted through day 21. (D) Serial treatment of high-dose roniciclib (1.3 mg/kg) slightly, but significantly induced body weight loss on day 10 when compared with control mice. This effect was not observed in mice treated with low-dose (1.0 mg/kg) roniciclib. K1 (E) and FTC-133 (F) xenograft tumors (arrowhead) were photographed on day 15. The molecular effects of roniciclib (1.3 mg/kg) treatment were evaluated in K1 (G) and FTC-133 tumors (H) using Western blot analysis. Arrow, roniciclib or placebo treatment.
Techniques Used: Drug discovery, Control, Western Blot
Figure Legend Snippet: Combination therapy of roniciclib and sorafenib in well-differentiated thyroid cancer cells. (A) Cytotoxicity was evaluated in BHP7–13, K1, WRO82–1 and FTC-133 cells treated with a series of six two-fold dilutions of sorafenib starting at 10 μmol/L. Dose-response curves were obtained on day 4 using LDH assays. (B) The median-effect dose (IC50) of sorafenib on day 4 was calculated for each cell line using CompuSyn software. (C) The cytotoxic effects of roniciclib and sorafenib alone and in combination after a 4-day treatment in BHP7–13, K1, WRO82–1 and FTC-133 cells were evaluated using LDH assays. (D) The combination index (CI) of roniciclib and sorafenib was calculated using CompuSyn software. The combination therapy of roniciclib and sorafenib had synergistic effects in WRO82–1 and FTC-133 cells, synergistic to additive effects in BHP7–13 cells and synergistic to antagonistic effects in K1 cells. Synergistic effects appeared when the affected fractions of BHP7–13 and K1 cells was lower (affected fraction < 0.9 and < 0.7, respectively). The horizontal line at CI = 1 was drawn for discrimination of synergism (CI < 1) and antagonism (CI > 1).
Techniques Used: Software
Figure Legend Snippet: Daily therapy of roniciclib and sorafenib in murine well-differentiated thyroid cancer xenograft tumor models. (A) Daily treatment of roniciclib (1.4 mg/kg) for 4 days significantly inhibited subcutaneous xenograft growth of K1 tumors compared with control mice on day 7. (B) Serial daily administration of roniciclib did not result in significant changes in body weight during the study period. (C) After FTC-133 flank tumors were established in nude mice, they were treated with oral gavage of placebo, roniciclib (1.4 mg/kg), sorafenib (25 mg/kg) or combination therapy once a day for three cycles of 4-day on and 3-day off therapy. Compared with control therapy, roniciclib, sorafenib and combination treatment all significantly inhibited tumor growth by day 3, and the inhibitory effects persisted through day 13. Combination therapy significantly retarded xenograft growth when compared with either single modality treatment on days 17 and 20. (D) No significant decreases in body weight were attributable to placebo, roniciclib, sorafenib or combination therapy compared with the baseline weight. Arrow, placebo, roniciclib, sorafenib and combination treatment.
Techniques Used: Control