Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: 3-O-acetyl-11-keto-β-boswellic acid exerts anti-tumor effects in glioblastoma by arresting cell cycle at G2/M phase

doi: 10.1186/s13046-018-0805-4

Figure Lengend Snippet: Proposed mechanistic scheme: AKBA suppresses glioblastoma by arresting cell cycle at G2/M phase. AKBA activates p21 which decreases expression of FOXM1 and its downstream target genes including Aurora A, Aurora B, PLK1, and cyclin B1. Inhibiting Aurora A suppresses the expression of PLK1 which leads to the inactivation of CDK1/cyclin B1 complex and arrests the cell cycle at the G2/M checkpoint. Inhibiting Aurora B decreases expression of TOP2A and inhibits mitosis

Article Snippet: After blocking with 5% fat-free milk in TBST for 1 h, membranes were immunoblotted with primary antibodies to caspase3, cleaved-caspase3, PARP, cleaved-PARP, p21, p-RB, PLK1, p-CDK1, and Aurora B (Cell Signaling Technology); p53, FOXM1, Aurora A, CDC-25C, CDK-1, cyclin B1, TOP2A, and GAPDH (Proteintech) at the appropriate dilutions with gentle shaking overnight at 4 °C.

Techniques: Expressing

Journal: Cancers

Article Title: Aurora Kinase A Inhibition Potentiates Platinum and Radiation Cytotoxicity in Non-Small-Cell Lung Cancer Cells and Induces Expression of Alternative Immune Checkpoints.

doi: 10.3390/cancers16162805

Figure Lengend Snippet: Figure 5. Knockdown of AURKA increases apoptosis induced by cisplatin or radiation. (A) Expres- sions of C-PARP, AURKA, and GADPH were shown in PC9 and A549 cells with and without the treatment of cisplatin and/or doxycycline for 48 h. (B) Expressions of C-PARP, AURKA, and GADPH were shown in PC9 and A549 cells (with and without the treatment of radiation and/or doxycycline for 48 h). The ratios of band intensities divided by GAPDH are noted at the top of each protein band.

Article Snippet: For Western blot analysis, antibodies against AURKA (catalog no. 91590), phosphoAurora A (Thr288) (catalog no. 3079), total PARP (catalog no. 9532), cleaved PARP (Asp214) (catalog no. 5625), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (catalog no. 5174) were sourced from Cell Signaling Technology (Boston, MA, USA).

Techniques: Knockdown

Journal: Cancers

Article Title: Aurora Kinase A Inhibition Potentiates Platinum and Radiation Cytotoxicity in Non-Small-Cell Lung Cancer Cells and Induces Expression of Alternative Immune Checkpoints.

doi: 10.3390/cancers16162805

Figure Lengend Snippet: Figure 6. Inhibiting AURKA by MLN8237 induces apoptosis and senescence. (A) Western blotting: the expression of cleaved PARP and GADPH in PC9 and A549 cells with and without treatment of cisplatin and/or MLN8237 for 48 h. (B) Representative picture of staining of senescence-associated beta-galactosidase in PC9 and A549 cells with and without treatment of cisplatin and/or MLN8237. (C) Quantitative analysis of staining of senescence-associated beta-galactosidase in PC9 and A549 cells with and without treatment of cisplatin and/or MLN8237.

Article Snippet: For Western blot analysis, antibodies against AURKA (catalog no. 91590), phosphoAurora A (Thr288) (catalog no. 3079), total PARP (catalog no. 9532), cleaved PARP (Asp214) (catalog no. 5625), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (catalog no. 5174) were sourced from Cell Signaling Technology (Boston, MA, USA).

Techniques: Western Blot, Expressing, Staining

Journal: EMBO Reports

Article Title: Aurora B‐dependent polarization of the cortical actomyosin network during mitotic exit

doi: 10.15252/embr.202152387

Figure Lengend Snippet: Maximum projection of 2 z slices of Hela cells immunostained for pERM following 10 min of forced mitotic exit in presence of DMSO, 1 µM AZD1152 and 1 µM Aurora A inhibitor I. Cells fail to polarize cortical pERM when treated with another Aurora B inhibitor AZD1152, but are not affected by Aurora‐A inhibition, suggesting that this function is specific to Aurora B during mitotic exit. Scale bar = 10 µm. Quantification of pERM intensity across the perimeter of cells as shown in Fig , where 5 and 6 represent regions closest to DNA, and 1 and 10 furthest. DMSO ( n = 28 cells) or Aur‐A inhibitor‐treated cells ( n = 8 cells) display an increase in pERM levels as the distance from the DNA increases, whereas cells treated with AZD1152 ( n = 19 cells) during exit fail to polarize cortical pERM. Data are represented as mean ± SD. Maximum projection of 2 z slices of Hela cells immunostained for pERM following 10 min of forced mitotic exit after siControl, siINCENP or siKLP2 treatment. While Control siRNA‐treated cells polarize their cortex, depletion of INCENP or MKLP2 leads to a failure in polarization. Note, the clearance of pERM close to DNA in control conditions, which does not occur following INCENP or MKLP2 depletion. Scale bar = 10 µm. Quantification of pERM intensity across the perimeter of the cells shown in (C), where 5 and 6 represent regions closest to DNA, and 1 and 10 furthest. Control siRNA‐treated cells ( n = 21 cells) show polarization of pERM. By contrast, this polarization is not seen following siRNA‐mediated silencing of INCENP ( n = 19 cells) or MKLP2 ( n = 19 cells). Data are represented as mean ± SD.

Article Snippet: 2 μM ZM447439 (Selleck) and 1 μM AZD1152 (Selleck) were used for Aurora B inhibition and 1 μM of Aurora A inhibitor I (Selleck‐S1451) was used for Aurora A inhibition.

Techniques: Inhibition, Control