Journal: Breast Cancer Research and Treatment

Article Title: MYC as a therapeutic target for the treatment of triple-negative breast cancer: preclinical investigations with the novel MYC inhibitor, MYCi975

doi: 10.1007/s10549-022-06673-6

Figure Lengend Snippet: Effects of combined treatment with MYCi975 and other compounds on cell proliferation MDA-MB-453, MDA-MB-468 and BT 549 cells were treated with various concentrations of MYCi975 in combination with a YM-155, b docetaxel or c doxorubicin for five days. Cell growth was then measured by the MTT assay. Combination index (CI) values were calculated using Compusyn software. CI values < 1 indicate drug-synergy. Data were calculated and graphed using GraphPad Prism 5. Data plotted are mean ± S.E.M ( n = 3).

Article Snippet: The cytotoxic drugs, docetaxel and doxorubicin were purchased from Sigma-Aldrich and Bio-techne, respectively while the survivin inhibitor YM-155 was obtained from Merck Life.

Techniques: MTT Assay, Software

Journal: Cancer letters

Article Title: KRAS-dependent cancer cells promote survival by producing exosomes enriched in Survivin.

doi: 10.1016/j.canlet.2021.05.031

Figure Lengend Snippet: Fig. 7. Exosomal Survivin induces drug resistance in human PDAC cells. (A and B) Western blot analysis using a Survivin antibody was performed on (A) MIA PaCa-2 and (B) PANC-1 cells that had been treated with DMSO, or 0.25 μM YM155. GAPDH was used as the loading control. The relative expression levels of Survivin were quantified and included below these blots. (C and D) Western blot analysis using a Survivin antibody was performed on the exosomes isolated from the cells described in (A and B). HSP90 was used as the loading control. The relative expression levels of Survivin were quantified and included below these blots. (E and F) Cell survival assays using trypan blue were performed on BxPC-3 cells that had been treated for 36 h with (E) DMSO and 0.30 μM paclitaxel (PTX), or (F) DMSO and the combination therapy of 1.0 μM SCH772984 and 6.3 μM chloroquine (SCH + CQ). (G and H) Cell survival assays using trypan blue were performed on BxPC-3 cells that had been treated for 36 h with (G) DMSO and 0.30 μM paclitaxel, or (H) DMSO and the combination therapy of 1.0 μM SCH772984 and 6.3 μM chloroquine (SCH + CQ), and exosomes isolated from MIA PaCa-2. The plots represent the increases in cell survival determined for each condition, compared to BxPC-3 treated with only 0.30 μM paclitaxel, or the combination therapy. (I and J) Cell survival assays using trypan blue were performed on BxPC-3 cells that had been treated for 36 h with (I) DMSO and 0.30 μM paclitaxel, or (J) DMSO and the combination therapy of 1.0 μM SCH772984 and 6.3 μM chlo roquine (SCH + CQ), and exosomes isolated from PANC-1. The plots represent the increases in cell survival determined for each condition, compared to BxPC- 3 treated with only 0.30 μM paclitaxel, or the combination therapy. The data shown in (E)-(J) represent the mean ± standard error. All experiments were performed a minimum of three independent times, and statistical signif icance was determined using Student’s t-tests; *p < 0.05, ***p < 0.001 and ****p < 0.0001.

Article Snippet: As indicated, cells were treated with various combinations of 1.0 μM SCH772984 (Selleck), 6.3 μM chloroquine (Sigma), and 0.25 μM YM155 (Selleck).

Techniques: Western Blot, Control, Expressing, Isolation

Journal: Drug Design, Development and Therapy

Article Title: Id-1 Promotes Reendothelialization In The Early Phase After Vascular Injury Through Activation Of NFkB/survivin Signaling Pathway

doi: 10.2147/DDDT.S208707

Figure Lengend Snippet: BAY 11–7082 and YM155 can down-regulate the expression of NF-κB and survivin in injured vessels. Notes: ( A ) Id1 is overexpressed after ad-Id1 injection. BAY 11–7082, YM155 can down-regulate the expression of NF-kappa B and survivin mRNA in injured vessels. (# compared with Ad-Id1 group, P <0.05, *compared with Ad-GFP group, P<0.05) ( B ) Id1 is overexpressed after ad-Id1 injection. BAY 11–7082, YM155 can down-regulate the expression of NF-kappa B and Survivin mRNA in injured vessels. (# compared with Ad-Id1 group, P<0.05, *compared with Ad-GFP group, P<0.05).

Article Snippet: BAY 11–7082 (the NFκB blocker), and YM155 (survivin blocker) were obtained from Santa Cruz Biotechnology.

Techniques: Expressing, Injection

Journal: Drug Design, Development and Therapy

Article Title: Id-1 Promotes Reendothelialization In The Early Phase After Vascular Injury Through Activation Of NFkB/survivin Signaling Pathway

doi: 10.2147/DDDT.S208707

Figure Lengend Snippet: Blocking κB and Survivin attenuates the inhibitory effect of Ad-Id1 on restenosis of injured vessel. Notes: ( A ) BAY 11–7082 and YM155 can attenuate Id1 over-expression and promote rapid re-endothelialization of injured vessels. (# P<0.05 vs Ad-Id1) ( B ) NF-kappa B/survivin signal blockade attenuates early reactive intimal hyperplasia induced by Ad-Id1 (# compared with Ad-GFP group, P <0.05).

Article Snippet: BAY 11–7082 (the NFκB blocker), and YM155 (survivin blocker) were obtained from Santa Cruz Biotechnology.

Techniques: Blocking Assay, Over Expression

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: YM155 IC 50 values in pancreatic cancer cell line.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques:

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: A, Concentration-dependent effects of a 24-hour treatment with YM155 on the expression of survivin and XIAP in PANC-1, MIAPaCa-2, and BxPC-3 cells were determined by Western blotting. B, The effect of YM155 on the expression of XIAP was compared with that of survivin knockdown by Western blotting. PANC-1 cells were treated with YM155 for 24 hours or transfected with 40 nM siRNA (siSurvivin, siXIAP, and scrambled siRNA) for 48 hours. *, nonspecific. C, Concentration-dependent effects of YM155 on the expression of anti-apoptotic (Bcl-xL and Mcl-1) and pro-apoptotic (Bid and Bad) proteins were examined in PANC-1, MIAPaCa-2, and BxPC-3 cells.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques: Concentration Assay, Expressing, Western Blot, Knockdown, Transfection

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: A, Levels of PI3K and survivin were analyzed by Western blotting after treating with YM155 or 30 µM LY294002 (control) for 24 hours, and 48 hours after transfection with 40 nM siRNA. B, Levels of phosphorylated ERK and expression of survivin were determined by Western blotting after treating for 24 hours with YM155 or 500 ng of AZD6244, and 48 hours after transfection of 40 nM siRNA. C, Levels of phosphorylated STAT3 and expression of survivin were analyzed by Western blotting after a 24-hours treatment with YM155 and 48 hours after transfection of 40 nM siRNA.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques: Western Blot, Control, Transfection, Expressing

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: A, PANC-1 cells were stimulated with 100 ng/ml EGF for 10 minutes before incubating with or without YM155 for 6 hours. Cetuximab (CTX; 100 ng/ml for 1 hour) was used as a control. Levels of phosphorylated (Y1068) EGFR and total EGFR were analyzed by Western blotting. B, YM155 diminished the expression of EGFR in a concentration-dependent manner in PANC-1, MIAPaCa-2 (cropped blots; full-length blots are presented in ), and BxPC-3 cells. The ratio of EGFR∶actin expression compared with the control is shown for each lane (using Multi-Gauge v2.3 software). C, Survivin and EGFR expression were detected in subcellular fractions of PANC-1 cells by Western blotting. Cytoplasmic (cyto) and nuclear (nu) fractions were isolated after exposure to YM155 for 24 hours. Aldolase (cytoplasmic) and H3 (nuclear) served as markers for the purity of subcellular fractions. Total lysates (total) were analyzed concurrently. D, YM155 (10 nM) induced the nuclear EGFR accumulation. PANC-1 cells were stained with anti-EGFR, anti-Alexa Fluor 488, and DAPI after the YM155 treatment. Scale bars: 10 µm.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques: Control, Western Blot, Expressing, Concentration Assay, Software, Isolation, Staining

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: A, After treatment of PANC-1 cells with YM155 for 24 hours, survivin, EGFR, and XIAP mRNA levels were determined using real-time RT-PCR. B, Survivin, EGFR, and XIAP levels in PANC-1 cells after treatment with 50 µg/ml cycloheximide (CHX) in the absence or presence of 100 nM YM155 for the indicated periods were examined by Western blotting. The ratio of survivin, EGFR, or XIAP∶actin expression compared with the control is shown for each lane. *, nonspecific.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques: Quantitative RT-PCR, Western Blot, Expressing, Control

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: A, YM155 induced lysosomal degradation of EGFR, XIAP, and survivin in PANC-1 cells. PANC-1 cells were treated with 100 nM YM155 (YM), 10 µM MG-132 (MG), 50 µM chloroquine (CQ), or 30 µM Z-VAD-fmk (Z-VAD) without or with YM155 for 24 hours. The expression ratios of EGFR, XIAP, or survivin to actin compared with the control are shown for each lane. ctrl, control; M+Y, MG-132+YM155; C+Y, chloroquine+YM155; Z+Y, Z-VAD-fmk+YM155. B, PANC-1 cells treated with 100 nM YM155 for 6 hours were immunoprecipitated (IP) with antibodies against EGFR, survivin or XIAP, and analyzed by Western blotting for ubiquitin. C, The time-course of EGFR phosphorylation at Y1045 in PANC-1 cells after treatment with YM155 (100 nM) is shown.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques: Expressing, Control, Immunoprecipitation, Western Blot, Ubiquitin Proteomics, Phospho-proteomics

Journal: PLoS ONE

Article Title: YM155 Induces EGFR Suppression in Pancreatic Cancer Cells

doi: 10.1371/journal.pone.0038625

Figure Lengend Snippet: Effects of YM155 on tumor growth (A) and body weight (B) in vivo were evaluated in MIAPaCa-2 xenografts (vehicle, n = 6; YM155, n = 8). Tumor volume was determined at the indicated times after the onset of treatment. YM155 was administered at dose of 50 mg/kg. The in vivo experimental schedule of YM155 is indicated at the bottom of each graph. Day 0 indicates the time at which subcutaneous tumors reached a size of 100 mm 3 and administration of YM155 was started. Statistical analyses of the effects of YM155 on tumor size were performed using Mann-Whitney tests (*p<0.05, **p<0.01, ***p<0.001, YM155 vs. vehicle). C, Average tumor sizes are depicted for each group on day 31. D, Immunohistochemical analyses in xenograft tumors on day 31 after the YM155 treatment were performed using antibodies against EGFR, survivin, and XIAP and stained with H&E.

Article Snippet: YM155 was obtained from Hanmi Pharmaceuticals (Seoul, Korea).

Techniques: In Vivo, MANN-WHITNEY, Immunohistochemical staining, Staining