Journal: American journal of hematology

Article Title: Voxelotor Treatment of a Patient With Sickle Cell Disease and Very Severe Anemia

doi: 10.1002/ajh.25389

Figure Lengend Snippet: Summary of measured fractions of hemoglobin modified with Voxelotor during treatment determined from oxygen binding curves a , Voxelotor dosage schedule and pertinent laboratory parameters

Article Snippet: We thank Global Blood Therapeutics for the gift of Voxelotor used in this study, the Department of Transfusion Medicine (DTM) at the NIH for transfusion support and Dr. Joshua Lehrer for helpful discussion and sharing results of unpublished work.

Techniques: Modification, Binding Assay

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Images of phosphorylated PTK (top) and STK (bottom) PamChip during the final cycle. (B) Phyla trees displaying the alterations of PTK and STK kinase activity in the HCC tumor with Imatinib (top), Rebastinib (middle), or Olverembatinib (bottom) compared to vehicle in men (left) and women (right). (C) Heatmaps showing the phosphorylation of 196 PTK substrates in men (top) and women (bottom) HCC tumor samples with vehicle, Imatinib, Rebastinib, or Olverembatinib.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques: Activity Assay, Phospho-proteomics

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Waterfall plot of the PTK Upstream Kinase Analysis (UKA) in men and women comparing Imatinib, Rebastinib, and Olverembatinib to vehicle for each sex. Blue arrow denotes the location of ABL. (B) Waterfall plot of the STK Upstream Kinase Analysis (UKA) in men and women comparing Imatinib, Rebastinib, and Olverembatinib to vehicle for each sex.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques:

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Waterfall plot of ABL substrates and Z-score plots of men (top) and women (bottom) HCC tumor with Imatinib (left), Rebastinib (middle), or Olverembatinib (right) compared to vehicle. Blue arrow denotes the location of ABL. (B) Heatmaps showing the phosphorylation of ABL substrates in men (top) and women (bottom) HCC tumor with Imatinib, Rebastinib, or Olverembatinib compared to vehicle. (C) The kinase activity of ABL and ARG/ABL2. The PerMed Score denote the percent change in kinase activity in the HCC tumor with ABL inhibitors compared to vehicle. The blue line denotes the average signal intensity of each substrate compared to the vehicle.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques: Phospho-proteomics, Activity Assay

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Images of phosphorylated PTK (left) and STK (right) PamChip during the final cycle. (B) Phyla trees displaying the alterations of PTK and STK kinase activity in the HepG2 with Imatinib (left), Rebastinib (middle), or Olverembatinib (right) compared to vehicle. (C) Waterfall plot of the PTK Upstream Kinase Analysis (UKA) in HepG2 comparing Imatinib (left), Rebastinib (middle), and Olverembatinib (right) to vehicle. Blue arrow denotes the location of ABL. (D) The kinase activity of ABL, ARG/ABL2, DDR1, and INSR. The PerMed Score denote the percent change in kinase activity in the HepG2 with AB inhibitors compared to vehicle. The blue line denotes the average signal intensity of each substrate compared to the vehicle.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques: Activity Assay

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Heatmap showing the phosphorylation of 196 PTK substrates in HepG2 with vehicle, Imatinib, Rebastinib, or Olverembatinib. (B) Waterfall plot of the STK Upstream Kinase Analysis (UKA) in HepG2 comparing Imatinib (left), Rebastinib (middle), and Olverembatinib (right) to vehicle. (C) Waterfall plots of ABL and ARG substrates in HepG2 with Imatinib (left), Rebastinib (middle), and Olverembatinib (right) compared to vehicle.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques: Phospho-proteomics

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Images of phosphorylated PTK PamChip during the final cycle in HLE, HepaRG, Huh7, and Hep3B2 cells. The kinase activity of ABL in the four cell lines. The PerMed Score denote the percent change in kinase activity in the cell lines with ABL inhibitors compared to vehicle. The blue line denotes the average signal intensity of each substrate compared to the vehicle. (B) Waterfall plot of the PTK Upstream Kinase Analysis (UKA) in HLE, HepaRG, Huh7, and Hep3B2 cells comparing Imatinib (left), Rebastinib (middle), and Olverembatinib (right) to vehicle. Blue arrow denotes the location of ABL. (C) The kinase activity of ARG/ABL2, INSR, DDR1, and SYK. The PerMed Score denote the percent change in kinase activity in the cell lines with ABL inhibitors compared to vehicle. The blue line denotes the average signal intensity of each substrate compared to the vehicle.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques: Activity Assay

Journal: medRxiv

Article Title: HEPATOCELLULAR CARCINOMA KINOME ATLAS AS AN EMPLOYABLE INSTRUMENTED PERSONALIZED MEDICINE

doi: 10.1101/2025.07.04.25328828

Figure Lengend Snippet: (A) Images of phosphorylated STK PamChip during the final cycle in HLE, HepaRG, Huh7, and Hep3B2 cells. (B) Waterfall plot of the STK Upstream Kinase Analysis (UKA) in HLE, HepaRG, Huh7, and Hep3B2 cells comparing Imatinib (left), Rebastinib (middle), and Olverembatinib (right) to vehicle. (C) The kinase activity of AKT2, ERK1, GSK3b, and AURA. The PerMed Score denote the percent change in kinase activity in the cell lines with ABL inhibitors compared to vehicle. The blue line denotes the average signal intensity of each substrate compared to the vehicle.

Article Snippet: The protein lysates and run basic mix were incubated with either vehicle (DMSO, Sigma-Aldrich, 472301), Imatinib (1 μM) (Selleckchem, S2475), Rebastinib (100 nM) (Selleckchem, S2634), or Olverembatinib (100 nM) (Selleckchem, S7194) for 30 minutes at room temperature while rocking prior to the addition of the ATP and fluorescently-label antibody.

Techniques: Activity Assay

Journal: Polymers

Article Title: Fiber Selection for Reinforced Additive Manufacturing

doi: 10.3390/polym13142231

Figure Lengend Snippet: Density and Tensile Strength of Ceramic Oxide Fibers.

Article Snippet: Dupont Alumina FP-2 [ ] , 3.70 , 1.724 , 0.466.

Techniques:

Journal: eLife

Article Title: BRAF V600E induces reversible mitotic arrest in human melanocytes via microrna-mediated suppression of AURKB

doi: 10.7554/eLife.70385

Figure Lengend Snippet: ( A ) Representative image of 15 H&E-stained melanocytic nevus. Border colors indicate two consecutive magnifications. Arrowheads indicate bi- (red) or multi- (blue) nucleation. ( B ) Example images of skin specimen containing a melanocytic nevus (circled) and phase-contrast microscopy of melanocytes isolated from nevus portion. Scale bar=400 µm. ( C ) Images of MLANA (purple) and Hoechst (green) co-staining of melanocytic nevus derived melanocytes in culture. Zoomed images show representative 2 N, 4 N, and 8 N cells. ( D ) Representative images of QPI coupled with fluorescence microscopy to identify adjacent mCherry-expressing and mCherry-negative melanocytes. Individual cells were identified at time zero, tracked, and monitored for division for 96 hr. ( E ) Mean and individual matched data points for the percent of n=3 mCherry-negative or mCherry-positive cells identified at time zero that divided over 96 hr. P value from paired t-test. ( F ) Mean and standard deviation for 48 hr growth rates of indicated cells treated with Barasertib. P values from unpaired t-tests comparing the 30 nM samples of melanoma lines to primary melanocytes (n=3). ( G ) Mean and standard deviation for relative QPI-derived dry mass per 501MEL cell at initial time point (black) compared to 48 hr treatment with Barasertib (gray) (n = 3). P values from unpaired t-tests. QPI, quantitative phase imaging.

Article Snippet: For each experiment, 100,000 melanocytes, 60,000 501Mel cells, or 150,000 HCIMel019 cells were plated per well and media containing indicated concentrations of barasertib (AURKB inhibitor; AZD1152-HQPA | AZD2811, Selleckchem, A1147) was added.

Techniques: Staining, Microscopy, Isolation, Derivative Assay, Fluorescence, Expressing, Standard Deviation, Imaging

Journal: eLife

Article Title: BRAF V600E induces reversible mitotic arrest in human melanocytes via microrna-mediated suppression of AURKB

doi: 10.7554/eLife.70385

Figure Lengend Snippet:

Article Snippet: For each experiment, 100,000 melanocytes, 60,000 501Mel cells, or 150,000 HCIMel019 cells were plated per well and media containing indicated concentrations of barasertib (AURKB inhibitor; AZD1152-HQPA | AZD2811, Selleckchem, A1147) was added.

Techniques: Derivative Assay, Western Blot, Recombinant, Sequencing, Control

Journal: bioRxiv

Article Title: Tie2 signaling in the tumor microenvironment orchestrates breast cancer cell dissemination through TMEM doorways

doi: 10.64898/2026.04.26.720938

Figure Lengend Snippet: A) Endothelial cells and macrophages were co-cultured to measure induction of VEGF-A protein expression. Macrophages were labelled with CellTracker TM Green to distinguish them from endothelial cells (top panel), the middle panel shows ZO-1 and DAPI stain to identify the endothelial cells and nuclei of both cell types respectively, and the bottom panel is magnified from the boxed region shown in middle panels, showing VEGF-A staining in macrophages in pseudo color LUT. Scale bars 10 µm. B) Immunofluorescence staining of VEGF-A (pseudo color) in macrophages (BAC1.2F5, M⏀) co-cultured with endothelial cells (HUVECs) or endothelial cell conditioned media (CM) in the presence of DMSO or Tie2 inhibitor rebastinib (50nM), as described in (A). Scale bars 5 µm. C) Quantification of immunofluorescence intensity of intracellular VEGF-A in macrophages from (B) n=3 experiments, **** P < 0.0001 analyzed by two-way ANOVA showing the inhibition of macrophage VEGF-A expression by Rebastinib. D) Immunofluorescence staining of VEGF-A (pseudo color) in macrophages (BAC1.2F5) stimulated with Ang2 (250ng/ml) in presence of DMSO or Tie2 inhibitor rebastinib (50nM). Scale bars 5 µm. E) Quantification of immunofluorescence intensity of intracellular VEGF-A in macrophages from (D) showing Tie2 signaling induces VEGF-A expression in macrophages and inhibition of Tie2 by Rebastinib decreases VEGF-A expression. n=3, *** P < 0.001, **** P < 0.0001 analyzed by two-way ANOVA. F) Immunofluorescence staining of VEGF-A (pseudo color) in macrophages (BMMs) transfected with ctrl siRNA or Tie2 siRNA stimulated with PBS or Ang2 (250ng/ml) as in (D). Scale bars 5 µm. G) Quantification of immunofluorescence intensity of intracellular VEGF-A in macrophages from (F) showing Tie2 knockdown in macrophages inhibits VEGF-A expression. n=3, **** P < 0.0001 analyzed by two-way ANOVA. H) Experimental diagram of macrophage treatment for data shown in (I-K). BAC1.2F5 macrophages were pretreated with DMSO control (Cont) or 50nM Rebastinib (Reb) and then cultured overnight with 250ng/ml Ang2. The next day, macrophages were treated with or without 3000U/mL CSF-1 for 45 minutes, fixed, stained for VEGF-A (I-J) and conditioned media was used for VEGF-A ELISA (K). I) VEGF immunofluorescence staining of BAC1.2F5 macrophages from (H), Scale bar 5 µm. J) Quantification of immunofluorescence intensity of intracellular VEGF-A in macrophages (I) showing VEGF-A expression within macrophages decreases with CSF-1 treatment. n=3, ****p<0.0001 analyzed by two-way ANOVA. K) VEGF-A ELISA from conditioned media obtained from macrophages from (H), denoted as fold change of secreted protein compared to control showing that CSF-1 signaling increases VEGF-A secretion and this is blocked with Tie2 inhibition n=3, **p < 0.001, ***p<0.001, ns=not significant, analyzed by two-way ANOVA.

Article Snippet: Rebastinib was kindly provided by Deciphera Pharmaceuticals and was reconstituted at a concentration of 10 mg/mL in 0.4% hydroxypropyl methylcellulose (HPMC).

Techniques: Cell Culture, Expressing, Staining, Immunofluorescence, Inhibition, Transfection, Knockdown, Control, Enzyme-linked Immunosorbent Assay

Journal: bioRxiv

Article Title: Tie2 signaling in the tumor microenvironment orchestrates breast cancer cell dissemination through TMEM doorways

doi: 10.64898/2026.04.26.720938

Figure Lengend Snippet: (A-D) PyMT and (E-H) tumor chunks were orthotopically transplanted into (A-D) FVB and (E-H) NOD-SCID mice, respectively. Mice were treated twice a week for four weeks with 10 mg/kg Rebastinib or vehicle p.o. and primary tumors from these mice were used for staining. (B, F) Panels show immunostaining of VEGF-A intensity in TMEM doorway macrophages in tumor tissues from these mice treated with or without Rebastinib. Sequential tumor sections were stained by IHC (TMEM doorways-Mena, Iba1, endomucin) and immunofluorescence (VEGF-A (green), Iba1 (white), and DAPI (blue)). TMEM doorways were identified as described in . The circle in the IHC (black) and IF (white) panels show the same TMEM doorways obtained from the alignment of serial sections, and the three cells making up the TMEM doorway are indicated with the yellow triangle in each panel (TM, TEC, TTC). The TMEM doorway macrophage (TM) in the IF image, stained with Iba1, is enlarged in the rightmost panel. Scale bars= 20 µm. (C-D, G-H) The Iba1 (white) in the IF-stained slide within the TMEM doorway circle ROI was used to identify TMEM doorway macrophages and the immunofluorescence intensity of VEGF-A expression (green) within (intracellular, C, G) and outside (extracellular, D,H) the Iba1 + TMEM doorway macrophage was quantified. n= 5-7 mice per group, each dot represents the average value for a mouse. *p<0.05, **p<0.01, ***p<0.001, analyzed by Student’s t -test.

Article Snippet: Rebastinib was kindly provided by Deciphera Pharmaceuticals and was reconstituted at a concentration of 10 mg/mL in 0.4% hydroxypropyl methylcellulose (HPMC).

Techniques: Staining, Immunostaining, Immunofluorescence, Expressing

Journal: bioRxiv

Article Title: Tie2 signaling in the tumor microenvironment orchestrates breast cancer cell dissemination through TMEM doorways

doi: 10.64898/2026.04.26.720938

Figure Lengend Snippet: A) Diagram of subluminal to luminal intravasation trans-endothelial migration (iTEM) assay, which is a model to measure ability of tumor cells to intravasate. Tumor cells (6DT1, green) cells are labeled with CellTracker TM green and plated on a confluent endothelium (3B-11 cells, brown) either alone or with RAW macrophages labeled with CellTracker FarRed. After 18 hours incubation, the cells are fixed and the endothelium is stained with ZO-1 antibodies to ensure endothelial confluence and tight junctions at locations of TC crossing. The number of green 6DT1 tumor cells which cross the endothelium are imaged using confocal microscopy and quantified using ImageJ software. B-D) 3B-11 endothelial cells (B), 6DT1 tumor cells (C), and RAW macrophages (D), were pretreated with 1 nM Rebastinib or vehicle control overnight and the next day, cells were washed and combined in the iTEM assay in the combinations shown in the figure. n=3 experiments, each point represents the average fold change tumor cell trans-endothelial migration compared to control ECs and tumor cells alone (first bars in each graph). *p<0.05, **p<0.01, analyzed by one-way ANOVA. E) Western blot of lysates from Control (sgCont, siCont) and Tie2 knockdown (sgTie2, siTie2) 3B-11 endothelial cells (ECs), 6DT1 tumor cells, and RAW macrophages (M⏀) using antibodies against Tie2 and GAPDH. Representative blots shown from n=3 experiments. F-H) Tie2 knockdown and control 3B-11 endothelial cells (F), 6DT1 tumor cells (G), and RAW macrophages (H), from (E) were combined in the iTEM assay in the combinations shown in the figure. n=3 experiments, each point represents the average fold change tumor cell trans-endothelial migration compared to control ECs and tumor cells alone (first bars in each graph). *p<0.05, **p<0.01, ***p<0.001, analyzed by one-way ANOVA.

Article Snippet: Rebastinib was kindly provided by Deciphera Pharmaceuticals and was reconstituted at a concentration of 10 mg/mL in 0.4% hydroxypropyl methylcellulose (HPMC).

Techniques: Migration, Labeling, Incubation, Staining, Confocal Microscopy, Software, Control, Western Blot, Knockdown

Journal: Acta Pharmacologica Sinica

Article Title: The LPI/GPR55 axis enhances human breast cancer cell migration via HBXIP and p-MLC signaling

doi: 10.1038/aps.2017.157

Figure Lengend Snippet: GPR55 is involved in breast cancer cell migration and increased filopodia formation. (A) The GPR55 protein levels in LM-MCF-7 and MDA-MB-231 cells transfected with siGPR55 were examined via Western blot analysis. (B) The migratory ability of LM-MCF-7 and MDA-MB-231 cells treated with 2.5 μmol/L LPI, 2.5 μmol/L CID16020046 or siGPR55 was examined based on a wound healing assay. The results were expressed as relative wound width (**P<0.01 vs control, Student's t-test). (C) The migratory ability of LM-MCF-7 cells with different treatments was determined using the modified Boyden's chamber assay (columns reflect the mean of six fields in which at least 100 cells were counted; *P<0.05, **P<0.01 vs control, Student's t-test). The results are representative of three independent experiments.

Article Snippet: CID16020046 (4-[4-(3-hydroxyphenyl)-3-(4-methylphenyl)-6-oxo-1H,4H,5H,6H-pyrrolo [3,4-c] pyrazol-5-yl] benzoic acid) was obtained from Tocris Bioscience (Bristol, UK) and diluted in DMSO.

Techniques: Migration, Transfection, Western Blot, Wound Healing Assay, Control, Modification, Boyden Chamber Assay

Journal: Acta Pharmacologica Sinica

Article Title: The LPI/GPR55 axis enhances human breast cancer cell migration via HBXIP and p-MLC signaling

doi: 10.1038/aps.2017.157

Figure Lengend Snippet: (D) The migratory ability of MDA-MB-231 cells with different treatments was determined using the modified Boyden's chamber assay (columns reflect the mean of six fields in which at least 100 cells were counted; *P<0.05, **P<0.01 vs control, Student's t-test). The results are representative of three independent experiments. (E) F-actin was visualized using immunofluorescence staining in cells treated with 2.5 μmol/L LPI, 2.5 μmol/L CID16020046 or siGPR55. Filopodia protrusions are indicated by the arrows. Scale bar, 10 μm.

Article Snippet: CID16020046 (4-[4-(3-hydroxyphenyl)-3-(4-methylphenyl)-6-oxo-1H,4H,5H,6H-pyrrolo [3,4-c] pyrazol-5-yl] benzoic acid) was obtained from Tocris Bioscience (Bristol, UK) and diluted in DMSO.

Techniques: Modification, Boyden Chamber Assay, Control, Immunofluorescence, Staining

Journal: Acta Pharmacologica Sinica

Article Title: The LPI/GPR55 axis enhances human breast cancer cell migration via HBXIP and p-MLC signaling

doi: 10.1038/aps.2017.157

Figure Lengend Snippet: HBXIP expression is significantly and positively associated with GPR55 expression in breast cancer. (A) HBXIP promoter activity was examined using dual-luciferase reporter gene assays in LM-MCF-7 and MDA-MB-231 cells treated with CID16020046 (*P<0.05, **P<0.01 vs control, Student's t-test). (B) HBXIP promoter activity was analyzed using dual-luciferase reporter gene assays in LM-MCF-7 and MDA-MB-231 cells treated with siRNA targeting GPR55. (C) The correlation between GPR55 and HBXIP expression was analyzed using qRT-PCR in the abovementioned tumor tissues (n=36, P<0.01, Wilcoxon signed-rank test). (D) The correlation between HBXIP mRNA levels and GPR55 mRNA levels was assessed in 8 human breast cancer cell lines (R2=0.9347, P<0.001).

Article Snippet: CID16020046 (4-[4-(3-hydroxyphenyl)-3-(4-methylphenyl)-6-oxo-1H,4H,5H,6H-pyrrolo [3,4-c] pyrazol-5-yl] benzoic acid) was obtained from Tocris Bioscience (Bristol, UK) and diluted in DMSO.

Techniques: Expressing, Activity Assay, Luciferase, Control, Quantitative RT-PCR

Journal: Acta Pharmacologica Sinica

Article Title: The LPI/GPR55 axis enhances human breast cancer cell migration via HBXIP and p-MLC signaling

doi: 10.1038/aps.2017.157

Figure Lengend Snippet: The LPI/GPR55 axis promotes breast cancer cell migration by activating HBXIP/p-ERK1/2/Capn4 and MLCK/p-MLC signaling. Examination of the expression levels of p-ERK1/2, ERK1/2, HBXIP, p-JNK, MLCK, p-MLC, β-catenin and Capn4 in LM-MCF-7 cells (A) and MDA-MB-231 cells (B) treated with various doses of CID16020046 and siGPR55. (C) HBXIP silencing reduced the expression of p-ERK1/2 and Capn4 in both LM-MCF-7 and MDA-MB-231 cells treated with 2.5 μmol/L LPI. (D) The expression levels of HBXIP, p-ERK1/2 and Capn4 were not influenced by the dephosphorylation of MLC via treating cells with 20 μmol/L ML-7.

Article Snippet: CID16020046 (4-[4-(3-hydroxyphenyl)-3-(4-methylphenyl)-6-oxo-1H,4H,5H,6H-pyrrolo [3,4-c] pyrazol-5-yl] benzoic acid) was obtained from Tocris Bioscience (Bristol, UK) and diluted in DMSO.

Techniques: Migration, Expressing, De-Phosphorylation Assay