Journal: Oncology Research

Article Title: Discovery of Two Novel Pyrazole Derivatives as Anticancer Agents Targeting Tubulin Polymerization and MAPK Signaling Pathways

doi: 10.32604/or.2026.074945

Figure Lengend Snippet: Gene expression analysis induced by P3C.1 and P3C.2 in three different cell lines. ( A ) Heatmap of differentially expressed genes of MDA-MB-231, ( B ) Jurkat and ( C ) CEM cells treated with P3C.1 and P3C.2, or with solvent control (DMSO). Each column represents the expression values of the different treatments performed for 6 h for each corresponding cell line, and each row denotes data from one transcript. The color legend of each expression values (log2 fold change) is displayed on the right. ( D ) Differentially expressed genes; up-regulated (green bars) and down-regulated (red bars) obtained for each cell line and treatments, considering only transcripts with a log2 fold change of >1.0, and a p -adjusted value of <0.05.

Article Snippet: In addition, the RAMOS (ATCC, CRL-1596), CEM (ATCC, CCL-119), JURKAT (ATCC, TIB-152), NALM-6 (ATCC, CRL-3273), RPMI-8226, MM.1S, MM.1R, U266, Rec-1, JVM-13, A549 (ATCC, CRM-CCL-185), HCC70 (ATCC, CRL-2315), HCC1419 (ATCC, CRL-2326), T47D (ATCC, CRL-2865), KMS-11, and OVCAR-5 cell lines were grown in Roswell Park Memorial Institute-1640 (RPMI-1640) culture media (Cytiva-Hyclone, SH30027FS, UT, USA,) supplemented with 10% FBS, 100 U/mL of penicillin, and 100 μg/mL of streptomycin.

Techniques: Gene Expression, Solvent, Control, Expressing

Journal: Oncology Research

Article Title: Discovery of Two Novel Pyrazole Derivatives as Anticancer Agents Targeting Tubulin Polymerization and MAPK Signaling Pathways

doi: 10.32604/or.2026.074945

Figure Lengend Snippet: P3C.1 and P3C.2 differentially expressed genes induced in common. ( A ) MDA-MB-231, ( B ) Jurkat, and CEM common DEGs identified for both compounds. ( C ) P3C.1 and P3C.2 induced 4 up-regulated genes in common (DUSP8, KLF6, KLF7 and BACH2) in MDA-MB-231, Jurkat and CEM cell lines.

Article Snippet: In addition, the RAMOS (ATCC, CRL-1596), CEM (ATCC, CCL-119), JURKAT (ATCC, TIB-152), NALM-6 (ATCC, CRL-3273), RPMI-8226, MM.1S, MM.1R, U266, Rec-1, JVM-13, A549 (ATCC, CRM-CCL-185), HCC70 (ATCC, CRL-2315), HCC1419 (ATCC, CRL-2326), T47D (ATCC, CRL-2865), KMS-11, and OVCAR-5 cell lines were grown in Roswell Park Memorial Institute-1640 (RPMI-1640) culture media (Cytiva-Hyclone, SH30027FS, UT, USA,) supplemented with 10% FBS, 100 U/mL of penicillin, and 100 μg/mL of streptomycin.

Techniques:

Journal: Oncology Research

Article Title: Discovery of Two Novel Pyrazole Derivatives as Anticancer Agents Targeting Tubulin Polymerization and MAPK Signaling Pathways

doi: 10.32604/or.2026.074945

Figure Lengend Snippet: Ingenuity pathways analysis of genes commonly found in P3C.1 and P3C.2-treated MDA-MB231, JURKAT, and CEM cells, identified canonical pathways implicating these genes in kinase-mediated signal transduction (see green asterisks * ), including RAF-independent MAPK1/3 activation, RAF/MAP kinase cascade, Protein Kinase A Signaling, and the SAPK/JNK signaling pathway, as well as cell signaling processes (see blue asterisks * ), and membrane dynamics (see blue asterisks * ). The figure shown was recreated from the original IPA histogram to enlarge features and improve legibility.

Article Snippet: In addition, the RAMOS (ATCC, CRL-1596), CEM (ATCC, CCL-119), JURKAT (ATCC, TIB-152), NALM-6 (ATCC, CRL-3273), RPMI-8226, MM.1S, MM.1R, U266, Rec-1, JVM-13, A549 (ATCC, CRM-CCL-185), HCC70 (ATCC, CRL-2315), HCC1419 (ATCC, CRL-2326), T47D (ATCC, CRL-2865), KMS-11, and OVCAR-5 cell lines were grown in Roswell Park Memorial Institute-1640 (RPMI-1640) culture media (Cytiva-Hyclone, SH30027FS, UT, USA,) supplemented with 10% FBS, 100 U/mL of penicillin, and 100 μg/mL of streptomycin.

Techniques: Transduction, Activation Assay, Membrane

Journal: Oncology Research

Article Title: Discovery of Two Novel Pyrazole Derivatives as Anticancer Agents Targeting Tubulin Polymerization and MAPK Signaling Pathways

doi: 10.32604/or.2026.074945

Figure Lengend Snippet: Connectivity map analyses revealed strong connectivity of P3C compounds with tubulin inhibitors. The top 20 perturbagens identified using P3C.1 and P3C.2 genes in common for ( A ) MDA-MB-231, and ( B ) Jurkat, and CEM cell lines. Tau scores of 90 or above have been previously recognized as strong and suitable for further investigation ( https://clue.io ).

Article Snippet: In addition, the RAMOS (ATCC, CRL-1596), CEM (ATCC, CCL-119), JURKAT (ATCC, TIB-152), NALM-6 (ATCC, CRL-3273), RPMI-8226, MM.1S, MM.1R, U266, Rec-1, JVM-13, A549 (ATCC, CRM-CCL-185), HCC70 (ATCC, CRL-2315), HCC1419 (ATCC, CRL-2326), T47D (ATCC, CRL-2865), KMS-11, and OVCAR-5 cell lines were grown in Roswell Park Memorial Institute-1640 (RPMI-1640) culture media (Cytiva-Hyclone, SH30027FS, UT, USA,) supplemented with 10% FBS, 100 U/mL of penicillin, and 100 μg/mL of streptomycin.

Techniques:

Journal: Cancers

Article Title: C3G Is Upregulated in Hepatocarcinoma, Contributing to Tumor Growth and Progression and to HGF/MET Pathway Activation

doi: 10.3390/cancers12082282

Figure Lengend Snippet: C3G knock-down reduces in vitro tumorigenic properties of HCC cells. Hep3B and HLE non-silenced (−) and C3G knock-down (shC3G) cells; and mHCC1 (non-silenced (−) and C3G knock-down (clones 2.17, 1.2 and 1.3)) were maintained in complete medium. ( A , B ) Top panels: Western-blot analysis of C3G expression in HCC cells, normalized with β-actin or tubulin. Middle panels: Representative macroscopic (whole dish) and microscopic (individual foci) photographs of anchorage-dependent growth assay. Bottom panels: Histograms show the mean ± S.E.M. of the number of foci (%) and the number of cells per focus (%). ( C ) Upper panels: Western-blot analysis of C3G expression in mHCC1 cells, normalized with β-actin. Middle panels: Representative macroscopic (whole dish) and microscopic (individual foci) photographs of anchorage-dependent growth assay. Lower panel: Histogram shows the mean ± S.E.M. of the number of foci. ( D ) Anchorage independent growth of Hep3B cells. Left panel: Histograms represent the mean ± S.E.M. of the number of foci (left) and cells per focus (right). Right panels: Representative microscope images of foci formation. ( E ) Adhesion assay in Hep3B cells. Histogram represents the mean ± S.E.M. of the percentage of adhered cells (%) after 15 and 30 min. Individual cells were counted with ImageJ. ( F ) Histograms showing the mean ± S.E.M. of the percentage of Hep3B cells in S+G2/M phases or ( G ) with a lower DNA content than 2C (apoptotic) analyzed by cytometry, when maintained in culture with 10% serum under adherent or suspension conditions for 6h. * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001, vs. non-silenced cells (−), ( A , B , D , E ) analyzed by Student’s t -test, ( A , B ) n > 3 or ( C , F , G ) one-way ANOVA; n ≥ 3.

Article Snippet: Then, membranes were probed with primary antibodies listed in CTAT table. β-Actin (Cell Signalling, Leiden, The Netherlands, #3700) or Tubulin (Santa Cruz Biotechnology, sc-2146) were used for normalization.

Techniques: Knockdown, In Vitro, Clone Assay, Western Blot, Expressing, Growth Assay, Microscopy, Cell Adhesion Assay, Cytometry, Suspension

Journal: BMC Immunology

Article Title: Comparative efficacy of glucocorticoid receptor agonists on Th2 cell function and attenuation by progesterone

doi: 10.1186/s12865-020-00383-8

Figure Lengend Snippet: A comparison of prednisolone- and dexamethasone-mediated reduction of type-2 cytokine mRNA levels in primary Th2 cells. Fold differences in mRNA level from corticosteroid (CS) treated cells compared to vehicle are provided ( n = 3). Quantification of IL-13 mRNA following steroid treatment ( a ). Comparison of CS ability to suppress IL-13 ( b ). The half maximal inhibitory concentration (IC 50 ) for prednisolone and dexamethasone required to suppress IL-13 mRNA expression ( c ). Quantification of IL-5 mRNA following CS treatment ( d ). Comparison of the ability of either CS to suppress IL-5 ( e ). A comparison of the IC 50 values for prednisolone and dexamethasone required to suppress IL-5 mRNA expression ( f ). Cell counts following culture in vehicle or increasing concentration of prednisolone or dexamethasone ( f ). Data represent mean and standard error. Pred, prednisolone; Dex, dexamethasone.* p < 0.05 determined by one-way ( a , d & g ) or two-way ( b & e ) RM ANOVA or t-test ( c & f )

Article Snippet: Fig. 4 Expression of the nuclear progesterone receptor (PGR) is undetectable in a Th2 cell line (CCRF-CEM) and primary Th2 cells, but present in a breast adenocarcinoma cell line (MCF-7) used as a positive control (n = 3; a ).

Techniques: Comparison, Concentration Assay, Expressing

Journal: BMC Immunology

Article Title: Comparative efficacy of glucocorticoid receptor agonists on Th2 cell function and attenuation by progesterone

doi: 10.1186/s12865-020-00383-8

Figure Lengend Snippet: A comparison of prednisolone- and dexamethasone-induced apoptosis in a Th2 cell line (CCRF-CEM). Data are expressed as percentage of 7AAD + cells ( a ) identifying dead cells. The half maximal dose (EC 50 ) for prednisolone and dexamethasone required to induce necrosis of cells ( b ). Percentage of Annexin V + 7AAD − cells, identifying apoptotic cells ( c ). A comparison of the EC 50 values for prednisolone and dexamethasone required to reach 50% maximal induction of apoptosis in cells ( d ; n = 11). Percentage of Annexin V + 7AAD − primary Th2 cells following treatment with dexamethasone, exhibiting a similar plateau effect as CCRF-CEM at 0.5 μM dexamethasone ( e ; n = 3). Comparison of CS-induced apoptosis in CCRF-CEM as fold-difference over vehicle ( f ). Data represent mean and standard error. Pred, prednisolone; Dex, dexamethasone. * p < 0.05 determined by two-way ( a & c ), t -test ( b & e ) or one-way RM ANOVA ( g )

Article Snippet: Fig. 4 Expression of the nuclear progesterone receptor (PGR) is undetectable in a Th2 cell line (CCRF-CEM) and primary Th2 cells, but present in a breast adenocarcinoma cell line (MCF-7) used as a positive control (n = 3; a ).

Techniques: Comparison

Journal: BMC Immunology

Article Title: Comparative efficacy of glucocorticoid receptor agonists on Th2 cell function and attenuation by progesterone

doi: 10.1186/s12865-020-00383-8

Figure Lengend Snippet: Corticosteroid-induced cell death is dampened by the female sex hormone progesterone. Dexamethasone-induced cell death ( a , % 7AAD + ) and apoptosis ( b , % Annexin V + 7AAD − ) of a Th2 cell line (CCRF-CEM) in the presence or absence of progesterone (2 μM, n = 5). Head-to-head comparison of apoptosis following treatment with prednisolone ( c ) or dexamethasone ( d ) with or without progesterone ( n = 4). The half maximal response (EC 50 ) for dexamethasone and prednisolone in the presence of progesterone ( e ). Influence of progesterone on the maximal response of prednisolone- or dexamethasone-induced apoptosis ( f ). Efficacy of prednisolone vs dexamethasone to induce apoptosis in the presence of prednisolone ( g ). Data represent mean and standard error. Pred, prednisolone; Dex, dexamethasone; Prog, progesterone; Pre, pretreatment. * p < 0.05 determined by one-way ( a - e ) or two-way ( f & g ) RM ANOVA

Article Snippet: Fig. 4 Expression of the nuclear progesterone receptor (PGR) is undetectable in a Th2 cell line (CCRF-CEM) and primary Th2 cells, but present in a breast adenocarcinoma cell line (MCF-7) used as a positive control (n = 3; a ).

Techniques: Comparison

Journal: BMC Immunology

Article Title: Comparative efficacy of glucocorticoid receptor agonists on Th2 cell function and attenuation by progesterone

doi: 10.1186/s12865-020-00383-8

Figure Lengend Snippet: Expression of the nuclear progesterone receptor (PGR) is undetectable in a Th2 cell line (CCRF-CEM) and primary Th2 cells, but present in a breast adenocarcinoma cell line (MCF-7) used as a positive control (n = 3; a ). Effect of progesterone with or without dexamethasone on expression of PIBF1 (n = 3, b ) . Progesterone reduced the dexamethasone-mediated increase in FKPB5 mRNA level, but had no effect when applied alone (n = 5, c ). Data represent mean and standard error. * p < 0.05 determined by one-way ANOVA

Article Snippet: Fig. 4 Expression of the nuclear progesterone receptor (PGR) is undetectable in a Th2 cell line (CCRF-CEM) and primary Th2 cells, but present in a breast adenocarcinoma cell line (MCF-7) used as a positive control (n = 3; a ).

Techniques: Expressing, Positive Control

Journal: BMC Immunology

Article Title: Comparative efficacy of glucocorticoid receptor agonists on Th2 cell function and attenuation by progesterone

doi: 10.1186/s12865-020-00383-8

Figure Lengend Snippet: RNA-sequencing of Th2 cells

Article Snippet: Fig. 4 Expression of the nuclear progesterone receptor (PGR) is undetectable in a Th2 cell line (CCRF-CEM) and primary Th2 cells, but present in a breast adenocarcinoma cell line (MCF-7) used as a positive control (n = 3; a ).

Techniques: