Presentation is loading. Please wait.

Presentation is loading. Please wait.

Figure S1, FGFR2 copy gain and overexpression in H716 cells A

Published by妗 乔 Modified over 6 years ago

Similar presentations

Presentation on theme: "Figure S1, FGFR2 copy gain and overexpression in H716 cells A"— Presentation transcript:

1 Figure S1, FGFR2 copy gain and overexpression in H716 cells A
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      View Key   NCI H716 colon adenocarcinoma B FGFR2 (MB 122)   KATOIII gastric cancer FGFR2 (MB 122)

2 Figure S1C: Selective FGFR2 overexpression in H716, KATOIII and SNU16 cell lines in Wooster Cell Line C Reporter: KatoIII SNU16 H716 18,823 measured genes 338 samples

3 Figure S2: FGF2 does not further activate FGFR2 in H716 or colon cancer cell lines.
p-FGFR2 Actin H H LS411N H RKO SW SW SW DLD1 -150 - 40 FGF2 FGFR2

4 Figure S3: AMBIT panel with 100nM PD173074
80-100%activity : Kinase % Control FGFR1 1.4 FGFR3 1.6 FGFR2 2.4 DDR1 18 MKNK1 34 FLT4 35 PIK3CB CSF1R 36 NEK4 54 NEK11 55 FGFR4 56 STK25 57 STK24 58 CHUK 62 NUAK1 67 MAPK13 MAP2K4 68 NTRK2 MATK 69 ERBB3 ABL1 70 RIOK2 71 AKT1 72 BTK DCLK1 CDK4 73 PIK3CA HIPK2 74 EGFR 76 MAP2K6 RPS6KA4 NUAK2 FLT3 77 HUNK MAPK9 STK3 KDR DYRK2 78 LCK MAP3K3 TAOK3 TRPM6 CDKL3 79 EIF2AK2 TSSK1B MAP3K2 80 PDGFRB PLK1

5 Figure S4: PD173074 Inhibits pFGFR2 and selectively inhibits NCI-H716 growth
20 40 60 80 100 Untreated Gleevec Tarceva Lapatinib PD173074 anti IGF1R PHA665752 PD168393 T = 0 T = 3 days B A IC50

6 Figure S5: pRSK S359/363 (ERK phosphorylation site) is inhibited by PD173074
-100 -75 PD : GAPDH

7 Figure S6: L-547 and Rapamycin inhibit Akt and S6RP phosphorylation
pAkt -60 1uM L : GAPDH Akt pS6RP S6RP -35 Rapamycin A B

8 . Figure S7: PD173074 causes cell death in NCI-H716 cells
PD nM Figure S7: PD causes cell death in NCI-H716 cells . Untreated

9 Figure S8: E cadherin and EPCAM are not expressed in H716 cells
Actin H H LS411N H RKO SW SW SW DLD1 -- 120 -150 -40 FGF2 CDH1 EPCAM -30

Download ppt "Figure S1, FGFR2 copy gain and overexpression in H716 cells A"

Similar presentations

NPV-BEZ235PKI-587 GDC-0980PD0325901 Supplemental Figure S1 Structures of Inhibitors NVP-BEZ235; PKI-587; GDC-0980 and PD0325901.

NPV-BEZ235PKI-587 GDC-0980PD Supplemental Figure S1 Structures of Inhibitors NVP-BEZ235; PKI-587; GDC-0980 and PD
Suppl. Figure 1 A B Suppl. Figure 1. Relative (A) miR-21 and (B) miR-224 expression levels in HCC tumors in different stages (I,II,III,IV) assessed by.

Suppl. Figure 1 A B Suppl. Figure 1. Relative (A) miR-21 and (B) miR-224 expression levels in HCC tumors in different stages (I,II,III,IV) assessed by.
Student Research Interest HER2 Receptor Signaling in Breast Cancer Cells Marc Y. Fink Biomedical Sciences LIU-Post.

Student Research Interest HER2 Receptor Signaling in Breast Cancer Cells Marc Y. Fink Biomedical Sciences LIU-Post.
The c-Met receptor contributes to motility and invasion in high grade STS; a potential therapeutic target Sarah E. Myers, Theresa G. Nguyen, Quan-Sheng.

The c-Met receptor contributes to motility and invasion in high grade STS; a potential therapeutic target Sarah E. Myers, Theresa G. Nguyen, Quan-Sheng.
Kyoto University, Japan

Kyoto University, Japan
HIGH-THROUGHPUT MUTATION PROFILING OF OSTEOSARCOMA PRIMARY TUMORS AND CELL LINES IDENTIFIES NEW MUTATIONS IN PREVIOUSLY UNASSOCIATED ONCOGENES AND TUMOR.

HIGH-THROUGHPUT MUTATION PROFILING OF OSTEOSARCOMA PRIMARY TUMORS AND CELL LINES IDENTIFIES NEW MUTATIONS IN PREVIOUSLY UNASSOCIATED ONCOGENES AND TUMOR.
Fig. S1 1 Oxygen consumption rate (pmol/sec/10⁶cells) shLKB1#1 control * untreated 25 μM erlotinib H358 Vector LKB1 Oxygen consumption rate (pmol/sec/10⁶cells)

Fig. S1 1 Oxygen consumption rate (pmol/sec/10⁶cells) shLKB1#1 control * untreated 25 μM erlotinib H358 Vector LKB1 Oxygen consumption rate (pmol/sec/10⁶cells)
Cell lineStatus FGFR1 DMS-114Gene amplification NCI-H520Gene amplification NCI-H1581Gene amplification FGFR2 NCI-H716Gene amplification KATO-IIIGene amplification.

Cell lineStatus FGFR1 DMS-114Gene amplification NCI-H520Gene amplification NCI-H1581Gene amplification FGFR2 NCI-H716Gene amplification KATO-IIIGene amplification.
Chromosome Tumor samplesNormal samples Supplemental Figure 1.

Chromosome Tumor samplesNormal samples Supplemental Figure 1.
Supplementary Figure S1 Inhibition of AKT and S6 phosphorylation. After 4 h treatment with 1 µM of GDC-0941, EVSA-T parental, resistant Clone1, Clone2,

Supplementary Figure S1 Inhibition of AKT and S6 phosphorylation. After 4 h treatment with 1 µM of GDC-0941, EVSA-T parental, resistant Clone1, Clone2,
The expression and signaling of FGFR3 in WM cells.

The expression and signaling of FGFR3 in WM cells.
Overall (regardless of smoking Hx) Prior or current smoking Hx

Overall (regardless of smoking Hx) Prior or current smoking Hx
Figure 1. Resistance mechanism against first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). (A) Mutations in the EGFR.

Figure 1. Resistance mechanism against first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). (A) Mutations in the EGFR.
Article title: PI3K independent activation of mTORC1 as a target in lapatinib-resistant ERBB2+ breast cancer cells   Journal: Breast Cancer Research and.

Article title: PI3K independent activation of mTORC1 as a target in lapatinib-resistant ERBB2+ breast cancer cells   Journal: Breast Cancer Research and.
From: Overexpression of the μ-Opioid Receptor in Human Non-Small Cell Lung Cancer Promotes Akt and mTOR Activation, Tumor Growth, and Metastasis Anesthes.

From: Overexpression of the μ-Opioid Receptor in Human Non-Small Cell Lung Cancer Promotes Akt and mTOR Activation, Tumor Growth, and Metastasis Anesthes.
Figure 1. Herbacetin binds to AKT1/2 and suppresses each respective kinase activity. The effect of herbacetin on (A) PI3K/AKT and (B) MAPK signaling pathway.

Figure 1. Herbacetin binds to AKT1/2 and suppresses each respective kinase activity. The effect of herbacetin on (A) PI3K/AKT and (B) MAPK signaling pathway.
Supplementary Figure 1 Lapatinib nM mM pEGFR MDA-MB231 EGFR pEGFR

Supplementary Figure 1 Lapatinib nM mM pEGFR MDA-MB231 EGFR pEGFR
Figure 1. Herbacetin binds to AKT1/2 and suppresses each respective kinase activity. The effect of herbacetin on (A) PI3K/AKT and (B) MAPK signaling pathway.

Figure 1. Herbacetin binds to AKT1/2 and suppresses each respective kinase activity. The effect of herbacetin on (A) PI3K/AKT and (B) MAPK signaling pathway.
Inhibition of FGFR fusion kinase activity repressed tumor growth in a mouse xenograft model. Inhibition of FGFR fusion kinase activity repressed tumor.

Inhibition of FGFR fusion kinase activity repressed tumor growth in a mouse xenograft model. Inhibition of FGFR fusion kinase activity repressed tumor.
CDK2 is highly expressed in colon cancer cells and curcumin selectively suppresses HCT116 cell proliferation. CDK2 is highly expressed in colon cancer.

CDK2 is highly expressed in colon cancer cells and curcumin selectively suppresses HCT116 cell proliferation. CDK2 is highly expressed in colon cancer.

Similar presentations

Ads by Google