Cancer Apoptosis Poster

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    26-Oct-2014
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Apoptosis evasion in cancer cells

Transcript of Cancer Apoptosis Poster

Apoptosis evasionin cancer cells1 DECOY RECEPTOR EXPRESSIONFasL FasL Fas Apo2L/Apo3L Apo2/Apo3 TNF TNFR1 Growth Factor Growth Factor Receptor Withdrawal of Growth Factors

FADD FADD Procaspase8 Procaspase8

FADD Procaspase8

TRADD TRAF2 RIP

2 ELEVATED ONCOGENE SIGNALINGRAS

PKC BID p90RSK

APOPTOSIS INHIBITING 3 UPREGULATED PATHWAYS

PI 3-K Ibs FLIP IKKs NF-B CIAP1 Caspase3 Caspase7 Caspase9 Apoptosis ICAD CAD APAF1 SMAC IBID BCLXL MMP HTRA2 Noxa Apoptosis CytoC Apoptosis EndoG AIF Depolarization Oncogenic Signal PUMA ANT BAX BAK VDAC PBR BCL2

Caspase8

BAD

Akt1 PTEN

PIP3

CypD BIM Mitochondria p53AIP1

Arts

POD PML ZIPK PAR4 Daxx NF-B PARP CAD ATM

EndoG DNA Fragmentation FLIP, CIAP2, BFL1, BCL2 AIF

p14(ARF)

4

p53 MUTATIONS

p53

BAX, BAK, BID, Ras, Noxa, PUMA, APAF1, Survivin

Apoptosis DNA Fragmentation

Chk2

p53

MDM2

How cancer cells evade apoptosis1Decoy Receptor Expression

2

Elevated Oncogene Signaling

3

Upregulated Apoptosis Inhibiting Pathways

4

Metabolic reprogramming

p53 Mutations

LEGEND ACTIVATION PROTEIN KINASES INDIRECT ACTIVATION DEATH-CAUSING PROTEASES DEATH-INDUCING LIGANDS INHIBITION GROWTH FACTOR TRANSLOCATION APOPTOSIS-INDUCING PROTEINS DEATH RECEPTORS TRANSCRIPTION FACTORLimitless replicative potential

Cancer cells can escape apoptotic programming by upregulating the expression of nonsignaling decoy receptors for the FAS ligand, which may prevent activation of the FAS receptor and downstream apoptosis.

Persistent, and/or elevated signaling from oncogenes can drive cell proliferation that can shift the balance over a cells apoptotic program.

Cancer cells can overcome apoptosis via the upregulation of apoptosis inhibiting pathways, such as the PI 3 kinase (PI 3K)Akt/PKB survival pathway and BCL2 overexpression. Loss of the tumor suppressor gene PTEN also inhibits apoptosis.

The pro-apoptotic regulator, p53, is a key tumor suppressor and is mutated in many cancers.

ed in esis sta gen Su io g an

ATP

im Esca m pe un f e c rom on tro l

DOWNSTREAM EFFECT

Tissue invasion & metastasis

Hallmarks of Cancer

STOP

Comprehensive Solutions for Cancer Research From Hallmarks to Biomarkers EMD Millipore is dedicated to developing and refining technologies for the study of cancer. Learn more about our extensive portfolio of high quality solutions for cancer research, including the Upstate, Chemicon, and Calbiochem brands of antibodies, small molecules, signaling pathway panels, invasion and apoptosis assays for immunochemistry, flow cytometry, and multiplex, at www.millipore.com/cancer.

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in

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ap

op to s

is

Insensitivity to proliferation inhibiting signals

EMD Millipore is a division of Merck KGaA, Darmstadt, GermanyEMD Millipore and the M logo are trademarks of Merck KGaA, Darmstadt, Germany. Upstate, Chemicon and Calbiochem are registered trademarks of EMD Chemicals Inc. Lit. No. PS2776EN00 06/12 LS SBU-12-06117 2012 EMD Millipore Corporation, Billerica, MA, 01821 USA. All rights reserved.

S pr elfol su ife f ra ci tio en n cy sig in na ls

GROWTH FACTOR RECEPTOR