PPAR Research / 2010 / Article / Tab 2

Review Article

Anticancer Role of PPARγ Agonists in Hematological Malignancies Found in the Vasculature, Marrow, and Eyes

Table 2

PPARγ and PPARγ ligands as potential therapy for hematological malignancies.

Hematological malignancy/cell linePPARγ agonistCommentsRef

HL-60troglitazoneInhibited cell proliferation by G1 arrest; induced differentiation to monocytes[366]

HL-6015d-PGJ2, troglitazoneInhibited cell proliferation; induced caspase-dependent apoptosis [367]

HL-60, K56215d-PGJ2, troglitazoneInduced apoptosis through Bax/Bcl-2 regulation [368]

Mono Mac 6, U93715d-PGJ2, troglitazoneInduced apoptosis; downregulated cyclooxygenase-2 [369]

HL-6015d-PGJ2PPARγ-independent TRAIL-induced apoptosis[370]

Jurkat, PC315d-PGJ2PPARγ-independent TRAIL-induced apoptosis [371]

EoL-1, U937, KPB-M15troglitazoneInhibited cell proliferation by G0/G1 arrest [372]

HL-60, K56215d-PGJ2, troglitazoneInhibited cell growth, adhesion, and invasion through Matrigel; inhibited MMP-2 and MMP-9 expression [230]

AMLDIM #34Inhibited cell growth; induced apoptosis through PPARγ-dependent and independent mechanism [365]

HL-60, U937, AML, CLLrosiglitazone, 15d-PGJ2, CDDOInhibited cell growth, induced differentiation, induced apoptosis when combined with RXR-selective ligands [373]

HL-60ThiazolidinedioneInhibited cell proliferation by G0/G1 arrest; induced apoptosis; induced differentiation[374]

U937troglitazoneInhibited cell proliferation by G1 arrest [375]

NB415d-PGJ2, pioglitazoneInhibited cell proliferation; induced differentiation and lipogenesis when combined with specific RXR ligands [376]

HL-60, AMLCDDO-MeInduced cell differentiation; induced apoptosis [214, 363, 364]

HL-60CDDOInduced apoptosis; induced differentiation and increased phagocytosis at sub-apoptotic doses [377]

APL, NB4, MR2CDDOEnhanced all-trans-retinoic acid-induced differentiation and apoptosis[378]

AMLCDDOInduced apoptosis in a caspase-dependent and independent manner [379]

U937CDDO-ImInhibited cell proliferation; induced differentiation through PPARγ-independent mechanism [50]

U937CDDO, CDDO-Me, CDDO-ImInduced apoptosis by increasing reactive oxygen species and decreasing intracellular glutathione [380]

THP-1rosiglitazoneInhibited 9-cis retinoic acid-induced cell growth[381]

THP-1troglitazone, rosiglitazoneInhibited MCP-1-induced migration [382]

K562, KU812, KCL22, BV173, SD1, SupB-15TZD18Inhibited cell growth through a PPARγ-independent mechanism; inhibited proliferation; induced apoptosis [359, 383]

K562troglitazone, pioglitazoneInhibited cell proliferation and erythroid phenotype; downregulated GATA-1[384]

B-ALL 15d-PGJ2, pioglitazoneInhibited cell growth by G1 arrest; induced apoptosis partially dependent on caspase signaling [385]

UTree-O2, Bay91, 380troglitazoneInhibited cell growth by G1 arrest; induced apoptosis; downregulates c-myc expression [386]
U266, RPMI 8226, BL-41, HS-Sultan15d-PGJ2Induced apoptosis; downregulation of NF-κB-dependent antiapoptotic proteins [387]

Jurkat, J-Jahn, T-ALL15d-PGJ2, PGD2Induced apoptosis through PPARγ-dependent mechanism[388]

Karpas 29915d-PGJ2, GW7845, rosiglitazoneInduced cell death at high ligand concentration but promoted cell survival at low doses [389]

CTCL and Sezary syndrome cell lines: MJ, Hut78, and HHCDDOInduced apoptosis through a PPARγ-independent mechanism by decreasing antiapoptotic protein Bcl-xL and activating caspase 3 [390]

GRANTA-519, Hbl-2, JeKo-115d-PGJ2, rosi-glitazone, pioglitazoneInduced apoptosis and downregulation of cyclin D1[391]

CLL B cellsCDDOInduced apoptosis in part by activation of caspase-8[392]

CLL B cells, JurkatCDDOInduced apoptosis through the intrinsic pathway[393]

DLBCLCDDOInhibited proliferation; induced apoptosis through a PPARγ-independent mechanism[47]

Primary B lymphocytes, Ramos, OCI-Ly19 DLBCLCDDO, CDDO-Im, Di-CDDOInduced apoptosis through a mitochondrial dependent pathway [394]

ANBL6, RPMI 822615d-PGJ2, ciglitazoneInduced apoptosis via caspase activation and mitochondrial depolarization [208]

LP-1, U-266, RPMI 8226-S, OPM-2, IM-9rosiglitazone, pioglitazone, 15d-PGJ2Inhibited tumor cell growth[395]

Waldenstrom's macroglobulinemiarosiglitazone, ciglitazoneInhibited cell growth; induced apoptosis[396]

multiple myeloma (MM) drug sensitive MM.1S or drug resistant MM.1R cells, KAS6/1, ANBL-615d-PGJ2, troglitazoneInhibited cell adhesion to BMSCs and adhesion-triggered IL-6 production; overcame resistance to dexamethasone (MM.1R cells)[212]

MM cells, U266, RPMI 8226, bone marrow mononuclear cellsCDDO, CDDO-ImInduced apoptosis by disruption of mitochondrial membrane potential [397]

Dexamethasone-resistant MM.R1, RPMI 8226/LR-5, RMPI 8226/Dox-40, U266CDDO-ImInduced apoptosis; decreased MM adhesion-triggered IL-6 production [398]

RPMI 8226, JJN3CDDO-ImInhibited Stat3 and Stat5 phosphorylation; induced Stat inhibitors SOCS-1 and SHP-1 [399]

Normal human B cells and B lymphoma cells (Daudi, Ramos, Raji)rosiglitazone, pioglitazone, 15d-PGJ2Inhibited cell proliferation; induced apoptosis[209]

MM cell lines (RPMI 8226 and U266); BMSCs, HS-5PPARγ over-expression; ciglitazonePPARγ overexpression inhibited proliferation and induced apoptosis in MM cells; inhibited IL-6 production in BMSCs[207]

B cell lymphoma (Raji, Ramos cell lines)PPARγ siRNASilencing of PPARγ induced cell proliferation and cell differentiation; PPARγ knockdown enhanced NF-κB activity in Ramos cells[206]