Table 2.
The use of curcumin in treatment and suppression of lymphoma.
| In vitro/In vivo | Cell line/Animal model | Study design | Molecular target | Biological mechanism | Remarks | Refs |
|---|---|---|---|---|---|---|
| In vitro In vivo |
Raji cells Xenograft model |
10 μM | VEGF Akt MMP-2 and -9 |
Proliferation Metastasis |
A combination of curcumin and omacetaxine suppresses proliferation and metastasis of cancer cells Inhibition of VEGF/Akt signaling Down-regulation of MMP-2 and MMP-9 |
118 |
| In vitro In vivo |
U937 and Raji cells Xenograft model |
0–80 μM | TGF-β/Smad | Proliferation | A combination of curcumin and HHT inhibits proliferation of lymphoma cells Inhibition of TGF-β/Smad axis Increasing E-cadherin levels Reducing N-cadherin levels |
121 |
| In vitro | ut-78, HH, MJ, My-La CD4+ and My-La CD8+ cells | 12–24 μM | – | Apoptosis DNA damage Autophagy |
Apoptosis induction Activation of caspase cascade DNA fragmentation Inducing dephosphorylation of Akt Autophagy induction |
135 |
| In vitro | PEL cells | 0–80 μM | JAK1 and STAT3 | Apoptosis Proliferation |
Apoptosis induction Decreasing proliferation of tumor cells Mediating loss of mitochondrial membrane potential Cytochrome C release Activation of caspase-3 Inhibition of JAK1 and STAT3 signaling |
136 |
| In vitro | MJ, Hut78, and HH cells | 5–20 μM | STAT3 Bcl-2 Survivin NF-kappaB Caspase-3 |
Apoptosis | Apoptosis induction Down-regulation of STAT3, Bcl-2 and survivin Inhibition of NF-kappaB signaling Activation of caspase-3 |
112 |
| In vivo | Lymphoma bearing mice | 50, 100 and 150 mg/kg | IL-1α and IL-1β | Inflammation | Inhibiting tumorigenesis via down-regulation of IL-1α and IL-1β Preventing inflammation |
137 |
| In vivo | Lymphoma bearing mice | 1.5, 3 and 4.5 mg/kg | IL-6 and TNF-α NF-kappaB |
– | Down-regulation of IL-6 and TNF-α Inhibition of NF-kappaB signaling |
138 |
| In vitro | H-RS and Jurkat cells | 2.5–100 μM | STAT3 and NF-kappaB | Apoptosis | Apoptosis induction Cell cycle arrest Suppressing STAT3 and NF-kappaB molecular pathways Down-regulation of Bcl-2, Bcl-xL, XIAP and survivin |
113 |
| In vitro | CH12F3 lymphoma cells | 0–6.5 μM | Caspase-3 | Apoptosis DNA damage |
Sensitizing cancer cells to DNA damage Apoptosis induction in a caspase-3 dependent manner |
139 |
| In vitro | Namalwa, Ramos and Raji cells | 2, 10 and 20 μmol/L | mTOR | Cell cycle progression | Cell cycle arrest at G2/M phase Increasing sensitivity of lymphoma cells to radiation Inhibiting mTOR phosphorylation |
140 |
| In vitro In vivo |
Lymphoma cells NOD/SCID mice |
0–40 μM 200 mg/kg |
Akt/mTOR PPARγ |
Apoptosis Cell cycle progression |
Apoptosis induction Cell cycle arrest at G2 phase PPARγ overexpression Inhibition of Akt/mTOR signaling |
141 |
| In vitro | AS283A, KK124, Pa682PB, BML895, and CA46 cells | 10 or 20 μmol/L | NF-kappaB Bax |
Apoptosis | Down-regulation of NF-kappaB Overexpression of Bax Apoptosis induction Reducing viability of tumor cells |
142 |
| In vitro | JeKo-1, Mino, SP-53, and Granta 519. JeKo-1 cells | 10, 25 and 50 μM | NF-kappaB | Apoptosis | Apoptosis induction Cell cycle arrest at G1/S phase Proliferation inhibition Inhibition of NF-kappaB signaling pathway |
143 |