Skip to main content
. 2000 Jun 20;97(13):7494–7499. doi: 10.1073/pnas.97.13.7494

Table 1.

Cell cycle effects of BBL22

Tissue type % G1
% S phase
% G2/M
Control BBL22 Control BBL22 Control BBL22
Breast cancer (estrogen receptor status)
 MCF7 (+) 68 46 12 10 10 40
 HS578t (−) 73 26 10 17 16 54
 HBL100 (−) 46 25 30 18 24 57
 MDA-MB-568 (−) 47 28 17 20 29 50
 BT474 (+) 67 25 20 15 12 60
Prostate cancer (androgen status)
 PC3 (independent) 64 33 16 8 20 54
 DU145 (independent) 71 34 15 20 9 32
 LNCaP* (dependent) 51 17* 22 22* 26 11*
Other epithelial carcinomas
 HeLa, cervical cancer 71 19 15 14 12 56
 T98, glioblastoma 70 22 15 14 14 64
Hematological malignancies
 K562, M6 (AML) 37 9 32 15 24 71
 Nalm16, B cell (ALL) 38 15 38 17 22 62
 Nalm6, B cell (ALL) 53 31 31 17 15 43
Nonmalignant breast epithelium
 MCF10A 37 33 25 25 36 38
 HS578BST 39 40 21 18 38 41
Nonmalignant prostate epithelium
 BPH1 70 66 17 15 12 15

Cells in exponential log growth phase were treated with 50 μM BBL22, and cell cycle kinetics were determined by propidium iodide staining and fluorescence-activated cell sorter analysis 24 h later. These results are representative of four independent experiments. AML, acute myeloid leukemia; ALL, acute lymphocytic leukemia. 

*

The sub-G1 apoptotic population comprised 49% of BBL22-treated LNCaP cells.