Transcription factor EGR-1 inhibits growth of hepatocellular carcinoma and esophageal carcinoma cell lines

Table 1 egr-1 transcription and expression in HCC tissue and its normal counterparts

Tissue	n	mRNA (%)	n	Protein (%)
Normal liver	8	0 (0.0)	2	0 (0.0)
Hepatic paracancerous tissue	22	21 (95.5)	5	4 (80.0)
Liver carcinoma	24	6 (25.0)a	3	0 (0.0)b

^aP = 0.000,

^bP = 0.143, vs hepatic paracancerous tissue

Table 2 egr-1 transcription and expression in EC tissue and its normal counterparts

Tissue	n	mRNA (%)	Protein (%)
Agressive carcinoma	47	8 (17.0)a	6 (12.8)b
Dysplasia	29	18 (62.1)	14 (48.3)
Normal epithelium	28	9 (32.1)	2 (7.1)

^aP = 0.000,

^bP = 0.001, vs dysplasia

Table 3 Cell cycle of HCC and EC cells expressing EGR-1 with FCM (number of fraction)

Cell clone	G1	G2/M	S
HHCC/EGR-1	0.77	0.08	0.15a
HHCC/φ	0.64	0.08	0.28
SMMC7721/EGR-1	0.70	0.09	0.21b
SMMC7721/φ	0.70	0.09	0.22
ECa109/EGR-1	0.73	0.11	0.18c
ECa109/φ	0.64	0.10	0.27

^aP = 0.038,

^bP = 1.000,

^cP = 0.048, vs their controls

Table 4 Nude mice tumorigenicity of gene transfected groups in HCC and EC cells

Cell clone	n	Tumorigenicity rate	Tumor growth rate (¯x ± s, mg·d-1)
HHCC/EGR-1	3	3/3	13.9 ± 5.2a
HHCC/Φ	3	3/3	70.9 ± 7.8
SMMC7721/EGR-1	3	3/3	18.7 ± 4.3b
SMMC7721/Φ	3	2/3	15.2 ± 13.0
ECa109/EGR-1	4	4/4	12.9 ± 2.1c
ECa109/Φ	4	4/4	47.1 ± 11.3

^aP = 0.001,

^bP = 0.681, P = 0.001, vs their controls