Increasing expression of presenilin 1, β-catenin, and p-PTEN and its regulatory roles on cell invasion in gastric cancer

Table 1 Characteristics of 116 patients with gastric cancer among presenilin-1, β-catenin, and phosphorylation of tensin homolog deleted on chromosome ten expressions

Clinicopathological features	PS-1		β-catenin		p-PTEN		P value
	Total (n)	High expression	P value	High expression	P value	High expression
Age (years)			0.056		0.068		0.028
≤ 60	63	33		31		24
> 60	53	37		35		31
Gender			0.673		0.919		0.604
Male	91	54		52		42
Female	25	16		14		13
Tumor site			0.147		0.272		0.405
Upper	40	19		23		18
Middle	22	15		16		13
Lower	46	32		24		22
Mixed	8	4		3		2
Tumor size (cm)			0.004		0.005		0.269
≤ 5	59	28		26		25
> 5	57	42		40		30
Grade of differentiation			0.405		0.389		0.439
Well and moderate	55	31		29		24
Poor and not	61	39		37		31
Neurovascular invasion			0.433		0.031		0.014
Negative	54	29		25		19
Positive	62	41		41		36
Depth of invasion			< 0.001		0.001		0.002
T1	4	1		0		1
T2	11	2		2		0
T3	48	25		26		22
T4	53	42		38		32
Lymphatic metastasis			< 0.001		< 0.001		0.003
N0	15	3		3		2
N1	20	7		7		7
N2	35	21		20		16
N3	46	39		36		30
Distal metastasis			0.041		0.112		0.004
M0	109	63		60		48
M1	7	7		6		7

p-PTEN: Phosphorylation of tensin homolog deleted on chromosome ten; PS-1: Presenilin-1; T: Tumor; N: Node; M: Metastasis.

Table 2 Correlation among expressions of presenilin 1, β-catenin and phosphorylation of tensin homolog deleted on chromosome ten

Protein	β-catenin expression			p-PTEN expression
	Low	High	r value	Low	High	r value
Presenilin-1 1 expression			0.362a			0.417a
Low	30	16		36	10
High	20	50		25	45
p-PTEN expression			0.338a
Low	36	25
High	14	41

^aP < 0.05. p-PTEN: Phosphorylation of tensin homolog deleted on chromosome ten.