Regulatory effect and mechanism of gastrin and its antagonists on colorectal carcinoma

doi:10.3748/wjg.v5.i5.408

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Oct 15, 1999 (publication date) through Feb 27, 2025

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Oct 15, 1999; 5(5): 408-416
Published online Oct 15, 1999. doi: 10.3748/wjg.v5.i5.408

Table 1 Effect of PG, PGL and SMS on the volume and weight of transp lanted carcinoma (x^-± s, n = 5)

Group	Volume (mm³)	Weight (g)
Control	1766 ± 36	3.04 ± 0.13
PG	1926 ± 98^a	3.37 ± 0.21^a
PGL	1750 ± 53^d	2.98 ± 0.16^c
SMS	210 ± 13^b^d	0.90 ± 0.14^b^d^a^a
PG + PGL	1708 ± 59^d	2.91 ± 0.23^c
PG + SMS	224 ± 19^b^d	0.95 ± 0.12^b^d

^aP < 0.05,

^bP < 0.01 vs control group;

^cP < 0.05,

^dP < 0.01 vs PG group.

Table 2 Effect of PG, PGL and SMS on cAMP, DNA and protein content (x^-± s, n = 5)

Group	CAMP (pmol/mL)	DNA (dalton)	Protein (dalton)
Control	2.74 ± 0.14	947 ± 16	364 ± 12
PG	3.18 ± 0.23^b	1004 ± 17^b	675 ± 18^b
PGL	2.72 ± 0.15^d	940 ± 21^d	356 ± 9^d
SMS	1.87 ± 0.14^b^d	684 ± 13^b^d	272 ± 11^b^d
PG + PGL	2.82 ± 0.17^c	940 ± 25^d	369 ± 14^d
PG + SMS	1.86 ± 0.17^b^d	687 ± 21^b^d	274 ± 13^b^d

^bP < 0.01 vs control group;

^cP < 0.05,

^dP < 0.01 vs PG group.

Table 3 Effect of PG, PGL and SMS on cell cycle and proliferation index (PI)

Group	G₀/G₁ (%)	S (%)	G₂M (%)	PI (%)
Control	64.92 ± 1.72	18.24 ± 1.20	16.84 ± 2.35	35.08 ± 1.72
PG	59.22 ± 1.18^b	20.16 ± 1.06^a	20.62 ± 2.05^a	40.78 ± 1.81^b
PGL	67.18 ± 2.23^d	18.04 ± 1.43^c	14.78 ± 1.09^d	32.82 ± 2.27^d
SMS	80.04 ± 2.29^b^d	14.90 ± 1.46^b^d	5.06 ± 1.61^b^d	19.96 ± 2.39^b^d
PG + PGL	67.76 ± 2.41^d	18.10 ± 1.40^c	14.34 ± 0.66^d	32.24 ± 2.41^d
PG + SMS	80.26 ± 2.73^b^d	15.22 ± 1.78^b^d	4.54 ± 1.25^b^d	19.22 ± 2.73^b^d

^aP < 0.05,

^bP < 0.01vs control group;

^cP < 0.05,

^dP < 0.01 vs PG group.

Table 4 Effect of PG on VCC, IP₃, [Ca²⁺] and PKC activity (pmol/min per mg protein) (x^-± s, n = 5)

Group (mg/L)	VCC (A)	IP₃ (CPM)	[Ca²⁺] I(nM)	Plasma PKC	Membrane PKC
Control	1.554 ± 0.009	8.83 ± 1.33	26.36 ± 2.91	2.39 ± 1.30	1.07 ± 0.28
PG6.25	1.555 ± 0.005	10.16 ± 1.33	30.16 ± 2.16	2.36 ± 0.84	1.09 ± 0.16
12.50	1.563 ± 0.010^a	11.18 ± 0.75^a	50.69 ± 2.30^a	2.30 ± 0.45	1.15 ± 0.15
25.00	1.580 ± 0.011^b	16.17 ± 0.75^b	101.44 ± 2.49^b	0.91 ± 0.34^a	2.65 ± 1.21^a
50.00	1.579 ± 0.008^b	14.10 ± 1.60^b	70.63 ± 4.17^b	0.92 ± 0.26^a	2.65 ± 0.60^a
100.00	1.578 ± 0.010^b	13.00 ± 2.53^b	62.59 ± 2.59^b	0.91 ± 0.14^a	2.66 ± 0.68^a

^aP < 0.05,

^bP < 0.01 vs control group.

Table 5 Effect of PG + PGL on VCC, IP₃, [Ca²⁺]i and PKC acti-vity (pmol/min per mg protein) (x^-± s, n = 5)

Group	PG (mg/L)	PGL (mg/L)	VCC (A)	IP₃ (CPM)	[Ca²⁺]i(nM)	Plasma PKC	Membrane PKC
Control	0.00	0.00	1.554 ± 0.009	8.83 ± 1.33	26.36 ± 2.91	2.39 ± 1.30	1.07 ± 0.28
PG	25.00	0.00	1.580 ± 0.011^b	16.17 ± 0.75^b	101.44 ± 2.49^b	0.91 ± 0.34^a	2.65 ± 0.21^a
PG + PGL	25.00	8.00	1.553 ± 0.016^d
	25.00	16.00	1.551 ± 0.008^d	9.17 ± 1.47^d	32.63 ± 2.86^d	2.33 ± 0.29^c	1.05 ± 0.09^c
	25.00	32.00	1.546 ± 0.011^d	9.00 ± 1.58^d	31.79 ± 4.41^d	2.30 ± 0.61^c	1.05 ± 0.20^c
	25.00	64.00	1.549 ± 0.011^d	9.33 ± 1.97^d	32.45 ± 2.46^d	2.32 ± 0.17^c	1.09 ± 0.12^c
	25.00	128.00	1.549 ± 0.014^d

^aP < 0.05,

^bP < 0.01 vs control group;

^cP < 0.05,

^dP < 0.01 vs PG group.

Table 6 Expression of gastrin, c-myc, c-fos, rasp21 and AgNORs

Group	n	gastrin positive (%)	c-myc positive (%)	c-fos positive (%)	rasp21 positive (%)	AgNORs (%)
Carcinoma tissue	48	19 (39.6)^b	26 (54.2)^b	23 (47.9)^b	26 (54.2)^b	7.10 ± 1.48^b
3 cm mucosa	48	2 (4.2)	12 (25.0)	9 (18.8)	10 (20.8)	3.65 ± 1.04^c
6 cm mucosa	48	0 (0)	7 (14.6)	4 (803)	6 (12.5)	2.88 ± 0.73
Normal	10	0 (0)	1 (10.0)	1 (10.0)	2 (20.0)	2.85 ± 0.60

^bP < 0.01 vs 3 cm, 6 cm and normal mucosa group.

^cP < 0.05 vs 6 cm and normal mucosa group.

Table 7 Expression of gastrin, c-myc, c-fos, rasp21 and AgNORs in different pathological carcinoma tissue

Group	n	Gastrin positive (%)	c-myc positive (%)	c-fos positive (%)	rasp21 positive (%)	AgNORs
Highly-differentiated	26	14 (53.9)^a	15 (57.7)	13 (50.0)	15 (57.7)	7.12 ± 1.80
Moderately-differentiated	12	4 (33.3)	5 (41.7)	7 (58.3)	6 (50.0)	7.25 ± 0.86
Poorly- and mucinous	10	1 (10.0)	6 (60.0)	3 (30.0)	5 (50.0)	7.11 ± 1.20

^aP < 0.05 vs poorly-differentiated and mucinous group.

Table 8 Relation between gastrin and c-myc, c-fos, rasp21 and AgNORs

Group	n	c-myc positive (%)	c-fos positive (%)	rasp21 positive (%)	AgNORs
Gastrin-positive	19	15 (78.9)^a	14 (73.7)^b	11 (57.9)	7.84 ± 1.30^b
Gastrin-negative	29	11 (37.9)	9 (31.0)	15 (51.7)	6.22 ± 1.40

^aP < 0.05,

^bP < 0.01 vs gastrin-negative group.

Citation: He SW, Shen KQ, He YJ, Xie B, Zhao YM. Regulatory effect and mechanism of gastrin and its antagonists on colorectal carcinoma. World J Gastroenterol 1999; 5(5): 408-416
URL: https://www.wjgnet.com/1007-9327/full/v5/i5/408.htm
DOI: https://dx.doi.org/10.3748/wjg.v5.i5.408