Effects of retinoic acid on metastasis and its related proteins in gastric cancer cells in vivo and in vitro.
Abstract
AIM: To investigate the effects of all-trans retinoic acid (ATRA) on metastasis
and its related proteins in human gastric cancer cells in vivo and in vitro.
METHODS: Gastric cancer cells, MGC80-3 and SGC-7901, were inoculated into spleen
subcapsule of nude mice, respectively. Nude mice were administered with ATRA (0.7
mg/kg, ig) every other day. Six weeks later, nude mice were sacrificed. All the
tumors formed in spleen and in liver were removed. Some of them were fixed, and
then embedded. Others were kept in liquid nitrogen for further use. Expression
level of proteins in tumor and in cell was analyzed by Western blot. Microvessel
in tumor section was shown by immunohistochemistry and adhesive ability of cell
to amnion was measured by adhesion assay.
RESULTS: When inoculated nude mice were treated with ATRA, the xenograft tumors
in spleen and metastatic tumors in liver were suppressed by 50 % respectively,
and inhibition of microvessel formation in xenograft and metastatic tumors was
also observed obviously. Although ATRA regulated expression of nm23 and mts1/p16
proteins at different patterns in vivo and in vitro, high ratio of nm23:mts1/p16
was in association with low adhesive activity of cells. In addition, ATRA induced
ICAM-1 protein expression in vivo and in vitro.
CONCLUSION: ATRA inhibits the growth of xenograft tumors and their metastasis to
liver. This process may be associated with regulation of metastatic related
proteins, including nm23, mts1/p16, and ICAM-1 in vivo and in vitro.
Keywords:
and its related proteins in human gastric cancer cells in vivo and in vitro.
METHODS: Gastric cancer cells, MGC80-3 and SGC-7901, were inoculated into spleen
subcapsule of nude mice, respectively. Nude mice were administered with ATRA (0.7
mg/kg, ig) every other day. Six weeks later, nude mice were sacrificed. All the
tumors formed in spleen and in liver were removed. Some of them were fixed, and
then embedded. Others were kept in liquid nitrogen for further use. Expression
level of proteins in tumor and in cell was analyzed by Western blot. Microvessel
in tumor section was shown by immunohistochemistry and adhesive ability of cell
to amnion was measured by adhesion assay.
RESULTS: When inoculated nude mice were treated with ATRA, the xenograft tumors
in spleen and metastatic tumors in liver were suppressed by 50 % respectively,
and inhibition of microvessel formation in xenograft and metastatic tumors was
also observed obviously. Although ATRA regulated expression of nm23 and mts1/p16
proteins at different patterns in vivo and in vitro, high ratio of nm23:mts1/p16
was in association with low adhesive activity of cells. In addition, ATRA induced
ICAM-1 protein expression in vivo and in vitro.
CONCLUSION: ATRA inhibits the growth of xenograft tumors and their metastasis to
liver. This process may be associated with regulation of metastatic related
proteins, including nm23, mts1/p16, and ICAM-1 in vivo and in vitro.