In collaboration with p53,
cyclins B1 and G1 regulate the G2/M transition, a key checkpoint in the active cell cycle, which can be monitored by Ki67. However, the
cyclin B1 expression remains unclear during colorectal
carcinogenesis and during later
metastasis to lymph nodes, and
cyclin G1 expression is not clear in
colorectal tumors. To clarify the variations of the two
cyclins in
colorectal tumors,
cyclin B1,
cyclin G1, p53, and Ki67 were immunohistochemically stained in 22 normal mucosa, 62
adenomas, 17
carcinomas in
adenomas, 194 primary
carcinomas, and 21
lymph node metastases; and the two
cyclins were examined by Western blot in other 10 pairs of normal mucosa and primary
carcinomas. Located in cytoplasms, nuclei or both,
cyclin B1 expression increased significantly from normal mucosa through
adenomas to primary
carcinomas, from
adenomas with mild dysplasia through those with moderate to those with severe, from peripheral
adenomas to their central
carcinomas, and from primary to metastatic foci. These increased expressions were confirmed by Western blot.
Cyclin B1 expression, however, declined significantly in primary
carcinomas showing large size, mucinous type, deep invasion, or short postoperative-patient-survival time. High
cyclin B1 was linked to high p53 in
adenomas, and to high Ki67 in
adenomas and primary
carcinomas. In contrast, found limited to nuclei,
cyclin G1 expression did not vary significantly from normal mucosa through to metastatic
carcinomas, and was not associated with clinicopathological parameters, p53 or Ki67. The unchanged expressions were confirmed by Western blot. Thus, increased
cyclin B1, but not
cyclin G1, may promote colorectal
carcinogenesis and later
metastasis to lymph nodes.