Correlation of matrix metalloproteinase suppressor genes RECK, VEGF, and CD105 with angiogenesis and biological behavior in esophageal squamous cell carcinoma.
OBJECTIVE
To explore the expression of reversion inducing cysteine-rich protein with Kazal motifs (RECK), vascular endothelial growth factor (VEGF) and endoglin (CD105) protein and its correlation with occurrence, development, invasion and metastasis in esophageal squamous cell carcinoma (ESCC).


METHODS
Streptavidin-peroxidase (SP) immunohisto-chemistry was used to detect expression of RECK and VEGF in 62 cases of ESCC, 31 cases of adjacent atypical hyperplastic epithelium and 62 cases of normal esophageal epithelium. CD105 Mb was used to assess microvessel density (MVD).


RESULTS
The expression of RECK was closely correlated with histological grade, infiltrative depth and lymphatic metastasis in ESCC (P < 0.05). The expression of RECK decreased during cancer development: normal esophageal epithelium (85.5%, 53/62), adjacent atypical hyperplastic epithelium (71.0%, 22/31), and carcinoma (59.7%, 37/62). There was a significant difference among the groups (P < 0.05). The expression of VEGF protein was closely correlated with infiltrative depth and lymphatic metastasis in ESCC (P < 0.05). The expression of VEGF protein increased during cancer development: normal esophageal epithelium (29.0%, 18/62), adjacent atypical hyperplastic epithelium (54.8%, 17/31), and carcinoma (67.7%, 42/62). There was a significant difference among the groups (P < 0.05). MVDCD105 increased in accordance with histological grade, but there was no significant difference (grade I, 36.92 +/- 10.85; grade II, 37.65 +/- 9.50; and grade III, 38.06 +/- 12.19). The MVDCD105 was closely correlated with infiltration and lymphatic metastasis in ESCC (P < 0.05). The expression of RECK was inversely correlated with the expression of VEGF and CD105.


CONCLUSIONS
RECK, VEGF and CD105 play important roles in the infiltration, metastasis and carcinogenesis in esophageal carcinoma. Angiogenesis in ESCC may be promoted by over-expression of CD105.
Li
Sheng-Lei
SL
Department of Pathology, The First Affiliated Hospital, Zhengzhou University, Henan Key Laboratory of Tumor Pathology, Zhengzhou 450052, He'nan Province, China.
Gao
Dong-Ling
DL
Zhao
Zhi-Hua
ZH
Liu
Zong-Wen
ZW
Zhao
Qiu-Min
QM
Yu
Jin-Xia
JX
Chen
Kui-Sheng
KS
Zhang
Yun-Han
YH
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism*; D002294:Carcinoma, Squamous Cell / Q000098:blood supply / Q000175:diagnosis / Q000378:metabolism*; D042241:Early Diagnosis; D000071063:Endoglin; D004938:Esophageal Neoplasms / Q000098:blood supply / Q000175:diagnosis / Q000378:metabolism*; D004947:Esophagus / Q000473:pathology; D005260:Female; D058851:GPI-Linked Proteins; D015870:Gene Expression; D006801:Humans; D006965:Hyperplasia / Q000175:diagnosis / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008875:Middle Aged; D009362:Neoplasm Metastasis; D009389:Neovascularization, Pathologic / Q000378:metabolism*; D011379:Prognosis; D011956:Receptors, Cell Surface / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; D058851:GPI-Linked Proteins; D008562:Membrane Glycoproteins; C115460:RECK protein, human; D011956:Receptors, Cell Surface; D042461:Vascular Endothelial Growth Factor A