[Correlation of expression of connexin to growth and progression of cervical carcinoma in situ].
OBJECTIVE
Gap junction intercellular communication (GJIC), mediated by connexin (CX), is the unique type of intercellular communication in carcinoma in situ (CIS). Changes in expression of CXs and function of GJIC may play roles in carcinogenesis of cervical cancer and progression of CIS. This study was to investigate the expression of CXs in normal epithelium (NE), hyperplasia, CIS, and invasive carcinoma (IC) of cervix, to explore correlation of expression of CXs to pathogenesis and progression of cervical CIS.


METHODS
Expression of CX43 (mRNA, protein), CX26 (mRNA), and Ki-67 (protein) in 30 specimens of cervical NE, 22 specimens of cervical hyperplasia, 30 specimens of cervical CIS, and 26 specimens of cervical IC were detected by immunohistochemistry and in situ hybridization.


RESULTS
In cervical NE, hyperplasia, CIS, and IC, positive rates of CX43 protein were 83%, 55%, 50%, and 30%, respectively, and positive rates of CX43 mRNA were 97%, 64%, 58%, and 46%, respectively; positive rates of CX26 mRNA was 93%, 68%, 55%, and 42%, respectively. Positive rates of CX43 (mRNA, protein) and CX26 (mRNA) were gradually decreased. Positive rate of CX was significantly lower in CIS group than in NE group (P < 0.05). The expressions of CX26 and CX43 were weaker in CIS group than in NE groupu their expressions were obviously decreased, or even vanished in the area of CIS adjacent to NE. Proliferating index (PI), indicated by expression of Ki-67 protein, was increased gradually in NE (5%), hyperplasia (12%), CIS (30%), and IC (62%)u the differences were significant (P < 0.05) between CIS group and other groups.


CONCLUSIONS
CX26 and CX43 may play important roles in carcinogenesis of cervical cancer. CXs may inhibit tumorigenesis and cell proliferation; it might be key factors in earlier stages when cellular malignant phenotypes have been established, or NE has been transformed into CIS.
Cao
Yu-Wen
YW
MOE Laboratory of Xinjiang Endemic and Ethnic Disease/ Department of Pathology, School of Medicine, Shihezi University, Shihezi, Xinjiang, 832002, P.R.China.
Lu
Tian-Cai
TC
Pan
Xiao-Lin
XL
Li
Feng
F
Zhong
Hao-Hao
HH
Sun
Yan
Y
Jiang
Jin-Fang
JF
Li
Li
L
D002278:Carcinoma in Situ / Q000378:metabolism*; D002294:Carcinoma, Squamous Cell / Q000378:metabolism*; D002584:Cervix Uteri / Q000378:metabolism; D000072259:Connexin 26; D018031:Connexin 43 / Q000096:biosynthesis* / Q000235:genetics; D017630:Connexins / Q000096:biosynthesis* / Q000235:genetics; D018450:Disease Progression; D004848:Epithelium / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D011230:Precancerous Conditions / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D002583:Uterine Cervical Neoplasms / Q000378:metabolism*
D018031:Connexin 43; D017630:Connexins; C000607042:GJB2 protein, human; D019394:Ki-67 Antigen; D012333:RNA, Messenger; D000072259:Connexin 26