Expression of Cell Competition Markers at the Interface between p53 Signature and Normal Epithelium in the Human Fallopian Tube.
There is a growing body of evidence regarding cell competition between normal and mutant mammalian cells, which suggest that it may play a defensive role in the early phase of carcinogenesis. In vitro study in the past has shown that overexpression of vimentin in normal epithelial cells at the contact surface with transformed cells is essential for the cell competition involved in epithelial defense against cancer. In this study, we attempted to examine cell competition in human tissue in vivo by investigating surgically resected human fallopian tubes that contain p53 signatures and serous tubal intraepithelial lesions (STILs), a linear expansion of p53-immunopositive/TP53 mutant tubal epithelial cells that are considered as precursors of pelvic high grade serous carcinoma. Immunofluorescence double staining for p53 and the cell competition marker vimentin was performed in 21 sections of human fallopian tube tissue containing 17 p53 signatures and 4 STILs. The intensities of vimentin expression at the interface between p53-positive cells at the end of the p53 signature/STIL and adjacent p53-negative normal tubal epithelial cells were compared with the background tubal epithelium. As a result, the average vimentin intensity at the interfaces relative to the background intensity was 1.076 (95% CI, 0.9412 - 1.211 for p53 signature and 0.9790 (95% CI, 0.7206 - 1.237) for STIL. Thus, it can be concluded that overexpression of the cell competition marker vimentin are not observed in human tissue with TP53 alterations.
Department of Cellular and Organ Pathology, Graduate School of Medicine, Akita University, Akita, Japan.|Department of Obstetrics and Gynecology, Graduate School of Medicine, Akita University, Akita, Japan.
Masahiko
M
Kito
Department of Cellular and Organ Pathology, Graduate School of Medicine, Akita University, Akita, Japan.
Daichi
D
Maeda
Department of Cellular and Organ Pathology, Graduate School of Medicine, Akita University, Akita, Japan.
Yukitsugu
Y
Kudo-Asabe
Department of Obstetrics and Gynecology, Graduate School of Medicine, Akita University, Akita, Japan.
Naoki
N
Sato
Department of Pathology, Oncology and Gynecology and Obstetrics, Johns Hopkins Medical Institutions, Baltimore, MD, United States of America.
Ie-Ming
IeM
Shih
Department of Pathology, Oncology and Gynecology and Obstetrics, Johns Hopkins Medical Institutions, Baltimore, MD, United States of America.
Tian-Li
TL
Wang
Department of Molecular Medicine and Biochemistry, Graduate School of Medicine, Akita University, Akita, Japan.
Masamitsu
M
Tanaka
Department of Obstetrics and Gynecology, Graduate School of Medicine, Akita University, Akita, Japan.
Yukihiro
Y
Terada
Department of Cellular and Organ Pathology, Graduate School of Medicine, Akita University, Akita, Japan.
Akiteru
A
Goto
D000328:Adult; D000368:Aged; D014408:Biomarkers, Tumor / Q000378:metabolism; D018284:Cystadenocarcinoma, Serous / Q000378:metabolism* / Q000473:pathology; D004848:Epithelium / Q000378:metabolism; D005185:Fallopian Tube Neoplasms / Q000378:metabolism* / Q000473:pathology; D005187:Fallopian Tubes / Q000378:metabolism*; D005260:Female; D006801:Humans; D008875:Middle Aged; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D014746:Vimentin / Q000378:metabolism*
D014408:Biomarkers, Tumor; D016159:Tumor Suppressor Protein p53; D014746:Vimentin