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Updated: May 13, 2026

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker
Published on: September 15, 2023
Disruption of precise regulation of αPKC expression and cellular localization is associated with cervical cancer
Xiaojiao Liu1, Ling Wang, Yangmei Shen
1Department of Gynecology, West China Second University Hospital, Sichuan University, Chengdu, People's Republic of China.
Purpose:
To understand the pathogenesis of cervical cancer (CC) associated with polarity protein αPKC and the potential roles of αPKC in clinical management of CC.
Methods:
Tissue samples were collected from women who received colposcopy biopsy or hysterectomy surgery, including 9 CIN1, 8 CIN2, 15 CIN3, and 12 invasive cervical squamous cancer (ICC). 16 normal controls were from the normal region of tumor samples, HE and immunofluorescence staining of αPKC were performed on these samples. ANOVA and Kruslal-wallis test were used to quantitate the abnormal distribution and expression level of αPKC among different cervical lesions.
Results:
Disruption of polarized apical localization and increased cytoplasmic accumulation of αPKC were identified in cervical lesions. In normal cervical epithelium, αPKC was detected on the apical membrane of endocervical columnar epithelial cells and of exocervical epithelial cells located at basal layer of squamous epithelium. While in squamous metaplasia, a precancerous lesion of cervical neoplasia, the polarized apical membrane localization of αPKC was disrupted, and intensed cytoplasmic accumulation was identified in the immature squamous metaplastic cells. Compared with normal cervix, number of epithelial cells with abnormal αPKC distribution was progressively increased in CINs and ICC (P < 0.05), and cytoplasmic accumulation of αPKC was increased in CIN2, CIN3, and ICC compared with CIN1 (P < 0.05).
Conclusions:
Disruption of polarized apical localization and increased cytoplasmic accumulation of αPKC were associated with CC progression, indicating that precise regulation of αPKC may play important roles in CC progression, and αPKC may be a potential molecular target for clinical diagnoses and treatment of CC.
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