The mechanism of PDX in regulating cervical cancer HeLa cell proliferation and tumor formation

Y. Chen, D.-J. Li, T.-T. Wu, H.-B. Ruan, M.-Y. Zheng

Department of Obstetrics and Gynecology, The First People’s Hospital of Wenling, Wenling, Zhejiang, China. ping19177331@163.com

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• Oncology

OBJECTIVE: As a gynecological malignant tumor, cervical cancer tends to occur in younger patients. Furin is an important member of precursor protein convertase that may affect malignant tumor metastasis and neovascularization. Pancreatic duodenal homeobox (PDX), as a transcription factor, can inhibit Furin. This study intends to explore the impact of PDX on cervical cancer HeLa cell proliferation and mechanism.

PATIENTS AND METHODS: PDX plasmid was transfected to cervical cancer HeLa cells. Cell proliferation, invasion, and migration were tested. HeLa cells were injected to Balb/c nude mice to observe the change of general status, tumor formation rate, tumor weight, and volume.

RESULTS: PDX expression was gradually increased after PDX transfection following time extension. Cell proliferation, invasion, and migration in experimental group were significantly lower than those in normal control (p < 0.05). The nude mice injected with PDX transfected HeLa cells showed markedly better general status, with reducing rate of tumor formation, tumor weight and volume compared with control.

CONCLUSIONS: PDX can suppress cervical cancer HeLa cell proliferation, cell invasion and migration, improve general status of tumor-bearing nude mice and reduce tumor weight and volume. Our data highlight the clinical benefits of PDX in inhibiting cervical cancer proliferation, invasion, and metastasis.

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