The long non-coding RNA PTTG3P promotes growth and metastasis of cervical cancer through PTTG1

• Published in: Aging (Albany, NY.) Vol. 11; no. 5; pp. 1333 - 1341
• Main Authors: Guo, Xiang-Cui, Li, Li, Gao, Zhi-Hui, Zhou, Hong-Wei, Li, Jun, Wang, Qian-Qing
• Format: Journal Article
• Language: English
• Published: United States Impact Journals 10.03.2019
• Subjects: Adult; Cadherins - genetics; Cadherins - metabolism; Cell Line, Tumor; Cell Movement; Cyclin B1 - metabolism; Female; Gene Expression Regulation, Neoplastic; Humans; Neoplasm Invasiveness; Research Paper; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Securin - genetics; Securin - metabolism; Snail Family Transcription Factors - genetics; Snail Family Transcription Factors - metabolism; Uterine Cervical Neoplasms - metabolism; Uterine Cervical Neoplasms - pathology; cancer growth and metastasis; Pituitary Tumor Transforming Gene 1 (PTTG1); cervical cancer; PTTG3P
• ISSN: 1945-4589; 1945-4589
• DOI: 10.18632/aging.101830

The outgrowth and metastasis of cervical cancer (CC) contribute to its malignancy. Pituitary Tumor Transforming Gene 1 (PTTG1) is upregulated in many types of cancer, and enhances tumor cell growth and metastasis. However, the activation and regulation of PTTG1 in CC, especially by its pseudogene PTTG3P, have not been shown. Here, we detected significantly higher levels of PTTG1 and PTTG3P in the resected CC tissue, compared to the paired adjacent normal cervical tissue. Interestingly, the PTTG3P levels positively correlated with the PTTG1 levels. High PTTG3P levels were associated with poor patients' survival. In vitro, PTTG1 were increased by PTTG3P overexpression, but was inhibited by PTTG3P depletion in CC cells. However, PTTG3P levels were not altered by modulation of PTTG1 in CC cells, suggesting that PTTG3P is upstream of PTTG1. Moreover, PTTG3P increased CC cell growth, likely through CCNB1-mediated increase in cell proliferation, rather than through decrease in cell apoptosis. Furthermore, PTTG3P increased CC cell invasiveness, likely through upregulation of SNAIL and downregulation of E-cadherin. Our work thus suggests that PTTG3P may promote growth and metastasis of CC through PTTG1.