Open AccessCDR1as is overexpressed in laryngeal squamous cell carcinoma to promote the tumour’s progression via miR‐7 signals
Author(s) -
Zhang Jianzhong,
Hu Huayong,
Zhao Yaoxin,
Zhao Yulin
Publication year - 2018
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12521
Subject(s) - gene knockdown , cancer research , microrna , downregulation and upregulation , suppressor , cell growth , in vivo , oncogene , biology , cell , cell culture , cancer , gene , cell cycle , genetics
Objectives To investigate the roles played by the circular RNA (circRNA) molecule ciRS‑7 (CDR1as) and tumour suppressor miRNA‐7 (miR‐7) in laryngeal squamous cell carcinoma (LSCC). Methods Specimens of LSCC tissue (n = 30) and corresponding relative normal tissue (n = 30) were collected to determine their levels and clinical significance of CDR1as/mir‐7 expression. The CDR1as and miR‐7 were overexpressed in LSCC cells to investigate its function and mechanism in vitro and in vivo. Results Patients with high TNM stages, poorly differentiated tumours, lymph node metastases and poor prognosis had high CDR1as levels but low miR‐7 levels. CDR1 expression was negatively associated with miR‐7 expression in LSCC. Overexpression of CDR1as in vitro enhanced cell vitality, and promoted the proliferation, migration, and invasion of two LSCC cell lines (Hep2 and AMC‐HN‐8.) However, these effects could be abrogated by knockdown of CDR1as or the forced expression of miR‐7. Mechanistically, overexpressed CDR1 molecules functioned as miR‐7 sponges and upregulated the key targets of miR‐7, CCNE1, and PIK3CD in Hep2 and AMC‐HN‐8 cells. In vivo studies demonstrated the tumourigenic role of CDR1as. Overexpression of CDR1as alone promoted tumour growth and increased expression of the proliferation indices ki‐67, CCNE1, and PIK3CD. Although the tumour suppressor miR‐7 effectively inhibited the tumour growth, this effect could be counteracted by co‐treatment with CDR1as in vivo. Conclusion CDR1as is an oncogene that promotes LSCC progression by regulating miR‐7 signals.