Open AccessLong noncoding RNA PXN‐AS1‐L promotes the malignancy of nasopharyngeal carcinoma cells via upregulation of SAPCD2
Author(s) -
Jia Xiaodong,
Niu Po,
Xie Cuncun,
Liu Hongjian
Publication year - 2019
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.2227
Subject(s) - nasopharyngeal carcinoma , biology , long non coding rna , cancer research , gene silencing , downregulation and upregulation , cell growth , microrna , cell migration , cell , medicine , gene , genetics , radiation therapy
Accumulating evidences highlight the critical roles of long noncoding RNAs (lncRNAs) in a variety of cancers. LncRNA PXN‐AS1‐L was previously shown to exert oncogenic roles in hepatocellular carcinoma. However, the expression, role, and molecular mechanism of PXN‐AS1‐L in nasopharyngeal carcinoma (NPC) malignancy remain unknown. Here, we determined that PXN‐AS1‐L is upregulated in NPC tissues and cell lines. Increased expression of PXN‐AS1‐L predicts worse prognosis of NPC patients. PXN‐AS1‐L overexpression promotes NPC cell proliferation, migration, and invasion in vitro, and NPC tumor growth in vivo. PXN‐AS1‐L silencing suppresses NPC cell proliferation, migration, and invasion in vitro. Mechanistically, PXN‐AS1‐L directly interacts with SAPCD2 mRNA 3′‐untranslated region, prevents the binding of microRNAs‐AGO silencing complex to SAPCD2 mRNA, and upregulates the mRNA and protein level of SAPCD2. SAPCD2 is also increased in NPC tissues. The expression of SAPCD2 is significantly positively associated with that of PXN‐AS1‐L in NPC tissues. Gain‐of‐function and loss‐of‐function experiments demonstrated that SAPCD2 also promotes NPC cell proliferation, migration, and invasion. Furthermore, depletion of SAPCD2 significantly reverses the roles of PXN‐AS1‐L in promoting NPC cell proliferation, migration, and invasion in vitro, and NPC tumor growth in vivo. In conclusion, lncRNA PXN‐AS1‐L is upregulated in NPC and promoted NPC malignancy by upregulating SAPCD2 via direct RNA‐RNA interaction.