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Long non‐coding RNA DBH‐AS1 promotes cancer progression in diffuse large B‐cell lymphoma by targeting FN1 via RNA‐binding protein BUD13
Author(s) -
Song Yanping,
Gao Feng,
Peng Yi,
Yang Xuejie
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11327
Subject(s) - antisense rna , gene knockdown , downregulation and upregulation , cancer research , messenger rna , biology , rna , microbiology and biotechnology , long non coding rna , gene , genetics
Diffuse large B‐cell lymphoma (DLBC) is a subtype of lymphoma with the worst prognosis. Existing treatment methods are not effective enough due to its high occurrence of metastasis. Therefore, identification of effective therapeutic targets is becoming increasingly important. In this research, long non‐coding RNA dopamine β hydroxylase antisense RNA 1 (DBH‐AS1) was found to be upregulated in DLBC tissues and cells. Knockdown of DBH‐AS1 suppressed the proliferation, migration, and invasion of cancer cells. Afterwards, RNA‐binding protein BUD13 homolog (BUD13) was found to be upregulated in cancer tissues and cells while binding to DBH‐AS1. Fibronectin 1 (FN1) was the downstream messenger RNA (mRNA) of BUD13. FN1 was upregulated in DLBC and was positively correlated with DBH‐AS1. Further rescue assays proved that DBH‐AS1 mediated FN1 expression by recruiting BUD13. In the meantime, BUD13 stabilized FN1 mRNA to promote FN1 expression. In this way, DBH‐AS1/BUD13/FN1 axis was confirmed. A set of rescue assays proved that DBH‐AS1 regulated DLBC progression via BUD13 and FN1. The function and mechanism of DBH‐AS1 were investigated for the first time in DLBC. DBH‐AS1 might become a therapeutic target in lymphoma treatment in the future.