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Long non‐coding RNA ELDR enhances oral cancer growth by promoting ILF 3‐cyclin E1 signaling
Author(s) -
Sur Subhayan,
Nakanishi Hiroshi,
Steele Robert,
Zhang Dapeng,
Varvares Mark A,
Ray Ratna B
Publication year - 2020
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.202051042
Subject(s) - cancer research , biology , long non coding rna , rna , cell growth , cancer , proliferating cell nuclear antigen , microbiology and biotechnology , gene , genetics
Oral squamous cell carcinoma ( OSCC ) is the sixth most common cancer with a 5‐year overall survival rate of 50%. Thus, there is a critical need to understand the disease process, and to identify improved therapeutic strategies. Previously, we found the long non‐coding RNA (lnc RNA ) EGFR long non‐coding downstream RNA ( ELDR ) induced in a mouse tongue cancer model; however, its functional role in human oral cancer remained unknown. Here, we show that ELDR is highly expressed in OSCC patient samples and in cell lines. Overexpression of ELDR in normal non‐tumorigenic oral keratinocytes induces cell proliferation, colony formation, and PCNA expression. We also show that ELDR depletion reduces OSCC cell proliferation and PCNA expression. Proteomics data identifies the RNA binding protein ILF 3 as an interacting partner of ELDR . We further show that the ELDR ‐ ILF 3 axis regulates Cyclin E1 expression and phosphorylation of the retinoblastoma ( RB ) protein. Intratumoral injection of ELDR ‐specific si RNA reduces OSCC and PDX tumor growth in mice. These findings provide molecular insight into the role of ELDR in oral cancer and demonstrate that targeting ELDR has promising therapeutic potential.