Abstract
Long non-coding RNA 00152 (LINC00152) is tumorigenic in multiple somatic malignancies. However, its prognostic significance and molecular mechanisms in the epithelial ovarian cancer (EOC) remain elusive. Here our study reveals that dysregulation of LINC00152 is a predictor of poor prognosis in patients with EOC and facilitates ovarian tumor growth and metastasis both in vitro and in vivo; the expression of LINC00152 positively correlates with the protein levels of BCL6 in EOC tissues and ovarian tumor cells; LINC00152 binds to Ser333 and Ser343 of BCL6 protein and stabilizes BCL6 from poly-ubiquitination thus facilitating the oncogenic functions in EOC. Moreover, overexpression of the mutant BCL6S333A/S343A fails to rescue the reduced proliferation and invasion caused by the knockdown of endogenous BCL6 in LINC00152-overexpressing cells. Our study might not only offer clues to the network of lncRNA-protein interactions but also provide potential therapeutic targets for the tumor pharmacology.
Highlights
Epithelial ovarian cancer (EOC) accounts for less than 3% of all malignancies in females, but is responsible for approximately 5% of total cancer deaths [1]
We found that the mRNA level of LINC00152 was abnormally increased in the ovarian tumor tissues and cell lines, and was accompanied with dysregulated biological functions, poorer clinical outcomes and increased cell proliferation and metastasis
Our study details the downstream targets of LINC00152 and the molecular mechanisms of B-cell CLL/lymphoma 6 (BCL6)-related lncRNAs in the tumorigenesis of EOC
Summary
Epithelial ovarian cancer (EOC) accounts for less than 3% of all malignancies in females, but is responsible for approximately 5% of total cancer deaths [1]. The non-coding RNA 00152 (LINC00152) is a lncRNA located at 2p11.2 [7] and has been involved in cell proliferation [8], cell-cycle arrest [7], epithelial-mesenchymal transition [9] and cell invasion [10] in order to facilitate tumor initiation and progression. Our former studies and studies from other researches have revealed that LINC00152 promotes tumor invasion and predicts poor prognosis in renal clear cell [11], lung [12], gastric [13] and hepatic carcinoma [5]; its role in the progression of EOC needs further exploration. Since lncRNAs could either repress [20] or prompt [21] the ubiquitination of target substrates, it is unclear whether the molecular mechanisms of LINC00152 in EOC are linked to the ubiquitination of downstream proteins
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