Abstract
BackgroundChromosome 14 open reading frame 166 (C14orf166) is upregulated in various tumors, but its role in breast cancer has not been reported.MethodsQuantitative real-time PCR and western blot were used to determine C14orf166 expression in normal breast epithelial cells (NBEC), breast cancer cells, and four matched pairs of breast cancer tissues and adjacent noncancerous tissues. Using immunohistochemistry, we determined C14orf166 expression in paraffin-embedded tissues from 121 breast cancer patients. Statistical analyses were performed to examine the associations among C14or166 expression, clinicopathological parameters and prognosis outcome of breast cancer. MTT and colony formation assay were used to determine the effect of C14orf166 on cell proliferation by overexpression or knockdown of C14orf166 level.ResultsC14orf166 was upregulated in breast cancer cell lines and tissues compared with the normal cells and adjacent normal breast tissues, high C14orf166 expression was positively with advancing clinical stage. The correlation analysis between C14orf166 expression and clinicopathological characteristics suggested C14orf166 expression was significantly correlated with clinical stages, T classification, N classification and PR expression, Kaplan–Meier curves with log rank tests showed patients with low C14orf166 expression had better survival, Cox-regression analysis suggested C14orf166 was an unfavorable prognostic factor for breast cancer patients. C14orf166 overexpression promoted breast cancer cell proliferation, whereas knockdown of C14orf166 inhibited this effect. Further analysis found C14orf166 overexpression inhibited cell cycle inhibitors P21 and P27 expression, and increased the levels of Cyclin D1 and phosphorylation of Rb, suggesting C14orf166 contributed to cell proliferation by regulating G1/S transition.ConclusionOur findings suggested C14orf166 could be a novel prognostic biomarker of breast cancer, it also contributes to cell proliferation by regulating G1/S transition.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-0805-0) contains supplementary material, which is available to authorized users.
Highlights
Chromosome 14 open reading frame 166 (C14orf166) is upregulated in various tumors, but its role in breast cancer has not been reported
C14orf166 is upregulated in breast cancer cells and tissues To investigate the role of C14orf166 in breast cancer, we first demonstrated C14orf166 expression in normal breast epithelial cells (NBEC) and breast cancer cells
Quantitative real-time PCR and western blot assay found C14orf166 expression was significantly upregulated in breast cancer cells compared to NBEC (Fig. 1a, b)
Summary
Chromosome 14 open reading frame 166 (C14orf166) is upregulated in various tumors, but its role in breast cancer has not been reported. Breast cancer is one of the leading causes of cancer death in women worldwide [1]. It is a heterogeneous tumor, Cheang et al J Transl Med (2016) 14:54 breast cancer have generated resistance to Trastumab [7]. C14orf166 plays critical role in transcription initiation, HCV infection, RNA metabolism, and centrosome architecture. It can interact with PA subunit of influenza virus polymerase to activate some genes transcription and promote influenza virus replication [8]. Knockdown of C14orf166 suppresses the synthesis of about 50 % RNA polymerase II transcripts, these suggest C14orf166 regulates gene transcription [9]. C14orf166 blocks the phosphorylation of ninein to regulation the function of ninein, ninein is required for the centrosome maturation, this suggests C14orf166 may participate in the centrosome architecture [12, 13]
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