Objective  To investigate the effect of long chain non-coding differentiation antagonizing nonprotein coding RNA (DANCR) on proliferation and apoptosis of nasopharyngeal carcinoma cells through targeted regulation of glucose-regulated protein 78 kDa (GRP78) and its mechanism.

  Methods  The expression of DANCR in nasopharyngeal carcinoma tissues and different nasopharyngeal carcinoma cell lines were detected with quantitative real-time PCR (qPCR). Double luciferase reporter was used to detect the interaction between DANCR and GRP78. The association of DANCR with clinical and pathological manifestations of nasopharyngeal carcinoma patients was analyzed. Clone formation assay was used to detect the effect of DANCR on the proliferation of nasopharyngeal carcinoma cells. The effect of DANCR on the apoptosis of nasopharyngeal carcinoma cells was detected with flow cytometry. The effect of DANCR on xenograft differentiation of nasopharyngeal carcinoma was evaluated with nude mouse tumorigenicity assay.

  Results  Compared with that in other nasopharyngeal carcinoma cell lines, the DANCR expression in nasopharygneal carcinoma cells (CNE-1) was significantly higher (2.38 ± 0.35) (P < 0.05). Double-luciferase experiments confirmed that DANCR can directly regulate the expression of GRP78 and fluorescence activity. The inhibition of DANCR expression can significantly attenuate the proliferation (number of cells/per plate: 188.2 ± 7.6 vs. 376.3 ± 19.3) and promote the apoptosis of nasopharyngeal carcinoma cells (59.3 ± 12.1% vs. 17.3 ± 4.2%) (both P < 0.05). The xenograft differentiation of nasopharyngeal carcinoma cells with the down-regulated expression of DANCR was inhibited at some extent, with the decreased transplanted tumor volume (0.71 ± 0.18 cm³ vs. 2.48 ± 0.34 cm³) and weight (0.73 ± 0.15 g vs. 2.28 ± 0.41g) (both P < 0.05).

  Conclusion  DANCR can inhibit the proliferation and promote the apoptosis of nasopharyngeal carcinoma cells through targeted regulation of GRP78 expression.