Login to Access Video or Poster Abstract: MP60-19
Sources of Funding: none

Introduction

Long noncoding RNAs (lncRNAs) are reported to serve as regulating role in carcinogenesis of various human malignancies. However, the function of lncRNAs and their underlying mechanism in renal cell carcinoma ( RCC ) is still unraveled. The aims of this study were to investigate the expression of lncRNA BX357664 in RCC and explore its function in RCC cell lines.

Methods

Previous microarray analysis was used to screen potential deregulated lncRNA. Real-time qualitative PCR (qRT-PCR) was used to further confirm the deregulation of BX357664 in 40 paired human RCC samples. Ability of migration, invasion and proliferation in RCC cells were detected by cell migration and invasion assay, cell proliferation assay and cell cycle assay. Western blot was performed to identify the influence of BX357664 on epithelial-mesenchymal transition (EMT), MMP9 and TGF-beta 1/p38/HSP27 signaling pathway in RCC.

Results

BX357664 was downregulated in tumor tissues in previous microarray analysis (P < 0.05), qRT-PCR was further performed to validate the BX357664 expression in 40 paired RCC tissues and adjacent normal tissues. The result was consistent with the microarray data(P < 0.05). Meanwhile, BX357664 expression was significantly lower in RCC cell lines (Caki-1 and Caki-2) compared with normal renal cell line HK-2(P < 0.05). After upregulation of BX357664 in RCC celllines, ability of migration, invasion and proliferation in RCC cells were significantly inhibited(P < 0.05). In addition, overexpression of BX357664 could block EMT, MMP9 through inhibiting TGF-beta 1/p38/HSP27 signaling pathway. Subsequently, upregulating the protein level of TGF-beta 1 with the present of BX357664 could rescue the malignant cell behaviors inhibited by BX357664 which indicated that BX357664 was attributed its inhibitory role to suppression of TGF-beta 1.

Conclusions

We have revealed a novel lncRNA BX357664, which might exhibit its inhibitory role in RCC metastasis and progression via block TGF-beta 1/p38/HSP27 pathway.

Funding

none