Dysregulation of long noncoding RNAs (lncRNAs) has been suggested to foster the carcinogenesis of hepatocellular carcinoma (HCC). To date, the role of long intergenic noncoding RNA01134 (LINC01134) in HCC have never been researched yet. Herein, we found that LINC01134 was highly expressed in HCC tissues in comparison with the matched normal liver tissues and increased LINC01134 expression correlated with shorter overall survival of patients with HCC. Additionally, we demonstrated LINC01134 downregulation significantly suppressed the proliferation ability and colony formation capacity of HCC cells. Furthermore, we revealed that LINC01134 functioned as a competitive endogenous RNA (ceRNA) for miR-4784 to upregulate structure-specific recognition protein 1 (SSRP1) in HCC cells. Meanwhile, miR-4784 inhibitor or restoration of SSRP1 could markedly attenuate the inhibitory effect of LINC01134 downregulation on HCC cells. Taken together, LINC01134 may promote the carcinogenesis of HCC at least partly via the miR-4784/SSRP1 axis. Therefore, LINC01134/miR-4784/SSRP1 axis should be developed as the promising therapeutic target for HCC.

长链非编码 RNA (lncRNA) 的失调已被认为会促进肝细胞癌 (HCC) 的癌变。迄今为止，尚未研究长基因间非编码 RNA01134 (LINC01134) 在 HCC 中的作用。在此，我们发现与匹配的正常肝组织相比，LINC01134 在 HCC 组织中高表达，并且 LINC01134 表达增加与 HCC 患者的总生存期缩短相关。此外，我们证明了 LINC01134 下调显着抑制了 HCC 细胞的增殖能力和集落形成能力。此外，我们发现 LINC01134 可作为 miR-4784 的竞争性内源 RNA (ceRNA) 上调 HCC 细胞中的结构特异性识别蛋白 1 (SSRP1)。同时，miR-4784抑制剂或SSRP1的恢复可以显着减弱LINC01134下调对HCC细胞的抑制作用。总之，LINC01134 可能至少部分通过 miR-4784/SSRP1 轴促进 HCC 的致癌作用。因此，LINC01134/miR-4784/SSRP1轴应该被开发为有前景的HCC治疗靶点。