LINC01133 aggravates the progression of hepatocellular carcinoma by activating the PI3K/AKT pathway.

LncRNAs exhibit crucial roles in various pathological diseases, including hepatocellular carcinoma (HCC). Therefore, it is significant to recognize the dysregulated lncRNAs in HCC progression. Recently, LINC01133 has been identified in several tumors. However, the biological role of LINC01133 in HCC remains poorly understood. Currently, we focused on the function of LINC01133 in HCC development. We observed that LINC01133 was significantly increased in HCC cells including HepG2, Hep3B, MHCC-97L, SK-Hep-1, and MHCC-97H cells compared with the normal human liver cell line HL-7702. In addition, PI3K/AKT signaling was highly activated in HCC cells. Knockdown of LINC01133 was able to inhibit HCC cell proliferation, cell colony formation, cell apoptosis, and blocked cell cycle arrest in the G1 phase. For another, downregulation of LINC01133 repressed HCC cell migration and invasion. Subsequently, the PI3K/AKT signaling pathway was strongly suppressed by silence of LINC01133 in Hep3B and HepG2 cells. Then, in vivo tumor xenografts models were established using Hep3B cells to explore the function of LINC01133 in HCC progression. Consistently, our study indicated that knockdown of LINC01133 dramatically repressed HCC tumor progression through targeting the PI3K/AKT pathway in vivo. Taken these together, we revealed that LINC01133 contributed to HCC progression by activating the PI3K/AKT pathway.

Zheng YF ，Zhang XY ，Bu YZ 《-》

Upregulation of lncRNA FER1L4 suppresses the proliferation and migration of the hepatocellular carcinoma via regulating PI3K/AKT signal pathway.

This study aimed to investigate the potential function of FER1L4 in the progression of hepatocellular carcinoma and uncover its underlying molecular mechanism. In the current study, quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the expression profile of FER1L4 in normal liver tissues and hepatocellular carcinoma tissues of human, as well as hepatocellular carcinoma (HCC) cell lines including HL-7702[L-02], HepG-2, Hep3b, and SMMC-7721. Then, HepG-2 cells were transfected with pcDNA3.1-FER1L4 (pcDNA3.1-empty as negative control) for gain-of-function analysis, followed with cell functional abnormality tests. Specifically, colony formation analysis and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide experiment were taken advantage to measure the cell proliferation, while cell migration and invasion were evaluated by wound healing assay and transwell experiment respectively. Additionally, cell apoptosis was detected by flow cytometry. Moreover, the effect of FER1L4 on PI3K/AKT signal pathway activation was investigated through analyzing phosphorylation of related proteins, p-AKT/AKT and p-PI3K/PI3K, via Western blot assay. Downregulation of FER1L4 in hepatocellular carcinoma tissues and cells was demonstrated by qRT-PCR analysis. Besides, FER1L4 overexpression evidently attenuated the cell proliferation, migration and invasion, but prompted cell apoptosis. Importantly, Western blot assays revealed that PII3K/AKT signal pathway were involved in mediating the progression regulation role of FER1L4 in HCC cells. Our study suggested that FER1L4 might alleviate progression of hepatocellular carcinoma via blocking PI3K/AKT pathway, which encourages a better understanding of the pathogenesis of HCC and may provide a novel potential therapeutic target for clinical treatment.

Wang X ，Dong K ，Jin Q ，Ma Y ，Yin S ，Wang S ... -  《-》

ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-κB signaling pathway.

Chen H ，Wang H ，Yu X ，Zhou S ，Zhang Y ，Wang Z ，Huang S ，Wang Z ... -  《BMC CANCER》

Secalonic Acid-F, a Novel Mycotoxin, Represses the Progression of Hepatocellular Carcinoma via MARCH1 Regulation of the PI3K/AKT/β-catenin Signaling Pathway.

Xie L ，Li M ，Liu D ，Wang X ，Wang P ，Dai H ，Yang W ，Liu W ，Hu X ，Zhao M ... -  《MOLECULES》

Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway.

Increasing studies have indicated that long noncoding RNAs (lncRNAs) exert important roles in hepatocellular carcinoma (HCC). Therefore, it is of great significance to identify the dysregulated lncRNAs in HCC. According to the previous reports, it has been suggested that DiGeorge syndrome critical region gene 5 (DGCR5) might participate in HCC and can serve as potential biomarker for HCC. In our current study, we concentrated on the biological function and roles of lncRNA-DGCR5 in HCC. It was indicated that DGCR5 was decreased in HCC tissues and HCC cells including HepG2, Hep3B, MHCC-97L, SNU-449, and SNU-182 cells compared with the normal human liver cell line LO2. Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. In addition, whether lncRNA-DGCR5 can regulate Wnt/β-catenin pathway during HCC progression is unclear. In our study, it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting β-catenin, cyclin D1 and increasing GSK-3β levels. Subsequently, in vivo tumor xenografts were established using HepG2 cells to investigate the function of DGCR5 in HCC development. Inconsistent with the in vitro findings, increase of DGCR5 dramatically suppressed HCC tumor progression in vivo. Taken these together, it was uncovered in our research that DGCR5 could play tumor suppressive role by targeting Wnt signaling in HCC progression.

Wang XL ，Shi M ，Xiang T ，Bu YZ ... -  《-》