scholarly journals Polyphyllin II inhibits liver cancer cell proliferation, migration and invasion through downregulated cofilin activity and the AKT/NF-κB pathway

Biology Open ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. bio046854 ◽  
Author(s):  
Dejiang Pang ◽  
Chengcheng Yang ◽  
Chao Li ◽  
Yuanfeng Zou ◽  
Bin Feng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell

scholarly journals MiR-155 Inhibits Malignant Biological Behavior of Human Liver Cancer Cells by Regulating SRPK1

2021 ◽  
Vol 20 ◽  
pp. 153303382095702
Author(s):  
Qi Wang ◽  
Guo-tai Wang ◽  
Wei-hong Lu
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Although the treatment of liver cancer has made great progress, the mechanism of its occurrence is not completely clear. miR-155 plays an important regulatory role in tumorigenesis and development, including survival, proliferation, migration and invasion. However, the role and regulatory mechanism of miR-155 in liver cancer has rarely been reported. We analyzed miR-155 expression in liver cancer tissue samples and cell lines by qRT-PCR. The expression of miR-155 was measured by qRT-PCR before and after miR-155-mimic and sh-miR-155 transfection. CCK-8 and clonogenic assays were used to detect the proliferation of liver cancer cells. Cell scratch and invasion assays were used to detect migration and invasion. RNA-seq was used to detect the difference in RNA expression in liver cancer cells. SRPK1 expression was detected in liver cancer cells before and after transfection by qRT-PCR and western blotting. We observed that miR-155 was downregulated in liver cancer tissues compared with normal tissues. Furthermore, we demonstrated that liver cancer cell proliferation, migration and invasion are markedly suppressed by miR-155. Importantly, we also demonstrated that SRPK1 is directly regulated by miR-155 during the process of liver cancer cell proliferation and metastasis. Finally, the overexpression of miR-155 inhibits malignant biological behavior of human liver cancer cells. We report the abnormal expression of the miR-155 cluster in liver cancer cells, which inhibits cancer cell proliferation and metastasis. In addition, we identified SRPK1 as a target gene of miR-155 during the process of liver cancer cell proliferation and metastasis.

scholarly journals MicroRNA-214 targets Wnt3a to suppress liver cancer cell proliferation

2017 ◽  
Vol 16 (5) ◽  
pp. 6920-6927 ◽  
Author(s):  
Yang Yang ◽  
Zhenghao Zhao ◽  
Ni Hou ◽  
Yulong Li ◽  
Xiaofei Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell

scholarly journals Deletion of low-density lipoprotein-related receptor 5 inhibits liver Cancer cell proliferation via destabilizing Nucleoporin 37

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Jinxiao Chen ◽  
Da Wo ◽  
En Ma ◽  
Hongwei Yan ◽  
Jun Peng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Hepg2 Cell ◽  
Cancer Cell ◽  
Hepg2 Cells ◽  
Nuclear Pore ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell ◽  
Independent Manner ◽  
Independent Functions

Abstract Background LRP5/6 are co-receptors in Wnt/β-catenin pathway. Recently, we discovered multiple β-catenin independent functions of LRP5/6 in tumor cells and in the diseased heart. Nucleoporin 37 (NUP37) is an important component of the nuclear pore complex (NPC), whose elevated expression is associated with worsened prognosis in liver cancer. Previous studies have shown that NUP37 interacted with YAP and activated YAP/TEAD signaling in liver cancer. Our preliminary findings showed a nuclear location of LRP5. We thus tested the hypothesis that LRP5 may act as a genuine regulator of YAP/TEAD signaling via modulating NUP37 in a β-catenin-independent way. Methods We performed siRNA knockdown of LRP5, LRP6, or β-catenin in liver cancer HepG2 cells to determine the effect on tumor cell proliferation. Protein expressions and interaction between LRP5 and NUP37 were determined using immunoprecipitation and western blot analyses. Results HepG2 cell proliferation was markedly inhibited by knockdown of LRP5 but not LRP6 or β-catenin, suggesting that LRP5 has a specific, β-catenin-independent role in inhibiting HepG2 cell proliferation. Knockdown of NUP37 by siRNA inhibited the proliferation of HepG2 cells, whereas overexpression of NUP37 reversed the decrease in cell proliferation induced by LRP5 knockdown. Immunoprecipitation assays confirmed that LRP5 bound to NUP37. Furthermore, LRP5 overexpression restored NUP37 knockdown-induced downregulation of YAP/TEAD pathway. Conclusions LRP5 deletion attenuates cell proliferation via destabilization of NUP37, in a β-catenin-independent manner. LRP5 therefore acts as a genuine regulator of YAP/TEAD signaling via maintaining the integrity of the NPC, and implicates a therapeutic strategy in targeting LRP5 for inhibiting liver cancer cell proliferation.

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