Human Colon and Liver Cancer Cell Proliferation Inhibition by Peptide Hydrolysates Derived from Heat-Stabilized Defatted Rice Bran

2008 ◽  
Vol 56 (24) ◽  
pp. 11643-11647 ◽  
Author(s):  
Arvind Kannan ◽  
Navam Hettiarachchy ◽  
Michael G. Johnson ◽  
Ramakrishna Nannapaneni
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Rice Bran ◽  
Human Colon ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell ◽  
Proliferation Inhibition ◽  
Defatted Rice Bran ◽  
Cell Proliferation Inhibition

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.

Sorafenib Affects Liver Cancer Cell Proliferation and Apoptosis by Regulating DJ-1-PTEN/PI3K/AKT Signaling Pathway

2020 ◽  
Vol 10 (8) ◽  
pp. 1219-1224
Author(s):  
Qiang Yu ◽  
Xiaoming Peng ◽  
Lihua Gong ◽  
Xiaoqiong Liu ◽  
Yuanyuan Shan
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Pten Expression ◽  
Akt Pathway ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell ◽  
Sorafenib Treatment ◽  
L Cells

Objective: To assess sorafenib's role in regulating DJ-1-PTEN/PI3 K/AKT pathway and affecting the biological effects of liver cancer cells. Methods: Human normal liver HL-7702, liver cancer MHC97-L, and HCCLM3 cells were cultured in vitro to measure DJ-1 and PTEN expression. MHC97-L and HCCLM3 cells were treated with 0, 1.0, 2.0 M of sorafenib followed by analysis of cell viability by CCK-8, and DJ-1 and PTEN expressions by Western blot. MHC97-L cells were separated into control group, 2.0 M Sorafenib treatment group, Sorafenib + pcDNA3.1-Blank group, and Sorafenib + pcDNA3.1-DJ-1 group. Cell proliferation was assessed by flow cytometry and EdU staining. Results: Compared with HL-7702 cells, DJ-1 expression was significantly increased, while PTEN level was significantly declined in MHC97-L and HCCLM3 cells. Sorafenib treatment significantly inhibited the proliferation activity of MHC97-L and HCCLM3 cells. Different concentrations of sorafenib significantly downregulated DJ-1 expression and enhanced PTEN expression in MHC97-L cells. pcDNA3.1-DJ-1 transfection on the basis of sorafenib treatment significantly elevated DJ-1 and p -AKT levels, reduced PTEN expression, decreased cell apoptosis, and enhanced cell proliferation. Conclusion: Sorafenib downregulates DJ-1 expression and affects PTEN/PI3K/AKT pathway activity to exert an anti-tumor effect that inhibits liver cancer cell proliferation and promotes cell apoptosis.

scholarly journals Vitamin D3 mediates miR‑15a‑5p inhibition of liver cancer cell proliferation via targeting E2F3

2020 ◽  
Vol 20 (1) ◽  
pp. 292-298
Author(s):  
Yulong Li ◽  
Qiang Lin ◽  
Su'e Chang ◽  
Rong Zhang ◽  
Jingjie Wang
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Vitamin D3 ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell
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