2021
DOI: 10.1016/j.phymed.2020.153373
|View full text |Cite
|
Sign up to set email alerts
|

Trans-chalcone induces death by autophagy mediated by p53 up-regulation and β-catenin down-regulation on human hepatocellular carcinoma HuH7.5 cell line

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
11
0

Year Published

2021
2021
2024
2024

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 18 publications
(11 citation statements)
references
References 21 publications
0
11
0
Order By: Relevance
“…Further mechanistic studies demonstrated that TChal could bind and degrade chromosome region maintenance 1 (CRM1), a nuclear export receptor involved in the active transport of tumor suppressors, and increase heat-shock protein 40 (HSP40) expression in U2OS osteosarcoma cells; the interaction of HSP40 with MDM2 blocked MDM2-mediated ubiquitination of p53, leading to the enhanced stability and activation of p53 [ 128 , 130 ]. Moreover, Siqueira et al reported that TChal could reestablish the p53 pathway and prevent the overexpression of Wnt/β-catenin tumor development, inducing autophagy-related cell death and decreasing the metastatic capacity of HCC HuH7.5 cells [ 131 ]. Seba et al reported that the chalcone derivative 4′-aminochalcone ( 48 ) inhibited the migration and invasion of osteosarcoma cells through the inhibition of extracellular matrix enzymatic degradation and the modulation of p53, regulating the epithelial-mesenchymal transition (EMT)-related genes [ 132 ].…”
Section: Representative Mechanisms Of Anticancer Action Of Chalconesmentioning
confidence: 99%
“…Further mechanistic studies demonstrated that TChal could bind and degrade chromosome region maintenance 1 (CRM1), a nuclear export receptor involved in the active transport of tumor suppressors, and increase heat-shock protein 40 (HSP40) expression in U2OS osteosarcoma cells; the interaction of HSP40 with MDM2 blocked MDM2-mediated ubiquitination of p53, leading to the enhanced stability and activation of p53 [ 128 , 130 ]. Moreover, Siqueira et al reported that TChal could reestablish the p53 pathway and prevent the overexpression of Wnt/β-catenin tumor development, inducing autophagy-related cell death and decreasing the metastatic capacity of HCC HuH7.5 cells [ 131 ]. Seba et al reported that the chalcone derivative 4′-aminochalcone ( 48 ) inhibited the migration and invasion of osteosarcoma cells through the inhibition of extracellular matrix enzymatic degradation and the modulation of p53, regulating the epithelial-mesenchymal transition (EMT)-related genes [ 132 ].…”
Section: Representative Mechanisms Of Anticancer Action Of Chalconesmentioning
confidence: 99%
“…260 Besides, the benefits of plant-derived, natural compounds is that they can inhibit β-catenin signaling to induce cytotoxicity against HCC cells, while they are safe and have no toxicity on normal cells or hematological profile. 116 A few experiments have evaluated synthetic small molecules as inhibitors of β-catenin signaling. C-82 is a small molecule and active form of PRI-724 that can induce cell cycle arrest at G0/G1 phase and prevents growth of HCC cells.…”
Section: Dovepressmentioning
confidence: 99%
“…In addition, chalcones capable of inducing autophagy include hydroxysafflor yellow A [ 143 ], cardamonin [ 105 ], panduratin A [ 163 ], bavachalcone (isolated from Cullen corylifolium) [ 111 ], trans-chalcone [ 164 ], or α,2′-dihydroxy-4,4′-dimethoxydihydrochalcone, isolated from Cedrela odorata (Meliaceae) [ 165 ].…”
Section: Induction Of Cell Deathmentioning
confidence: 99%