Parthenolide inhibits proliferation and invasion, promotes apoptosis, and reverts the cell–cell adhesion loss through downregulation of NF‐κB pathway TNF‐α‐activated in colorectal cancer cells

孤雌内酯 肿瘤坏死因子α 细胞凋亡 细胞粘附 下调和上调 细胞生长 癌症研究 NF-κB 粘附 生物 细胞生物学 细胞 化学 免疫学 医学 生物化学 基因 有机化学
作者
Adriana Sartorio Gehren,Waldemir Fernandes de Souza,Annie Cristhine Moraes Sousa‐Squiavinato,Diego Alfonso Arregui Ramos,Bruno Ricardo Barreto Pires,Eliana Abdelhay,José Andrés Morgado‐Díaz
出处
期刊:Cell Biology International [Wiley]
卷期号:47 (9): 1638-1649 被引量:2
标识
DOI:10.1002/cbin.12060
摘要

Abstract The activation of the nuclear factor‐κB (NF‐κB) pathway has been associated with the development and progression of colorectal cancer (CRC). Parthenolide (PTL), a well‐known inhibitor of the NF‐κB pathway, has emerged as an alternative treatment. However, whether PTL activity is tumor cell‐specific and dependent on the mutational background has not been defined. This study investigated the antitumor role of PTL after tumor necrosis factor‐α (TNF‐α) stimulation in various CRC cell lines with different mutational statuses of TP53 . We observed that CRC cells displayed different patterns of basal p‐IκBα levels; PTL reduced cell viability according to p‐IκBα levels and p‐IκBα levels varied among the cell lines according to the time of TNF‐α stimulation. High concentrations of PTL reduced more effectively p‐IκBα levels than low doses of PTL. However, PTL increased total IκBα levels in Caco‐2 and HT‐29 cells. In addition, PTL treatment downregulated p‐p65 levels in HT‐29 and HCT‐116 cells stimulated by TNF‐α in a dose‐dependent manner. Moreover, PTL induced cell death via apoptosis and reduced the proliferation rate of TNF‐α‐treated HT‐29 cells. Finally, PTL downregulated the messenger RNA levels of interleukin‐1β, a downstream cytokine of NF‐κB, reverted the E‐cadherin‐mediated disorganization of cell–cell contacts, and decreased the invasion of HT‐29 cells. Together, these results suggest a differential antitumoral activity of PTL on CRC cells with different mutational statuses of TP53 , modulating cell death, survival, and proliferation underlying the NF‐κB pathway TNF‐α‐induced. Therefore, PTL has emerged as a potential treatment for CRC in an inflammatory NF‐κB‐dependent manner.
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