Asset Details
Do you wish to reserve the book?
Cinobufagin inhibits M2-like tumor-associated macrophage polarization to attenuate the invasion and migration of lung cancer cells
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Cinobufagin inhibits M2-like tumor-associated macrophage polarization to attenuate the invasion and migration of lung cancer cells
Do you wish to request the book?
Cinobufagin inhibits M2-like tumor-associated macrophage polarization to attenuate the invasion and migration of lung cancer cells
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Cinobufagin inhibits M2-like tumor-associated macrophage polarization to attenuate the invasion and migration of lung cancer cells
2024
Overview
Macrophages have crucial roles in immune responses and tumor progression, exhibiting diverse phenotypes based on environmental cues. In the present study, the impact of cinobufagin (CB) on macrophage polarization and the consequences on tumor-associated behaviors were investigated. Morphological transformations of THP-1 cells into M0, M1 and M2 macrophages were observed, including distinct changes in the size, shape and adherence properties of these cells. CB treatment inhibited the viability of A549 and LLC cells in a concentration-dependent manner, with an IC50 of 28.8 and 30.12 ng/ml, respectively. CB at concentrations of <30 ng/ml had no impact on the viability of M0 macrophages and lung epithelial (BEAS-2B) cells. CB influenced the expression of macrophage surface markers, reducing CD206 positivity in M2 macrophages without affecting CD86 expression in M1 macrophages. CB also altered certain expression profiles at the mRNA level, notably downregulating macrophage receptor with collagenous structure (MARCO) expression in M2 macrophages and upregulating tumor necrosis factor-α and interleukin-1β in both M0 and M1 macrophages. Furthermore, ELISA analyses revealed that CB increased the levels of pro-inflammatory cytokines in M1 macrophages and reduced the levels of anti-inflammatory factors in M2 macrophages. CB treatment also attenuated the migration and invasion capacities of A549 and LLC cells stimulated by M2 macrophage-conditioned medium. Additionally, CB modulated peroxisome proliferator-activated receptor γ (PPARγ) and MARCO expression in M2 macrophages and epithelial-mesenchymal transition in A549 cells, which was partially reversed by rosiglitazone, a PPARγ agonist. Finally, CB and cisplatin treatments hindered tumor growth in vivo, with distinct impacts on animal body weight and macrophage marker expression in tumor tissues. In conclusion, the results of the present study demonstrated that CB exerted complex regulatory effects on macrophage polarization and tumor progression, suggesting its potential as a modulator of the tumor microenvironment and a therapeutic for cancer treatment.
Publisher
D.A. Spandidos,Spandidos Publications,Spandidos Publications UK Ltd
