Iscador Qu inhibits doxorubicin-induced senescence of MCF7 cells.
Tatjana Srdic-RajicJuan F SantibañezKsenija KanjerNevena Tisma-MileticMilena CavicDaniel GalunMarko JevricNevena KardumAleksandra Konic-RisticTamara Zoranovic PryjdaPublished in: Scientific reports (2017)
Chemotherapy in patients with inoperable or advanced breast cancer inevitably results in low-dose exposure of tumor-cell subset and senescence. Metabolically active senescent cells secrete multiple tumor promoting factors making their elimination a therapeutic priority. Viscum album is one of the most widely used alternative anti-cancer medicines facilitating chemotherapy tolerance of breast cancer patients. The aim of this study was to model and investigate how Viscum album extracts execute additive anti-tumor activity with low-dose Dox using ER + MCF7 breast cancer cells. We report that cotreatment of MCF7 with Viscum album and Dox abrogates G2/M cycle arrest replacing senescence with intrinsic apoptotic program. Mechanistically, this switch was associated with down-regulation of p21, p53/p73 as well as Erk1/2 and p38 activation. Our findings, therefore, identify a novel mechanistic axis of additive antitumor activity of Viscum album and low dose-Dox. In conclusion, ER + breast cancer patients may benefit from addition of Viscum album to low-dose Dox chemotherapy due to suppression of cancer cell senescence and induction of apoptosis.
Keyphrases
- low dose
- breast cancer cells
- cell cycle arrest
- induced apoptosis
- cell death
- high dose
- endothelial cells
- dna damage
- locally advanced
- pi k akt
- stress induced
- endoplasmic reticulum stress
- oxidative stress
- signaling pathway
- high glucose
- drug delivery
- single cell
- squamous cell carcinoma
- quality improvement
- cell proliferation
- cell therapy
- mesenchymal stem cells
- drug induced
- estrogen receptor
- cancer therapy
- cell cycle
- bone marrow