Inhibition of the FEN1-PBX1 axis elicits cellular senescence in breast cancer via the increased intracellular reactive oxygen species levels.

Background: Cellular senescence is a state of irreversible cell growth arrest. As such, senescence induction is viewed as an efficacious countermeasure in cancer treatment. Flap endonuclease 1 (FEN1) has been reported to participate in tumor growth, metastasis and immunomodulation.

Cobalt carbonate nanorods enhance chemotherapy via neutralization of acidic tumor microenvironment and generation of carbonate radical anions for necrosis.

One of the hallmarks of cancer is the acidic extracellular space surrounding the tumor, which is linked to metabolic reprogramming and the use of glycolysis. Additionally, the acidic tumor microenvironment (TME) establishes a physiological barrier called "ion trapping" and significantly lowers the ability of cells to absorb weak-base chemotherapy agents. Although CO containing agents and nanoformulations could effectively neutralize the tumor acidity, the CO based therapeutic effect was insufficiently investigated.

The endonuclease FEN1 mediates activation of STAT3 and facilitates proliferation and metastasis in breast cancer.

Background: The metastasis accounts for most deaths from breast cancer (BRCA). Understanding the molecular mechanisms of BRCA metastasis is urgently demanded. Flap Endonuclease 1 (FEN1), a pivotal factor in DNA metabolic pathways, contributes to tumor growth and drug resistance, however, little is known about the role of FEN1 in BRCA metastasis.