Serum albumin exposure enhances cell invasiveness and paclitaxel resistance in human neuroblastoma cells, with attenuation by valeriana-type iridoid glycosides.
Ajay UpretyTrung Huy NgoSanjaya PrajapatiShambhu JoshiJoo-Won NamSoo Young KimPublished in: FASEB journal : official publication of the Federation of American Societies for Experimental Biology (2024)
Neuroblastoma, a prevalent extracranial solid tumor in children, arises from undifferentiated nerve cells. While tumor vasculature, often characterized by increased permeability, influences metastasis and recurrence, the direct impact of blood-borne molecules on tumor progression remains unclear. In the present study, we focused on the effect of exposure to albumin, one of the most abundant proteins in the serum, on human neuroblastoma cells. Albumin exposure elevated oxidative stress and led to mitochondria dysfunction via the activation of TGFβ and PI3K pathways, accompanied by an increase in the metastatic and invasive properties of neuroblastoma cells. Proteins relevant to the induction of autophagy were upregulated in response to prolonged albumin exposure. Additionally, pre-exposure to albumin before treatment resulted in increased resistance to paclitaxel. Two valeriana-type iridoid glycosides, patrisophoroside and patrinalloside, recently isolated from Nardostachys jatamansi significantly mitigated the effect of albumin on oxidative stress, cell invasiveness, and chemoresistance. These findings illuminate the potential role of blood-borne molecules, such as albumin, in the progression and metastasis of neuroblastoma, as well as the possible therapeutic implications of valeriana-type iridoid glycosides in anti-cancer treatment.
Keyphrases
- induced apoptosis
- oxidative stress
- cell cycle arrest
- endoplasmic reticulum stress
- endothelial cells
- cell death
- signaling pathway
- small cell lung cancer
- squamous cell carcinoma
- stem cells
- young adults
- dna damage
- single cell
- cell therapy
- pi k akt
- mesenchymal stem cells
- poor prognosis
- heat stress
- middle cerebral artery
- internal carotid artery
- reactive oxygen species
- replacement therapy