Peroxiredoxin I and II as novel therapeutic molecular targets in cervical cancer treatment through regulation of endoplasmic reticulum stress induced by bleomycin.
Lian-Hui WeiDa-Yu MaXiao-Yu GuoYing-Ying HaoMei-Hua JinYing-Hao HanXun JinTaeho KwonPublished in: Cell death discovery (2024)
Cervical cancer, significantly affecting women worldwide, often involves treatment with bleomycin, an anticancer agent targeting breast, ovarian, and cervical cancers by generating reactive oxygen species (ROS) to induce cancer cell death. The Peroxiredoxin (PRDX) family, particularly PRDX1 and 2, plays a vital role in maintaining cellular balance by scavenging ROS, thus mitigating the damaging effects of bleomycin-induced mitochondrial and cellular oxidative stress. This process reduces endoplasmic reticulum (ER) stress and prevents cell apoptosis. However, reducing PRDX1 and 2 levels reverses their protective effect, increasing apoptosis. This research highlights the importance of PRDX1 and 2 in cervical cancer treatments with bleomycin, showing their potential to enhance treatment efficacy by managing ROS and ER stress and suggesting a therapeutic strategy for improving outcomes in cervical cancer treatment.
Keyphrases
- cell death
- endoplasmic reticulum stress
- reactive oxygen species
- oxidative stress
- pulmonary fibrosis
- dna damage
- induced apoptosis
- endoplasmic reticulum
- cell cycle arrest
- diabetic rats
- type diabetes
- squamous cell carcinoma
- cell proliferation
- combination therapy
- polycystic ovary syndrome
- skeletal muscle
- young adults
- insulin resistance
- high glucose
- childhood cancer
- drug induced
- squamous cell
- heat shock protein
- weight loss
- breast cancer risk