Bladder cancer cells prevent cisplatin-induced oxidative stress by upregulating Nestin1 expression.

ABSTRACT:

Objective

Redox adaptation plays a critical role in cancer cells' drug tolerance and sensitivity. The antioxidative response is induced by nuclear factor erythroid 2-related factor 2 (Nrf2), which triggers the transcriptional activation of genes related to chemosensitivity, glutathione synthesis, and cell protection. Although Nestin1 is known to regulate cellular redox homeostasis by regulating Nrf2 in lung cancer cells, its regulatory effect on the antioxidative state of bladder cancer (BC) cells remains unclear.

Methods

The oxidative stress levels in two cisplatin-treated BC cell lines (T24 and J82) were examined using 2',7'-dichlorofluorescin diacetate staining and real-time quantitative reverse transcription-PCR (RT-qPCR) assays. The cell viability, growth, and apoptosis

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC8581882 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature