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The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Ferroptosis is a lysosomal cell death process

Gao, Huan, Bai, Yuansong, Jia, Yuanyuan, Zhao, Yanan, Kang, Rui, Tang, Daolin, Dai, Enyong·2018·Biochemical and Biophysical Research Communications

Abstract

Ferroptosis is a form of regulated cell death resulting from iron accumulation and lipid peroxidation. While impaired ferroptosis is tightly linked to human diseases and conditions, the mechanism and regulation of ferroptosis remain largely unknown. Here, we demonstrate that STAT3 is a positive regulator of ferroptosis in human pancreatic ductal adenocarcinoma (PDAC) cell lines. Activation of the MAPK/ERK pathway, but not inhibition of system Xc-, was required for STAT3 activation during erastin-induced ferroptosis. Importantly, pharmacological inhibition and genetic silencing of STAT3 through small molecules (e.g., cryptotanshinone and S3I-201) or siRNA blocked erastin-induced ferroptosis in PDAC cells. Mechanically, STAT3-mediated cathepsin B expression was required for ferroptosis. Consequently, inhibition of lysosome-dependent cell death by pharmacological blockade of cathepsin activity (using CA-074Me) or vacuolar type H+-ATPase (using bafilomycin A1) limited erastin-induced ferroptosis. These studies indicate that ferroptosis is a lysosomal cell death process.

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Metadata

Authors
Gao, H., Bai, Y., Jia, Y., Zhao, Y., Kang, R., Tang, D., & Dai, E.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2018-09
Volume
503
Issue
3
Pages
1550-1556
ISSN
0006-291X (ISSN-L)
OpenAlex
W2883276664
Cited by
244
References
11
FWCI
12.85
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Ferroptosis is a lysosomal cell death process. https://app.cochat.ai/papers/10.1016/j.bbrc.2018.07.078
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Gao, H., Bai, Y., Jia, Y., Zhao, Y., Kang, R., Tang, D., & Dai, E. (2018). Ferroptosis is a lysosomal cell death process. Biochemical and Biophysical Research Communications. https://doi.org/10.1016/j.bbrc.2018.07.078

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