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Cited by 1,042

The DOI matches its Crossref record; 147 of the 147 references it cites were found in a registry or an index.

Apoptosis, autophagy, necroptosis, and cancer metastasis

Open access
Su, Zhenyi, Yang, Zuozhang, Xu, Yongqing, Chen, Yongbin, Yu, Qiang·2015·Molecular Cancer

Abstract

Metastasis is a crucial hallmark of cancer progression, which involves numerous factors including the degradation of the extracellular matrix (ECM), the epithelial-to-mesenchymal transition (EMT), tumor angiogenesis, the development of an inflammatory tumor microenvironment, and defects in programmed cell death. Programmed cell death, such as apoptosis, autophagy, and necroptosis, plays crucial roles in metastatic processes. Malignant tumor cells must overcome these various forms of cell death to metastasize. This review summarizes the recent advances in the understanding of the mechanisms by which key regulators of apoptosis, autophagy, and necroptosis participate in cancer metastasis and discusses the crosstalk between apoptosis, autophagy, and necroptosis involved in the regulation of cancer metastasis.

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Crossref · 10.1186/s12943-015-0321-5

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Metadata

Authors
Su, Z., Yang, Z., Xu, Y., Chen, Y., & Yu, Q.
Venue
Molecular Cancer
Published
2015-02-21
Volume
14
Issue
1
Pages
48-48
ISSN
1476-4598 (ISSN-L)
OpenAlex
W2166616170
Cited by
1,042
References
147
FWCI
23.93
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Apoptosis, autophagy, necroptosis, and cancer metastasis. https://app.cochat.ai/papers/10.1186/s12943-015-0321-5
The paper
Su, Z., Yang, Z., Xu, Y., Chen, Y., & Yu, Q. (2015). Apoptosis, autophagy, necroptosis, and cancer metastasis. Molecular Cancer. https://doi.org/10.1186/s12943-015-0321-5

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.