Apoptotic sphingolipid ceramide in cancer therapy

Wei Ching Huang, Chia Ling Chen, Yee Shin Lin, Chiou-Feng Lin

Research output: Contribution to journalReview article

Abstract

Apoptosis, also called programmed cell death, is physiologically and pathologically involved in cellular homeostasis. Escape of apoptotic signaling is a critical strategy commonly used for cancer tumorigenesis. Ceramide, a derivative of sphingolipid breakdown products, acts as second messenger for multiple extracellular stimuli including growth factors, chemical agents, and environmental stresses, such as hypoxia, and heat stress as well as irradiation. Also, ceramide acts as tumor-suppressor lipid because a variety of stress stimuli cause apoptosis by increasing intracellular ceramide to initiate apoptotic signaling. Defects on ceramide generation and sphingolipid metabolism are developed for cancer cell survival and cancer therapy resistance. Alternatively, targeting ceramide metabolism to correct these defects might provide opportunities to overcome cancer therapy resistance.
Original languageEnglish
JournalJournal of Lipids
Publication statusPublished - 2011
Externally publishedYes

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Sphingolipids
Ceramides
Neoplasms
Apoptosis
Therapeutics
Second Messenger Systems
Cell Survival
Intercellular Signaling Peptides and Proteins
Carcinogenesis
Homeostasis
Cell Death
Hot Temperature
Lipids

Cite this

Apoptotic sphingolipid ceramide in cancer therapy. / Huang, Wei Ching; Chen, Chia Ling; Lin, Yee Shin; Lin, Chiou-Feng.

In: Journal of Lipids, 2011.

Research output: Contribution to journalReview article

Huang, Wei Ching ; Chen, Chia Ling ; Lin, Yee Shin ; Lin, Chiou-Feng. / Apoptotic sphingolipid ceramide in cancer therapy. In: Journal of Lipids. 2011.
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AB - Apoptosis, also called programmed cell death, is physiologically and pathologically involved in cellular homeostasis. Escape of apoptotic signaling is a critical strategy commonly used for cancer tumorigenesis. Ceramide, a derivative of sphingolipid breakdown products, acts as second messenger for multiple extracellular stimuli including growth factors, chemical agents, and environmental stresses, such as hypoxia, and heat stress as well as irradiation. Also, ceramide acts as tumor-suppressor lipid because a variety of stress stimuli cause apoptosis by increasing intracellular ceramide to initiate apoptotic signaling. Defects on ceramide generation and sphingolipid metabolism are developed for cancer cell survival and cancer therapy resistance. Alternatively, targeting ceramide metabolism to correct these defects might provide opportunities to overcome cancer therapy resistance.

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