Abstract
As a central cellular program to sense and transduce stress signals, the integrated stress response (ISR) pathway has been implicated in cancer initiation and progression. Depending on the genetic mutation landscape, cellular context, and differentiation states, there are emerging pieces of evidence showing that blockage of the ISR can selectively and effectively shift the balance of cancer cells toward apoptosis, rendering the ISR a promising target in cancer therapy. Going beyond its pro-survival functions, the ISR can also influence metastasis, especially via proteostasis-independent mechanisms. In particular, ISR can modulate metastasis via transcriptional reprogramming, in the help of essential transcription factors. In this review, we summarized the current understandings of ISR in cancer metastasis from the perspective of transcriptional regulation.
Highlights
Transcriptional Control of Metastasis by Integrated Stress Response SignalingSi Lu1,2†, Li-Xian Yang1,2†, Zi-Jian Cao1,2†, Jiang-Sha Zhao1,2*, Jia You3* and Yu-Xiong Feng1,2*
Development of secondary lesions in organs or tissues that are physically disconnected with the original primary cancer is termed metastasis
Over a million cancer cells can be released by the primary lesion into the circulation every day, but only a very minor portion of them is capable of colonizing a distant organ, even fewer can flourish into clinical detectable macro-metastasis [25]
Summary
Si Lu1,2†, Li-Xian Yang1,2†, Zi-Jian Cao1,2†, Jiang-Sha Zhao1,2*, Jia You3* and Yu-Xiong Feng1,2*. Edited by: Wenbo Li, University of Texas Health Science Center at Houston, United States. Reviewed by: Shanshan Pang, Chongqing University, China Zhijie Jason Liu, The University of Texas Health Science Center at San Antonio, United States. Specialty section: This article was submitted to Cancer Genetics, a section of the journal
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