NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development

Transient receptor potential (TRP) channels, particularly those involved in nociception (nociceptive TRP channels), are implicated in both pain and cancer development. Activation of these channels by diverse stimuli triggers calcium influx, leading to mitochondrial oxidative stress and reactive oxyg...

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Main Authors: Tzu-Yin Chen, Tohru Yoshioka, Wen-Li Hsu
Format: Article
Language:English
Published: IMR Press 2025-03-01
Series:Frontiers in Bioscience-Landmark
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Online Access:https://www.imrpress.com/journal/FBL/30/3/10.31083/FBL31328
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author Tzu-Yin Chen
Tohru Yoshioka
Wen-Li Hsu
author_facet Tzu-Yin Chen
Tohru Yoshioka
Wen-Li Hsu
author_sort Tzu-Yin Chen
collection DOAJ
description Transient receptor potential (TRP) channels, particularly those involved in nociception (nociceptive TRP channels), are implicated in both pain and cancer development. Activation of these channels by diverse stimuli triggers calcium influx, leading to mitochondrial oxidative stress and reactive oxygen species (ROS) accumulation. This ROS production contributes to both nociceptive signaling (causing pain) and aging processes, including genomic instability, a key driver of carcinogenesis. Although a direct causal link between pain and cancer onset remains elusive, the shared involvement of nociceptive TRP channels strongly suggests a correlation. This opinion article proposes targeting the crosstalk between nociceptive TRP channels and ROS as a promising therapeutic strategy to mitigate cancer and cancer-associated pain simultaneously. While further research is needed to definitively establish a causal relationship between pain and cancer risk, the available evidence suggests that inhibiting this pathway may offer significant benefits for both cancer prevention and treatment.
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institution Kabale University
issn 2768-6701
language English
publishDate 2025-03-01
publisher IMR Press
record_format Article
series Frontiers in Bioscience-Landmark
spelling doaj-art-4cd71b618fe7421b8c4e57a89f0760022025-08-20T03:42:25ZengIMR PressFrontiers in Bioscience-Landmark2768-67012025-03-013033132810.31083/FBL31328S2768-6701(25)01657-0NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer DevelopmentTzu-Yin Chen0Tohru Yoshioka1Wen-Li Hsu2National Center for Geriatrics and Welfare Research, National Health Research Institutes, 632007 Yunlin, TaiwanRegenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, 80708 Kaohsiung, TaiwanNational Center for Geriatrics and Welfare Research, National Health Research Institutes, 632007 Yunlin, TaiwanTransient receptor potential (TRP) channels, particularly those involved in nociception (nociceptive TRP channels), are implicated in both pain and cancer development. Activation of these channels by diverse stimuli triggers calcium influx, leading to mitochondrial oxidative stress and reactive oxygen species (ROS) accumulation. This ROS production contributes to both nociceptive signaling (causing pain) and aging processes, including genomic instability, a key driver of carcinogenesis. Although a direct causal link between pain and cancer onset remains elusive, the shared involvement of nociceptive TRP channels strongly suggests a correlation. This opinion article proposes targeting the crosstalk between nociceptive TRP channels and ROS as a promising therapeutic strategy to mitigate cancer and cancer-associated pain simultaneously. While further research is needed to definitively establish a causal relationship between pain and cancer risk, the available evidence suggests that inhibiting this pathway may offer significant benefits for both cancer prevention and treatment.https://www.imrpress.com/journal/FBL/30/3/10.31083/FBL31328nociceptive transient receptor potential channelcancer progressionpainmitochondrial ca2+ overloadros
spellingShingle Tzu-Yin Chen
Tohru Yoshioka
Wen-Li Hsu
NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development
Frontiers in Bioscience-Landmark
nociceptive transient receptor potential channel
cancer progression
pain
mitochondrial ca2+ overload
ros
title NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development
title_full NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development
title_fullStr NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development
title_full_unstemmed NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development
title_short NO Pain! No Cancer? The Crosstalk Between Nociception, ROS, and Cancer Development
title_sort no pain no cancer the crosstalk between nociception ros and cancer development
topic nociceptive transient receptor potential channel
cancer progression
pain
mitochondrial ca2+ overload
ros
url https://www.imrpress.com/journal/FBL/30/3/10.31083/FBL31328
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AT wenlihsu nopainnocancerthecrosstalkbetweennociceptionrosandcancerdevelopment