ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Corticotropin-releasing factor mediates bone cancer induced pain through neuronal activation in rat spinal cord.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Long noncoding RNA NONRATT007487.2 drives cancer-induced bone pain progression through direct interaction with CXCL1.The Korean journal of pain · 2025Article
- The relationship between chronic pain and health-related quality of life: the mediating roles of frailty and depression in chronic disease patients.Frontiers in public health · 2025Article
- Modulation of Rat Cancer-Induced Bone Pain is Independent of Spinal Microglia Activity.Cancers · 2020Article
- Small-Conductance CaFrontiers in pharmacology · 2020Article
- Whole-Brain Mapping of Monosynaptic Afferent Inputs to Cortical CRH Neurons.Frontiers in neuroscience · 2019Article
- Article
- Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats.Neuroscience bulletin · 2017Article
- Article
- The Walker 256 Breast Cancer Cell- Induced Bone Pain Model in Rats.Frontiers in pharmacology · 2016Review
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7 authors at 1 institution in 1 country.
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Abstract
Corticotropin-releasing factor (CRF) serves as a neuromodulator in the hypothalamic-pituitary-adrenal axis, playing an essential role in depression, anxiety, and pain regulation. However, its biological role in bone cancer induced pain has not been investigated. In the present study, we aimed to elucidate the expression and distribution of CRF in spinal cord using a rodent model of bone cancer pain. Our study showed that implantation of Walker 256 mammary gland carcinoma cells into the tibia of rats significantly increased CRF expression in the spinal cord in a time-dependent manner. The upregulated expression of CRF mainly expressed in the superficial dorsal horn of spinal cord. Moreover, immunofluorescence double staining showed that CRF was extensively colocalized with neurons, but hardly with astrocytes or microglia. In addition, intrathecal injection of CRF receptor antagonist (α-helical-CRF) significantly inhibited heat hyperalgesia, mechanical allodynia, and the expression of c-Fos in spinal dorsal horn of bone cancer pain rats. In summary, our study demonstrates that CRF plays an important role in the development and maintenance of bone cancer pain via activation of neurons.
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