ArticleMolecular pain2011
Cancer-induced bone pain sequentially activates the ERK/MAPK pathway in different cell types in the rat spinal cord.
Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- Bone metastasis and pain research through the dual lens of bibliometrics and bioinformatics: knowledge structure, frontiers, and core pathway analysis (2015-2024).Frontiers in medicine · 2025Pooled it
- A systematic review and meta-analysis on the use of traditional Chinese medicine compound kushen injection for bone cancer pain.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2014Pooled it
- Cancer pain: molecular mechanisms and management.Molecular biomedicine · 2025Review
- Discovery of a CCR2-targeting pepducin therapy for chronic pain.Pharmacological research · 2024Article
- Evaluation of pain related behaviors and disease related outcomes in an immunocompetent mouse model of prostate cancer induced bone pain.Journal of bone oncology · 2023Article
- Knockdown of PAR2 alleviates cancer-induced bone pain by inhibiting the activation of astrocytes and the ERK pathway.BMC musculoskeletal disorders · 2022Article
- Spinal Nrf2 translocation may inhibit neuronal NF-κB activation and alleviate allodynia in a rat model of bone cancer pain.Journal of neurochemistry · 2021Article
- Evidence of the Involvement of Spinal EZH2 in the Development of Bone Cancer Pain in Rats.Journal of pain research · 2021Article
- Modulation of Rat Cancer-Induced Bone Pain is Independent of Spinal Microglia Activity.Cancers · 2020Article
- Liquiritin Alleviates Pain Through Inhibiting CXCL1/CXCR2 Signaling Pathway in Bone Cancer Pain Rat.Frontiers in pharmacology · 2020Article
- Transcriptional Regulation of Voltage-Gated Sodium Channels Contributes to GM-CSF-Induced Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- microRNA-329 reduces bone cancer pain through the LPAR1-dependent LPAR1/ERK signal transduction pathway in mice.Therapeutic advances in medical oncology · 2019Article
- The Somatostatin Receptor-4 Agonist J-2156 Alleviates Mechanical Hypersensitivity in a Rat Model of Breast Cancer Induced Bone Pain.Frontiers in pharmacology · 2018Article
- Anti-rheumatic drug iguratimod protects against cancer-induced bone pain and bone destruction in a rat model.Oncology letters · 2017Article
- Molecular signaling underlying bulleyaconitine A (BAA)-induced microglial expression of prodynorphin.Scientific reports · 2017Article
- Monocyte chemoattractant protein-1 contributes to morphine tolerance in rats with cancer-induced bone pain.Experimental and therapeutic medicine · 2017Article
- P2YJournal of pain research · 2017Article
- Glial contributions to visceral pain: implications for disease etiology and the female predominance of persistent pain.Translational psychiatry · 2016Review
- Interleukin-17A Acts to Maintain Neuropathic Pain Through Activation of CaMKII/CREB Signaling in Spinal Neurons.Molecular neurobiology · 2016Article
- Analgesic effect and possible mechanism of SCH772984 intrathecal injection on rats with bone cancer pain.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies have demonstrates that, after nerve injury, extracellular signal-regulated protein kinase (ERK) activation in the spinal cord-initially in neurons, then microglia, and finally astrocytes. In addition, phosphorylation of ERK (p-ERK) contributes to nociceptive responses following inflammation and/or nerve injury. However, the role of spinal cells and the ERK/MAPK pathway in cancer-induced bone pain (CIBP) remains poorly understood. The present study analyzed activation of spinal cells and the ERK/MAPK pathway in a rat model of bone cancer pain.
resultsA Sprague Dawley rat model of bone cancer pain was established and the model was evaluated by a series of tests. Moreover, fluorocitrate (reversible glial metabolic inhibitor) and U0126 (a MEK inhibitor) was administered intrathecally. Western blots and double immunofluorescence were used to detect the expression and location of phosphorylation of ERK (p-ERK). Our studies on pain behavior show that the time between day 6 and day 18 is a reasonable period ("time window" as the remaining stages) to investigate bone cancer pain mechanisms and to research analgesic drugs. Double-labeling immunofluorescence revealed that p-ERK was sequentially expressed in neurons, microglia, and astrocytes in the L4-5 superficial spinal cord following inoculation of Walker 256 cells. Phosphorylation of ERK (p-ERK) and the transcription factor cAMP response element-binding protein (p-CREB) increased in the spinal cord of CIBP rats, which was attenuated by intrathecal injection of fluorocitrate or U0126.
conclusionsThe ERK inhibitors could have a useful role in CIBP management, because the same target is expressed in various cells at different times.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.