CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

Xu, Chengfei; Zhao, Baoxia; Xu, Long; Wang, Yahui; Liu, Beibei; Xu, Miao; He, Qing; Ni, Chaobo; Fu, Jie; Kong, Min; Lin, Xiao; Ni, Huadong; Yao, Ming

doi:10.1177/17448069221135743

Cited by 9 publications

(2 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The rats were allowed to acclimatize to the experimental environment for 2 days before the commencement of the study. Consistent with previous investigations, 48 , 49 , 50 the rats were anesthetized using 5 mg/mL sodium pentobarbital. All animal experiments were conducted within the time frame of 8:00 am to 8:00 pm .…”

Section: Methodsmentioning

confidence: 81%

N4-acetylcytidine acetylation of neurexin 2 in the spinal dorsal horn regulates hypersensitivity in a rat model of cancer-induced bone pain

Xu,

Zheng,

Chen

et al. 2024

Molecular Therapy - Nucleic Acids

Self Cite

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 81%

N4-acetylcytidine acetylation of neurexin 2 in the spinal dorsal horn regulates hypersensitivity in a rat model of cancer-induced bone pain

Xu,

Zheng,

Chen

et al. 2024

Molecular Therapy - Nucleic Acids

Self Cite

View full text Add to dashboard Cite

“…The role of CXCR1 in the processes of nociception remains unclear; however, recently, it was proven that this receptor is expressed by spinal cord neurons and upregulated during the development of bone cancer pain [148]. CXCR1 has four ligands: CXCL5, CXCL6, CXCL7, and CXCL8.…”

Section: Chemokines In Neuropathic Painmentioning

confidence: 99%

Targeting Members of the Chemokine Family as a Novel Approach to Treating Neuropathic Pain

Pawlik

Mika

2023

Molecules

View full text Add to dashboard Cite

Neuropathic pain is a debilitating condition that affects millions of people worldwide. Numerous studies indicate that this type of pain is a chronic condition with a complex mechanism that tends to worsen over time, leading to a significant deterioration in patients’ quality of life and issues like depression, disability, and disturbed sleep. Presently used analgesics are not effective enough in neuropathy treatment and may cause many side effects due to the high doses needed. In recent years, many researchers have pointed to the important role of chemokines not only in the development and maintenance of neuropathy but also in the effectiveness of analgesic drugs. Currently, approximately 50 chemokines are known to act through 20 different seven-transmembrane G-protein-coupled receptors located on the surface of neuronal, glial, and immune cells. Data from recent years clearly indicate that more chemokines than initially thought (CCL1/2/3/5/7/8/9/11, CXCL3/9/10/12/13/14/17; XCL1, CX3CL1) have pronociceptive properties; therefore, blocking their action by using neutralizing antibodies, inhibiting their synthesis, or blocking their receptors brings neuropathic pain relief. Several of them (CCL1/2/3/7/9/XCL1) have been shown to be able to reduce opioid drug effectiveness in neuropathy, and neutralizing antibodies against them can restore morphine and/or buprenorphine analgesia. The latest research provides irrefutable evidence that chemokine receptors are promising targets for pharmacotherapy; chemokine receptor antagonists can relieve pain of different etiologies, and most of them are able to enhance opioid analgesia, for example, the blockade of CCR1 (J113863), CCR2 (RS504393), CCR3 (SB328437), CCR4 (C021), CCR5 (maraviroc/AZD5672/TAK-220), CXCR2 (NVPCXCR220/SB225002), CXCR3 (NBI-74330/AMG487), CXCR4 (AMD3100/AMD3465), and XCR1 (vMIP-II). Recent research has shown that multitarget antagonists of chemokine receptors, such as CCR2/5 (cenicriviroc), CXCR1/2 (reparixin), and CCR2/CCR5/CCR8 (RAP-103), are also very effective painkillers. A multidirectional strategy based on the modulation of neuronal–glial–immune interactions by changing the activity of the chemokine family can significantly improve the quality of life of patients suffering from neuropathic pain. However, members of the chemokine family are still underestimated pharmacological targets for pain treatment. In this article, we review the literature and provide new insights into the role of chemokines and their receptors in neuropathic pain.

show abstract

ALKBH5 modulates bone cancer pain in a rat model by suppressing NR2B expression

Song,

Cao,

Yang

et al. 2024

Biotech and App Biochem

View full text Add to dashboard Cite

Currently, the clinical treatment of bone cancer pain (BCP) is mainly related to its pathogenesis. The aim of the present study was to elucidate the potential role of N6‐methyladenosine (m6A) in BCP in the spinal cord dorsal root ganglia (DRG) of BCP rats and its specific regulatory mechanism in N‐methyl‐d‐aspartate receptor subunit 2B (NR2B). A rat model of BCP was constructed by tibial injection of Walker256 cells, and ALKBH5 and NR2B expression in the spinal cord DRG was detected. ALKBH5 was silenced or overexpressed in PC12 cells to verify the regulatory effect of ALKBH5 on NR2B. The specific mechanism underlying the interaction between ALKBH5 and NR2B was investigated using methylated RNA immunoprecipitation and dual‐luciferase reporter gene assays. The results showed increased expression of m6A, decreased expression of ALKBH5, and increased expression of NR2B in the DRG of the BCP rat model. Overexpression of ALKBH5 inhibited NR2B expression, whereas interference with ALKBH5 caused an increase in NR2B expression. In NR2B, interference with ALKBH5 caused an increase in m6A modification, which caused an increase in NR2B. Taken together, ALKBH5 affected the expression of NR2B by influencing the stability of the m6A modification site of central NR2B, revealing that ALKBH5 is a therapeutic target for BCP.

show abstract

CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

Cited by 9 publications

References 45 publications

N4-acetylcytidine acetylation of neurexin 2 in the spinal dorsal horn regulates hypersensitivity in a rat model of cancer-induced bone pain

N4-acetylcytidine acetylation of neurexin 2 in the spinal dorsal horn regulates hypersensitivity in a rat model of cancer-induced bone pain

Targeting Members of the Chemokine Family as a Novel Approach to Treating Neuropathic Pain

ALKBH5 modulates bone cancer pain in a rat model by suppressing NR2B expression

Contact Info

Product

Resources

About