The nonreceptor protein tyrosine kinase Src participates in every step of cancer-induced bone pain

Li, Yaoyuan; Bao, Yanju; Zheng, Hongliang; Qin, Yinggang; Bai, Hua

doi:10.1016/j.biopha.2021.111822

Cited by 7 publications

(3 citation statements)

References 128 publications

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“…Src and Fyn are Evidence-Based Complementary and Alternative Medicine members of the Src family kinases of nonreceptor tyrosine kinases, mediating diferent intracellular signaling pathways. Src family kinases have been identifed as important in terms of progression, invasion, metastasis, bone pain, and drug resistance in human cancer, including NSCLC [24][25][26]. Src and Fyn are activators of PI3K and can mediate the PI3K/ AKT/mTOR pathway [27].…”

Section: Discussionmentioning

confidence: 99%

A Mechanism Exploration for the Yi‐Fei‐San‐Jie Formula against Non‐Small‐Cell Lung Cancer Based on UPLC‐MS/MS, Network Pharmacology, and In Silico Verification

Mo³

et al. 2023

Evidence-Based Complementary and Alternative Medicine

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Non-small-cell lung cancer (NSCLC) is one of the most prevalent cancers worldwide. A Yi-Fei-San-Jie formula (YFSJF), widely used in NSCLC treatment in south China, has been validated in clinical studies. However, the pharmacological mechanism behind it remains unclear. In this study, 73 compounds were identified using ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), with 58 enrolled in network pharmacology. The protein-protein interaction network, functional enrichment analysis, and compound-target-pathway network were constructed using 74 overlapping targets from 58 drugs and NSCLC. YFSJF has many targets and pathways in the fight against NSCLC. PIK3R1, PIK3CA, and AKT1 were identified as key targets, and the PI3K/AKT pathway was identified as the key pathway. According to the Human Protein Atlas (THPA) database and the Kaplan–Meier Online website, the three key targets had varying expression levels in normal and abnormal tissues and were linked to prognosis. Molecular docking and dynamics simulations verified that hub compounds have a strong affinity with three critical targets. This study revealed multiple compounds, targets, and pathways for YFSJF against NSCLC and suggested that YFSJF might inhibit PIK3R1, PIK3CA, and AKT1 to suppress the PI3K/AKT pathway and play its pharmacological role.

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Section: Discussionmentioning

confidence: 99%

A Mechanism Exploration for the Yi‐Fei‐San‐Jie Formula against Non‐Small‐Cell Lung Cancer Based on UPLC‐MS/MS, Network Pharmacology, and In Silico Verification

Mo³

et al. 2023

Evidence-Based Complementary and Alternative Medicine

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“…Glial cells located near the periaqueductal gray matter (PAG) of the midbrain are also activated in tumor-bearing mice, and a several cytokines such as IL-1 and IL-6 are secreted to activate the PI3K-AKT pathway in PAG, leading to central sensitization and cancer pain. Blocking this signal pathway can reduce mechanical and thermal hyperalgesia in rats with bone cancer ( 44 ).…”

Section: Mechanism Of Cibpmentioning

confidence: 99%

Management of pain in patients with bone metastases

Jing

Zhao

et al. 2023

Front. Oncol.

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Cancer-induced bone pain (CIBP) has a considerable impact on patients’ quality of life as well as physical and mental health. At present, patients with CIBP are managed according to the three-step analgesic therapy algorithm proposed by the World Health Organization. Opioids are commonly used as the first-line treatment for moderate-to-severe cancer pain but are limited due to addiction, nausea, vomiting and other gastrointestinal side effects. Moreover, opioids have a limited analgesic effect in some patients. In order to optimize the management of CIBP, we must first identify the underlying mechanisms. In some patients, surgery, or surgery combined with radiotherapy or radiofrequency ablation is the first step in the management of CIBP. Various clinical studies have shown that anti-nerve growth factor (NGF) antibodies, bisphosphonates, or RANKL inhibitors can reduce the incidence and improve the management of cancer pain. Herein, we review the mechanisms of cancer pain and potential therapeutic strategies to provide insights for optimizing the management of CIBP.

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“…Up to 75% of patients with bone metastasis tumors have moderate to severe pain, which has a serious impact on the patients’ mood and quality of life [ 2 ] . Cancer-induced bone pain (CIBP) is a complicated pain condition consisting of basal, spontaneous, or exercise-induced pain [ 3 , 4 ]. Clinically available drug treatment options for CIBP are limited by their inability to sufficiently relieve pain or their intolerable side effects [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Nav1.6 Mediated by the p38 MAPK Pathway in the Dorsal Root Ganglia Contributes to Cancer-Induced Bone Pain in Rats

Lin

Chen

et al. 2022

Cells

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Cancer-induced bone pain (CIBP) occurs frequently among advanced cancer patients. Voltage-gated sodium channels (VGSCs) have been associated with chronic pain, but how VGSCs function in CIBP is poorly understood. Here, we aimed to investigate the specific role of VGSCs in the dorsal root ganglia (DRGs) in CIBP. A CIBP rat model was generated by the intratibial inoculation of MRMT-1 breast carcinoma cells. Transcriptome sequencing was conducted to assess the gene expression profiles. The expression levels of key genes and differentiated genes related to activated pathways were measured by Western blotting and qPCR. We implanted a catheter intrathecally for the administration of lentivirus and drugs. Then, the changes in the mechanical withdrawal threshold (MWT) were measured. We identified 149 differentially expressed mRNAs (DEmRNAs) in the DRGs of CIBP model rats. The expression of Nav1.6, which was among these DEmRNAs, was significantly upregulated. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the DEmRNAs showed that they were mainly enriched in the mitogen-activated protein kinase (MAPK) pathway. The decrease in MWT induced by bone cancer was attenuated by Nav1.6 knockdown. Western blot analysis revealed that a p38 inhibitor decreased the expression of Nav1.6 and attenuated pain behavior. Our study shows that the upregulation of Nav1.6 expression by p38 MAPK in the DRGs of rats contributes to CIBP.

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The nonreceptor protein tyrosine kinase Src participates in every step of cancer-induced bone pain

Cited by 7 publications

References 128 publications

A Mechanism Exploration for the Yi‐Fei‐San‐Jie Formula against Non‐Small‐Cell Lung Cancer Based on UPLC‐MS/MS, Network Pharmacology, and In Silico Verification

A Mechanism Exploration for the Yi‐Fei‐San‐Jie Formula against Non‐Small‐Cell Lung Cancer Based on UPLC‐MS/MS, Network Pharmacology, and In Silico Verification

Management of pain in patients with bone metastases

Upregulation of Nav1.6 Mediated by the p38 MAPK Pathway in the Dorsal Root Ganglia Contributes to Cancer-Induced Bone Pain in Rats

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