A positive feedback loop of heparanase/ syndecan1/nerve growth factor regulates cancer pain progression
1
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
Background: The purpose of this research was to assess the role of heparanase (HPSE)/syndecan1 (SDC1)/nerve growth factor (NGF) on cancer pain from melanoma. Methods: The influence of HPSE on the biological function of melanoma cells and cancer pain in a mouse model was evaluated. Immunohistochemical staining was used to analyze HPSE and SDC1. HPSE, NGF, and SDC1 were detected using western blot. Inflammatory factors were detected using ELISA assay. Results: HPSE promoted melanoma cell viability, proliferation, migration, invasion, and tumor growth, as well as cancer pain, while SST0001 treatment reversed the promoting effect of HPSE. HPSE up-regulated NGF, and NGF feedback promoted HPSE. High expression of NGF reversed the inhibitory effect of HPSE down-regulation on melanoma cell phenotype deterioration, including cell viability, proliferation, migration, and invasion. SST0001 down-regulated SDC1 expression. SDC1 reversed the inhibitory effect of SST0001 on cancer pain. Conclusions: The results showed that HPSE promoted melanoma development and cancer pain by interacting with NGF/SDC1. It provides new insights to better understand the role of HPSE in melanoma and also provides a new direction for cancer pain treatment.
Abstract
Background: The purpose of this research was to assess the role of heparanase (HPSE)/syndecan1 (SDC1)/nerve growth factor (NGF) on cancer pain from melanoma. Methods: The influence of HPSE on the biological function of melanoma cells and cancer pain in a mouse model was evaluated. Immunohistochemical staining was used to analyze HPSE and SDC1. HPSE, NGF, and SDC1 were detected using western blot. Inflammatory factors were detected using ELISA assay. Results: HPSE promoted melanoma cell viability, proliferation, migration, invasion, and tumor growth, as well as cancer pain, while SST0001 treatment reversed the promoting effect of HPSE. HPSE up-regulated NGF, and NGF feedback promoted HPSE. High expression of NGF reversed the inhibitory effect of HPSE down-regulation on melanoma cell phenotype deterioration, including cell viability, proliferation, migration, and invasion. SST0001 down-regulated SDC1 expression. SDC1 reversed the inhibitory effect of SST0001 on cancer pain. Conclusions: The results showed that HPSE promoted melanoma development and cancer pain by interacting with NGF/SDC1. It provides new insights to better understand the role of HPSE in melanoma and also provides a new direction for cancer pain treatment.
참고문헌 (40)
- Neufeld NJ, "Cancer pain : a review of epidemiology, clinical quality and value impact", Future Oncol, 13, pp.833~841 (2017)
- Lovell M, "Australian survey of current practice and guideline use in adult cancer pain assessment and management : perspectives of palliative care physicians", J Palliat Med, 16, pp.1403~1409 (2013)
- Magee D, "Cancer pain: where are we now?", Pain Manag, 9, pp.63~79 (2019)
- Sanderson RD, "Heparanase regulation of cancer, autophagy and inflammation : new mechanisms and targets for therapy", FEBS J, 284, pp.42~55 (2017)
- Rivara S, "Heparanase : a rainbow pharmacological target associated to multiple pathologies including rare diseases", Future Med Chem, 8, pp.647~680 (2016)
- Doweck I, "Opposing effects of heparanase and heparanase-2 in head & neck cancer", Adv Exp Med Biol, 1221, pp.847~856 (2020)
- Hermano E, "Heparanase accelerates obesity-associated breast cancer progression", Cancer Res, 79, pp.5342~5354 (2019)
- Heyman B, "Mechanisms of heparanase inhibitors in cancer therapy", Exp Hematol, 44, pp.1002~1012 (2016)
- Jiang X, "Inhibition of triple-negative breast cancer tumor growth by electroacupuncture with encircled needling and its mechanisms in a mice xenograft model", Int J Med Sci, 16, pp.1642~1651 (2019)
- Demir IE, "Nerve growth factor & TrkA as novel therapeutic targets in cancer", Biochim Biophys Acta, 1866, pp.37~50 (2016)
- Wang W, "The role of nerve growth factor and its receptors in tumorigenesis and cancer pain", Biosci Trends, 8, pp.68~74 (2014)
- Di Donato M, "Nerve growth factor induces proliferation and aggressiveness in prostate cancer cells", Cancers(Basel), 11, pp.784~ (2019)
- Hayakawa Y, "Nerve growth factor promotes gastric tumorigenesis through aberrant cholinergic signaling", Cancer Cell, 31, pp.21~34 (2017)
- Han L, "Sonic hedgehog signaling pathway promotes pancreatic cancer pain via nerve growth factor", Reg Anesth Pain Med, 45, pp.137~144 (2020)
- Teixeira FCOB, "Involvement of Syndecan-1and heparanase in cancer and inflammation", Adv Exp Med Biol, 1221, pp.97~135 (2020)
- Jayatilleke KM, "Heparanase and the hallmarks of cancer", J Transl Med, 18, pp.453~ (2020)
- Sayyad MR, "Syndecan-1 facilitates breast cancer metastasis to the brain", Breast Cancer Res Treat, 178, pp.35~49 (2019)
- Chute C, "Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases", Breast Cancer Res, 20, pp.66~ (2018)
- Calixto-Campos C, "Quercetin reduces Ehrlich tumor-induced cancer pain in mice", Anal Cell Pathol (Amst), 2015, pp.285708~ (2015)
- Pellati F, "Cannabis sativa L. and nonpsychoactive cannabinoids : their chemistry and role against oxidative stress, inflammation, and cancer", Biomed Res Int, 2018, pp.1691428~ (2018)
- Masola V, "Role of heparanase in tumor progression : molecular aspects and therapeutic options", Semin Cancer Biol, 62, pp.86~98 (2020)
- Hermano E, "Macrophage polarization in pancreatic carcinoma : role of heparanase enzyme", J Natl Cancer Inst, 106 (2014)
- Vlodavsky I, "Heparanase : from basic research to therapeutic applications in cancer and inflammation", Drug Resist Updat, 29, pp.54~75 (2016)
- Ramani VC, "Targeting heparanase overcomes chemoresistance and diminishes relapse in myeloma", Oncotarget, 7, pp.1598~1607 (2016)
- Hao NB, "Hepatocyte growth factor(HGF)upregulates heparanase expression via the PI3K", Akt, Cancer Lett, pp.2015, 361[DOI]
- Luan Q, "Mutual enhancement between heparanase and vascular endothelial growth factor : a novel mechanism for melanoma progression", Cancer Lett, 308, pp.100~111 (2011)
- Wei RR, "CTC clusters induced by heparanase enhance breast cancer metastasis", Acta Pharmacol Sin, 39, pp.1326~1337 (2018)
- Barash U, "Involvement of heparanase in the pathogenesis of mesothelioma : basic aspects and clinical applications", J Natl Cancer Inst, 110, pp.1102~1114 (2018)
- Ramani VC, "Chemotherapy induces expression and release of heparanase leading to changes associated with an aggressive tumor phenotype", Matrix Biol, 55, pp.22~34 (2016)
- Renz BW, "β2 adrenergic-neurotrophin feedforward loop promotes pancreatic cancer", Cancer Cell, 33, pp.75~90 (2018)
- Salvo E, "TNFα promotes oral cancer growth, pain, and Schwann cell activation", Sci Rep, 11, pp.1840~ (2021)
- Lin H, "Nerve growth factor regulates liver cancer cell polarity and motility", Mol Med Rep, 23, pp.288~ (2021)
- Garrido MP, "NGF", TRKA decrease miR-145-5p levels in epithelial ovarian cancer cells, 2020, pp.21, 7657~
- Faulkner S, "Nerve growth factor and its receptor tyrosine kinase TrkA are overexpressed in cervical squamous cell carcinoma", FASEB Bioadv, 2, pp.398~408 (2020)
- Parimon T, "Syndecan-1 controls lung tumorigenesis by regulating miRNAs packaged in exosomes", Am J Pathol, 188, pp.1094~1103 (2018)
- Binder Gallimidi A, "Syndecan-1deficiency promotes tumor growth in a murine model of colitis-induced colon carcinoma", PLoS One, 12, pp.e0174343~ (2017)
- Zhang Y, "Cell surface-anchored syndecan-1 ameliorates intestinal inflammation and neutrophil transmigration in ulcerative colitis", J Cell Mol Med, 21, pp.13~25 (2017)
- Ibrahim SA, "Syndecan-1 is a novel molecular marker for triple negative inflammatory breast cancer and modulates the cancer stem cell phenotype via the IL-6", STAT3, Notch and EGFR signaling pathways, 2017, pp.16, 57~
- Yang Y, "MicroRNA-494 acts as a tumor suppressor in pancreatic cancer, inhibiting epithelial-mesenchymal transition, migration and invasion by binding to SDC1", Int J Oncol, 53, pp.1204~1214 (2018)
- Yu S, "Heparanase-1-induced shedding of heparan sulfate from syndecan-1 in hepatocarcinoma cell facilitates lymphatic endothelial cell proliferation via VEGF-C", ERK pathway, 2017, pp.485, 432~439
