Interleukin-24 inhibits cell migration and invasion in the neuroblastoma cell line SH-SY5Y

Zhuo, Baobiao; Wang, Rong; Zhang, Hongwei; Qin, Haihui; Yin, Yue; Shi, Yingchun

doi:10.3892/or.2013.2756

Cited by 6 publications

(6 citation statements)

References 33 publications

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“…However, it has been observed that IL-24 inhibits neuroblastoma cell migration and invasion by regulating numerous invasion-associated molecules in vitro (15,16). These observations are consistent with the results of other studies, which reported that IL-24 inhibited migration and invasion of human ovarian, liver and lung cancer cells in vitro (17)(18)(19).…”

Section: Introductionsupporting

confidence: 89%

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Interleukin-24 inhibits osteosarcoma cell migration and invasion via the JNK/c-Jun signaling pathways

et al. 2017

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Abstract. Approximately 25% of osteosarcoma patients present with clinically detectable metastatic disease at the time of initial diagnosis. High-dose chemotherapy and/or surgery for the treatment of primary metastatic osteosarcoma is ineffective, and <20% of patients will survive 5 years from diagnosis. Therefore, the treatment of metastases is critical for the improvement of the prognosis of primary metastatic osteosarcoma patients. We have previously observed that overexpression of interleukin-24 (IL-24) inhibits neuroblastoma cell proliferation, migration and invasion in vitro. The present study investigated whether IL-24 may be a novel agent for osteosarcoma metastasis-suppressive treatment. It was observed that IL-24 is able to inhibit migration and invasion in spontaneously metastasizing human 143B osteosarcoma cells via the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway. IL-24 was effective in inhibiting JNK and c-Jun phosphorylation to downregulate matrix metalloproteinase (MMP)-2 and MMP-9, which contributed to the suppression of cell migration and invasion. It was concluded that IL-24 may be a potent agent in the inhibition of highly metastatic 143B osteosarcoma cells, and IL-24 may have translational potential as an effective therapeutic agent for the treatment of metastatic osteosarcoma.

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Section: Introductionsupporting

confidence: 89%

“…Previously, our and others' data have demonstrated that overexpressed IL-24 may inhibit migration and invasion in human ovarian, liver and lung cancer cells and neuroblastoma in vitro (15,(17)(18)(19). In the present study, anti-proliferative effects were observed following overexpression of IL-24 in osteosarcoma cells.…”

Section: Discussionmentioning

confidence: 91%

Interleukin-24 inhibits osteosarcoma cell migration and invasion via the JNK/c-Jun signaling pathways

et al. 2017

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“…The anti-tumor activity of IL24 is mainly attributed to endogenous gene expression ( Mohammad et al, 2019 ). The evidence shows that overexpression of IL24 has been found to inhibit the migration of pancreatic cancer, lung cancer, neuroblastoma, and hepatocellular carcinoma cells ( Zhuo et al, 2013 ; Han et al, 2015 ; Janani et al, 2015 ; Jia et al, 2016 ). Emerging evidence has shown the relationship between IL24 and AhR.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been found that the activation of the AhR signaling pathway by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 6-formylindolo[3,2-b]carbazole (FICZ) can inhibit the migration of glioblastoma by inducing the expression of downstream target gene Interleukin 24 (IL24) ( Liu et al, 2021 ). IL24 is a tumor suppressor, which can inhibit the migration and invasion of neuroblastoma, lung cancer cells ( Zhuo et al, 2013 ; Janani et al, 2015 ). Thus, the AhR-IL24 axis was proposed as an important mechanism in the inhibitory regulation of glioblastoma cell migration ( Liu et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Rutaecarpine Inhibits U87 Glioblastoma Cell Migration by Activating the Aryl Hydrocarbon Receptor Signaling Pathway

Liu

Chen

Zhu

et al. 2021

Front. Mol. Neurosci.

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Glioblastoma is the most frequent and aggressive primary astrocytoma in adults. The high migration ability of the tumor cells is an important reason for the high recurrence rate and poor prognosis of glioblastoma. Recently, emerging evidence has shown that the migration ability of glioblastoma cells was inhibited upon the activation of aryl hydrocarbon receptor (AhR), suggesting potential anti-tumor effects of AhR agonists. Rutaecarpine is a natural compound with potential tumor therapeutic effects which can possibly bind to AhR. However, its effect on the migration of glioblastoma is unclear. Therefore, we aim to explore the effects of rutaecarpine on the migration of human glioblastoma cells U87 and the involvement of the AhR signaling pathway. The results showed that: (i) compared with other structural related alkaloids, like evodiamine and dehydroevodiamine, rutaecarpine was a more potent AhR activator, and has a stronger inhibitory effect on the glioblastoma cell migration; (ii) rutaecarpine decreased the migration ability of U87 cells in an AhR-dependent manner; (iii) AhR mediated the expression of a tumor suppressor interleukin 24 (IL24) induced by rutaecarpine, and AhR-IL24 axis was involved in the anti-migratory effects of rutaecarpine on the glioblastoma. Besides IL24, other candidates AhR downstream genes both associated with cancer and migration were proposed to participate in the migration regulation of rutaecarpine by RNA-Seq and bioinformatic analysis. These data indicate that rutaecarpine is a naturally-derived AhR agonist that could inhibit the migration of U87 human glioblastoma cells mostly via the AhR-IL24 axis.

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“…SH-SY5Y cell is a MYCN non-amplified cell line, however, it have been commonly used for evaluating anti-migratory and anti-invasive effects of drug candidates for suppressing primary neuroblastoma metastasis54,55 . Thus, MYCN amplification status have been used for risk classification in current neuroblastoma trials.…”

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confidence: 99%

Discovery of a novel ROCK2 inhibitor with anti-migration effects via docking and high-content drug screening

et al. 2016

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Rho-associated protein kinase (ROCK) mediated the reorganization of the actin cytoskeleton and has been implicated in the spread and metastatic process of cancer. In this study, structure-based high-throughput virtual screening was used to identify candidate compounds targeting ROCK2 from a chemical library. Moreover, high-content screening based on neurite outgrowth of SH-SY5Y cells (a human neuroblastoma cell line) was used for accelerating the identification of compounds with characteristics of ROCK2 inhibitors. The effects of bioactive ROCK2 inhibitor candidates were further validated using other bioassays including cell migration and wound healing in SH-SY5Y cells. Through the combined virtual and high-content drug screening, the compound 1,3-benzodioxol-5-yl[1-(5-isoquinolinylmethyl)-3-piperidinyl]-methanone (BIPM) was identified as a novel and potent ROCK2 inhibitor. Exposure of SH-SY5Y cells to BIPM led to significant changes in neurite length, cell migration and actin stress fibers. Further experiments demonstrated that BIPM was able to significantly inhibit phosphorylation of cofilin, a regulatory protein of actin cytoskeleton. These results suggest that BIPM could be considered as a promising scaffold for the further development of ROCK2 inhibitors for anti-cancer metastasis.

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Interleukin-24 inhibits cell migration and invasion in the neuroblastoma cell line SH-SY5Y

Cited by 6 publications

References 33 publications

Interleukin-24 inhibits osteosarcoma cell migration and invasion via the JNK/c-Jun signaling pathways

Interleukin-24 inhibits osteosarcoma cell migration and invasion via the JNK/c-Jun signaling pathways

Rutaecarpine Inhibits U87 Glioblastoma Cell Migration by Activating the Aryl Hydrocarbon Receptor Signaling Pathway

Discovery of a novel ROCK2 inhibitor with anti-migration effects via docking and high-content drug screening

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