sIL-24 peptide, a human interleukin-24 isoform, induces mitochondrial-mediated apoptosis in human cancer cells

Valiyari, Samira; Salami, Mona; Mahdian, Reza; Shokrgozar, Mohammad Ali; Oloomi, Mana; Farsani, Azadeh Mohammadi; Bouzari, Saeid

doi:10.1007/s00280-017-3370-1

Cited by 9 publications

(3 citation statements)

References 35 publications

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“…Bax is a pro-apoptotic protein, which can release cytochrome c from the mitochondria and induce changes in mitochondrial permeability, ultimately resulting in severe morphological changes in mitochondrial structure. Bcl-2 is an anti-apoptotic protein that regulates apoptosis by controlling the permeability of the mitochondrial membrane ( Lv et al, 2018 ; Valiyari et al, 2017 ). As a result, the Bcl-2/Bax ratio can affect mitochondrial membrane permeability and is closely associated with the mitochondrial-mediated apoptotic pathway.…”

Section: Discussionmentioning

confidence: 99%

RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down Syndrome

Liu

Zhang

Ren³

et al. 2023

Molecules and Cells

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Down syndrome (DS) is the most common autosomal aneuploidy caused by trisomy of chromosome 21. Previous studies demonstrated that DS affected mitochondrial functions, which may be associated with the abnormal development of the nervous system in patients with DS. Runt-related transcription factor 1 (RUNX1) is an encoding gene located on chromosome 21. It has been reported that RUNX1 may affect cell apoptosis via the mitochondrial pathway. The present study investigated whether RUNX1 plays a critical role in mitochondrial dysfunction in DS and explored the mechanism by which RUNX1 affects mitochondrial functions. Expression of RUNX1 was detected in induced pluripotent stem cells of patients with DS (DS-iPSCs) and normal iPSCs (N-iPSCs), and the mitochondrial functions were investigated in the current study. Subsequently, RUNX1 was overexpressed in N-iPSCs and inhibited in DS-iPSCs. The mitochondrial functions were investigated thoroughly, including reactive oxygen species levels, mitochondrial membrane potential, ATP content and lysosomal activity. Finally, RNA-sequencing was used to explore the global expression pattern. It was observed that the expression levels of RUNX1 in DS-iPSCs were significantly higher than those in normal controls. Impaired mitochondrial functions were observed in DS-iPSCs. Of note, overexpression of RUNX1 in N-iPSCs resulted in mitochondrial dysfunction, while inhibition of RUNX1 expression could improve the mitochondrial function in DS-iPSCs. Global gene expression analysis indicated that overexpression of RUNX1 may promote the induction of apoptosis in DS-iPSCs by activating the PI3K/Akt signaling pathway. The present findings indicate that abnormal expression of RUNX1 may play a critical role in mitochondrial dysfunction in DS-iPSCs.

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Section: Discussionmentioning

confidence: 99%

RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down Syndrome

Liu

Zhang

Ren³

et al. 2023

Molecules and Cells

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“…A specific IL-24 isoform that can block the secretion of IL-24 could be used as a therapeutic strategy. Five alternatively spliced isoforms of IL-24 induce apoptosis in cancer cells [ 70 ]. At the same time, an IL-24 splicing variant interacts with full-length IL-24 in the ER and inhibits secretion, blocking the antiapoptotic effect of full-length IL-24 [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

Interleukin 24: Signal Transduction Pathways

Smith,

Lopez,

Kim

et al. 2023

Cancers

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Interleukin 24 is a member of the IL-10 family with crucial roles in antitumor, wound healing responses, host defense, immune regulation, and inflammation. Interleukin 24 is produced by both immune and nonimmune cells. Its canonical pathway relies on recognition and interaction with specific Interleukin 20 receptors in the plasma membrane and subsequent cytoplasmic Janus protein tyrosine kinases (JAK)/signal transducer and activator of the transcription (STAT) activation. The identification of noncanonical JAK/STAT-independent signaling pathways downstream of IL-24 relies on the interaction of IL-24 with protein kinase R in the cytosol, respiratory chain proteins in the inner mitochondrial membrane, and chaperones such as Sigma 1 Receptor in the endoplasmic reticulum. Numerous studies have shown that enhancing or inhibiting the expression of Interleukin 24 has a therapeutic effect in animal models and clinical trials in different pathologies. Successful drug targeting will require a deeper understanding of the downstream signaling pathways. In this review, we discuss the signaling pathway triggered by IL-24.

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“…Cancer has high mortality and morbidity rates and is regarded as one of the most important health problems around the world (Valiyari et al, 2017[ 26 ]). The anticancer drug function is very important in cancer treatment, such that the drug preferentially kills cancer cells without any significant toxic effect on normal cells (Boohaker et al, 2012[ 2 ]).…”

Section: Introductionmentioning

confidence: 99%

A-NGR fusion protein induces apoptosis in human cancer cells

Mohammadi-Farsani

Roudkenar

Golkar

et al. 2018

EXCLI Journal; 17:Doc590; ISSN 1611-2156

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sIL-24 peptide, a human interleukin-24 isoform, induces mitochondrial-mediated apoptosis in human cancer cells

Abstract: Our results suggest that the sIL-24 peptide is a promising candidate for potential treatment of human cancers.

Cited by 9 publications

References 35 publications

RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down Syndrome

RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down Syndrome

Interleukin 24: Signal Transduction Pathways

A-NGR fusion protein induces apoptosis in human cancer cells

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