Interaction network mapping among IL-32 isoforms

Kang, Jeong Woo; Park, Yun Sun; Lee, Dong Hun; Kim, Man Sub; Bak, Yesol; Ham, Sun Young; Park, Su Ho; Kim, Heejong; Ahn, Joong Hoon; Hong, Jin Tae; Yoon, Do‐Young

doi:10.1016/j.biochi.2014.01.013

Cited by 69 publications

(83 citation statements)

References 18 publications

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“…IL-32 gene was found to be located on human chromosome 16p13.3 and was reported to exist in nine different isoforms by mRNA alternative splicing including IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , and IL-32 s (small), with specific activities and properties. Moreover, these isoforms can interact with each other intracellularly to control their respective activities and IL-32 is the most active isoform [105][106][107]. IL-32 is not assigned to any of the cytokine families, due to the lack of homology with other well-known cytokines.…”

Section: Il-32mentioning

confidence: 99%

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

et al. 2017

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In recent years, the landscape of pro- and anti-inflammatory cytokines has rapidly expanded with the identification of new members proven to be involved at different extent in the pathogenesis of chronic immune mediated inflammatory diseases including rheumatoid arthritis (RA). The advance of our understanding of mediators involved in the pathogenesis of RA and in consequence, the development of novel targeted therapies is necessary to provide patients not responding to currently available strategies with novel compounds. The aim of this review article is to provide an overview on recently identified cytokines, emphasizing their pathogenic role and therapeutic potential in RA. A systematic literature review was performed to retrieve articles related to every cytokine discussed in the review. In some cases, evidence from animal models and RA patients is already consistent to move forward into drug development. In others, conflicting observation and the paucity of data require further investigations.Forty years after the discovery of IL-1, the landscape of cytokines is continuously expanding with increasing possibilities to develop novel therapeutic strategies in RA. Electronic supplementary material The online version of this article (10.1186/s41927-017-0001-8) contains supplementary material, which is available to authorized users.

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Section: Il-32mentioning

confidence: 99%

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

et al. 2017

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“…In addition, it was suggested that the NK4 protein contained ArgGly-Asp (RGD) motif, important in cell adhesion (15). The NK4 transcript contains a potential signal sequence cleavage site between amino acid 31 and 32, indicating that NK4 can be secreted by the classical secretion pathway (12,13). Nevertheless, for the next 13 years, the biological function of NK4 was not known.…”

Section: History Of the Il-32mentioning

confidence: 99%

“…Authors demonstrated high polymorphism of the NK4 gene. Sequence analysis revealed that the NK4 -encoded protein had a predicted molecular mass of 27 kDa (12)(13)(14). In addition, it was suggested that the NK4 protein contained ArgGly-Asp (RGD) motif, important in cell adhesion (15).…”

Section: History Of the Il-32mentioning

confidence: 99%

“…IL-32α is the most abundant while IL-32β is the most common transcript (12,18,19). The different isoforms of IL-32 originate by splicing of pre-mRNA of the isoform IL-32γ.…”

Section: Isoformsmentioning

confidence: 99%

“…IL-32 gene was found to be located on human chromosome 16p13.3 and was reported to exist in nine different isoforms by mRNA alternative splicing including IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , IL-32 , and IL-32s (small), and all of them have specific activities and properties (12,17,15). IL-32α is the most abundant while IL-32β is the most common transcript (12,18,19).…”

Section: Isoformsmentioning

confidence: 99%

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Interleukin-32 in Infection, Inflammation and Cancer Biology

Pavlovic

Jovanović

Arsenijević

2020

Serbian Journal of Experimental and Clinical Research

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Modulatory effects of point‐mutated IL‐32θ (A94V) on tumor progression in triple‐negative breast cancer cells

Park,

Kim

et al. 2023

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Breast cancer is a frequently diagnosed cancer and the leading cause of death among women worldwide. Tumor‐associated macrophages stimulate cytokines and chemokines, which induce angiogenesis, metastasis, proliferation, and tumor‐infiltrating immune cells. Although interleukin‐32 (IL‐32) has been implicated in the development and modulation of several cancers, its function in breast cancer remains elusive. Mutation of interleukin‐32θ (IL‐32θ) in the tissues of patients with breast cancer was detected by Sanger sequencing. RT‐qPCR was used to detect the mRNA levels of inflammatory cytokines, chemokines, and mediators. The secreted proteins were detected using respective enzyme‐linked immunosorbent assays. Evaluation of the inhibitory effect of mutant IL‐32θ on proliferation, migration, epithelial–mesenchymal transition (EMT), and cell cycle arrest in breast cancer cells was conducted using MTS assays, migration assays, and Western blotting. A point mutation (281C>T, Ala94Val) was detected in IL‐32θ in both breast tumors and adjacent normal tissues, which suppressed the expression of pro‐inflammatory factors, EMT factors, and cell cycle related factors. Mutated IL‐32θ inhibited the expression of inflammatory factors by regulating the NF‐κB pathway. Furthermore, mutated IL‐32θ suppressed EMT markers and cell cycle related factors through the FAK/PI3K/AKT pathway. It was inferred that mutated IL‐32θ modulates breast cancer progression. Mutated IL‐32θ (A94V) inhibited inflammation, EMT, and proliferation in breast cancer by regulating the NF‐κB (p65/p50) and FAK‐PI3K‐GSK3 pathways.

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Interaction network mapping among IL-32 isoforms

Cited by 69 publications

References 18 publications

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

Interleukin-32 in Infection, Inflammation and Cancer Biology

Modulatory effects of point‐mutated IL‐32θ (A94V) on tumor progression in triple‐negative breast cancer cells

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