Chitinase 3 like-1 activates the Akt pathway, inducing NF-κB-dependent release of pro-inflammatory cytokines and promoting the proliferative ability in nasopharyngeal carcinoma cells

Li, Dajun; Fan, Gai; Zhou, Yeqi

doi:10.1016/j.cyto.2024.156631

Cytokine

2024

DOI: 10.1016/j.cyto.2024.156631

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Chitinase 3 like-1 activates the Akt pathway, inducing NF-κB-dependent release of pro-inflammatory cytokines and promoting the proliferative ability in nasopharyngeal carcinoma cells

Dajun Li,

Gai Fan,

Yeqi Zhou

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2024

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Chitinase 3‐like 1 overexpression aggravates hypoxia–reoxygenation injury in IEC‐6 cells by inhibiting the PI3K/AKT signalling pathway

Mi,

Jin,

Zhang

et al. 2024

Experimental Physiology

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Intestinal ischaemia–reperfusion (I/R) is a common clinical pathology with high incidence and mortality rates. However, the mechanisms underlying intestinal I/R injury remain unclear. In this study, we investigated the role and mechanism of chitinase 3‐like 1 (CHI3L1) during intestinal I/R injury. Therefore, we analysed the expression levels of CHI3L1 in the intestinal tissue of an intestinal I/R rat model and explored its effects and mechanism in a hypoxia–reoxygenation (H/R) IEC‐6 cell model. We found that intestinal I/R injury elevated CHI3L1 levels in the serum, ileum and duodenum, whereas H/R enhanced CHI3L1 expression in IEC‐6 cells. The H/R‐induced inhibition of proliferation and apoptosis was alleviated by CHI3L1 knockdown and aggravated by CHI3L1 overexpression. In addition, CHI3L1 knockdown alleviated, and CHI3L1 overexpression aggravated, the H/R‐induced inflammatory response and oxidative stress. Mechanistically, CHI3L1 overexpression weakened the activation of the phosphoinositide 3‐kinase (PI3K)/AKT pathway, suppressed the nuclear translocation of Nrf2, and promoted the nuclear translocation of nuclear factor κB (NF‐κB). Moreover, CHI3L1 knockdown had the opposite effect on the PI3K/AKT pathway, Nrf2, and NF‐κB. Moreover, the PI3K inhibitor LY294002 blocked the effect of CHI3L1 knockdown on the H/R‐induced inhibition of proliferation, apoptosis, inflammatory response and oxidative stress. In conclusion, CHI3L1 expression was induced during intestinal I/R and H/R injury in IEC‐6 cells, and CHI3L1 overexpression aggravated H/R injury in IEC‐6 cells by inhibiting the PI3K/AKT signalling pathway. Therefore, CHI3L1 may be an effective target for controlling intestinal I/R injury.

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Chitinase 3‐like 1 overexpression aggravates hypoxia–reoxygenation injury in IEC‐6 cells by inhibiting the PI3K/AKT signalling pathway

Mi,

Jin,

Zhang

et al. 2024

Experimental Physiology

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Chitinase 3 like-1 activates the Akt pathway, inducing NF-κB-dependent release of pro-inflammatory cytokines and promoting the proliferative ability in nasopharyngeal carcinoma cells

Cited by 1 publication

References 52 publications

Chitinase 3‐like 1 overexpression aggravates hypoxia–reoxygenation injury in IEC‐6 cells by inhibiting the PI3K/AKT signalling pathway

Chitinase 3‐like 1 overexpression aggravates hypoxia–reoxygenation injury in IEC‐6 cells by inhibiting the PI3K/AKT signalling pathway

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