Inhibition of JAK2/STAT3 signaling pathway protects mice from the DDP-induced acute kidney injury in lung cancer

Zhang, Lei; Lü, Peng; Guo, Xu; Liu, Ting; Luo, Xu; Zhu, Yitang

doi:10.1007/s00011-019-01258-4

Cited by 26 publications

(24 citation statements)

References 52 publications

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“…A xenograft model in mice suggests that tan IIA could function to effectively increase the antitumor effect of DDP in vivo (Figure 6). H&E staining indicated that the drugs had no obvious toxic and side effects on the heart, lung, liver, kidney, and brain tissues (Supplementary Figure S1), which is contrary to other relevant research that DDP (10 mg/kg) could induce tubular dilatation, cast formation, and vacuolization in the kidneys (51). This may be due to the fact that we used a lower concentration of DDP (3 mg/kg).…”

Section: Discussioncontrasting

confidence: 70%

RETRACTED: Combination of Tanshinone IIA and Cisplatin Inhibits Esophageal Cancer by Downregulating NF-κB/COX-2/VEGF Pathway

et al. 2020

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Cisplatin (DDP) represents one of the common drugs used for esophageal squamous cell carcinoma (ESCC), but side effects associated with DDP and drug resistance lead to the failure of treatment. This study aimed to understand whether tanshinone IIA (tan IIA) and DDP could generate a synergistic antitumor effect on ESCC cells. Tan IIA and DDP are demonstrated to restrain ESCC cell proliferation in a time-and dose-dependent mode. Tan IIA and DDP at a ratio of 2:1 present a synergistic effect on ESCC cells. The combination suppresses cell migration and invasion abilities, arrests the cell cycle, and causes apoptosis in HK and K180 cells. Molecular docking indicates that tan IIA and DDP could be docked into active sites with the tested proteins. In all treated groups, the expression levels of E-cadherin, β-catenin, Bax, cleaved caspase-9, P21, P27, and c-Fos were upregulated, and the expression levels of fibronectin, vimentin, Bcl-2, cyclin D1, p-Akt, pERK , p-JNK, P38, COX-2, VEGF, IL-6, NF-κB, and c-Jun proteins were downregulated. Among these, the combination induced the most significant difference. Our results suggest that tan IIA could be a novel treatment for combination therapy for ESCC.

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Section: Discussioncontrasting

confidence: 70%

RETRACTED: Combination of Tanshinone IIA and Cisplatin Inhibits Esophageal Cancer by Downregulating NF-κB/COX-2/VEGF Pathway

et al. 2020

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“…Numerous studies have demonstrated that the occurrence and development of sepsis-mediated AKI is accompanied by changes and dysfunction of various genes, RNAs, and proteins, especially the regulating apoptotic and inflammatory role of microRNA (miR). [2] Therefore, exploring new mechanisms for AKI to effectively regulate the expression of these abnormal molecules exerts a significant effect.…”

Section: Introductionmentioning

confidence: 99%

A novel role of the miR‐152‐3p/ERRFI1/STAT3 pathway modulates the apoptosis and inflammatory response after acute kidney injury

Zhang

Huo

et al. 2020

J Biochem & Molecular Tox

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Acute kidney injury (AKI) is one of the most common and serious complications in the development of sepsis. Many microRNAs are closely related to the occurrence, development, and prognosis of sepsis AKI (but the effect and mechanism of miR‐152‐3p in it is unclear). Meanwhile, the ERBB receptor feedback inhibitor 1 (ERRFI1) has a negative regulatory effect on signal transducer and activator of transcription 3 (STAT3) phosphorylation on uterine epithelial cells. But, the relationship between miR‐152‐3p and renal function, inflammatory factors, prognosis in AKI, and the mechanism is not clear. Analyzing sepsis‐induced AKI rats and the cell model, our results revealed that miR‐152‐3p was upregulated in septic AKI patients and positively correlated with serum creatinine, urea nitrogen, interleukin 1β (IL‐1β) and tumor necrosis factor α (TNF‐α). Downregulation of miR‐152‐3p with the inhibitor could dramatically attenuate caspase‐3, bromodeoxyuridine and IL‐1β, and TNF‐α in the AKI rats' model. Furthermore, downregulation of miR‐152‐3p attenuated lipopolysaccharide‐induced apoptosis and inflammatory response in HK‐2 and HEK293 cells. To further explore the mechanisms, we found ERRFI1 was appreciably downregulated and STAT3 was upregulated in AKI, whereas ERRFI1 was radically upregulated and STAT3 was greatly downregulated after the addition of miR‐152‐3p inhibitor, no matter in vivo or in vitro. Summarily, our study confirmed that miR‐152‐3p could promote the expression of STAT3 by targeting ERRFI1, aggravate cell apoptosis and inflammatory response, and thereby aggravate kidney injury in sepsis AKI.

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“…JAK2/STAT3 is an important signaling pathway involving the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) family, which is involved in cell proliferation, apoptosis, immunity, and inflammation [37]. For example, Zhang et al reported that suppression of the JAK2/STAT3 pathway alleviated DDP-induced lung cancer in mice with improved oxidative stress and apoptosis [38]. Wu et al demonstrated that suppression of the JAK2/STAT3 pathway alleviated the apoptosis of liver cancer cells [39].…”

Section: Discussionmentioning

confidence: 99%

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

Yang

Liu

et al. 2019

Biomolecules

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T-2 toxin is one of the most toxic type A trichothecene mycotoxins in nature, and it exhibits reproductive toxicity. Betulinic acid (BA) is a natural pentacyclic triterpene compound found in species of Betula, and it has been reported to have antioxidant activity. The aim of the present study was to investigate the protective effect of BA on T-2-toxin-induced testicular injury in mice and explore its molecular mechanism. Sixty adult male mice were randomly divided into groups. The mice were pretreated orally with BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and the T-2 toxin (4 mg/kg body weight) was administered via intraperitoneal injection to induce oxidative stress after the last administration of BA. BA pretreatment significantly increased the secreted levels of testosterone and sperm motility. Moreover, BA pretreatment significantly increased the total antioxidant capacity (T-AOC), the activity of SOD and CAT, and the content of GSH, and it reduced the content of MDA. Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax). BA also increased the expression of B-cell lymphoma-2 (Bcl-2). We suggest that BA reduced the oxidative damage induced by T-2 toxin, and that these protective effects may be partially mediated by the JAK2/STAT3 signaling pathway.

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Inhibition of JAK2/STAT3 signaling pathway protects mice from the DDP-induced acute kidney injury in lung cancer

Cited by 26 publications

References 52 publications

RETRACTED: Combination of Tanshinone IIA and Cisplatin Inhibits Esophageal Cancer by Downregulating NF-κB/COX-2/VEGF Pathway

RETRACTED: Combination of Tanshinone IIA and Cisplatin Inhibits Esophageal Cancer by Downregulating NF-κB/COX-2/VEGF Pathway

A novel role of the miR‐152‐3p/ERRFI1/STAT3 pathway modulates the apoptosis and inflammatory response after acute kidney injury

Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice

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