IL-8 promotes proliferation and inhibition of apoptosis via STAT3/AKT/NF-κB pathway in prostate cancer

Guo, Yidi; Zang, Ying; Lv, Lianzheng; Cai, Feng; Qian, Tingting; Zhang, Guoying; Feng, Qi Sheng

doi:10.3892/mmr.2017.7747

Cited by 49 publications

(42 citation statements)

References 42 publications

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“…AKT is directly phosphorylated by PDK1 at T308, and forms an activation loop between SIN1, mTORC2 and p-AKT (T308), leading to the phosphorylation of AKT S473 by mTORC2 (30,31). In addition, it has been reported that STAT/AKT pathway inhibition could cause apoptosis in prostate cancer (32). In the present study, it was identified that p-AKT (T308) and p-STAT3 (Y703) decreased following exposure to 6 µg/ml EEIHL, indicating STAT3/AKT inhibition following EEIHL treatment.…”

Section: Discussionsupporting

confidence: 55%

Ethyl acetate extract from Inulaï¿½helenium L. inhibits the proliferation of pancreatic cancer cells by regulating the STAT3/AKT pathway

et al. 2018

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Sesquiterpene lactones are bioactive compounds that have been identified as responsible for the anticancer activity of the medicinal herb, Inula helenium L. (IHL). However, the mechanisms of action involved in the anti‑pancreatic cancer activity of IHL have yet to be elucidated. The present study used an optimized extraction strategy to obtain sesquiterpene lactones from IHL (the resulting product termed ethyl acetate extract of IHL; EEIHL), and examined the potential mechanisms involved in the anti‑pancreatic cancer activity of EEIHL. Ethanol and ethyl acetate were used to extract sesquiterpene lactones from IHL to give the final product EEIHL. Cell Counting Kit‑8, colony formation and Annexin V/propidium iodide assays were used to detect the anti‑proliferative activity of EEIHL. Cell migration was determined with a wound healing assay. mRNA and protein expression levels were analyzed by reverse transcription‑quantitative polymerase chain reaction and western blot analyses, respectively. It was identified that low concentrations of EEIHL caused CFPAC‑1 cell cycle arrest in the G0/G1 phase, whereas high concentrations of EEIHL induced mitochondria‑dependent apoptosis. In addition, EEIHL could inhibit the phosphorylation of the signal transducer and activator of transcription (STAT)3/AKT pathway, potentially resulting in impeded cell mobility. In conclusion, EEIHL could activate mitochondrial‑dependent apoptosis and inhibit cell migration through the STAT3/AKT pathway in CFPAC-1 cells.

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Section: Discussionsupporting

confidence: 55%

Ethyl acetate extract from Inulaï¿½helenium L. inhibits the proliferation of pancreatic cancer cells by regulating the STAT3/AKT pathway

et al. 2018

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“…Next, we investigated the biological function of this mitotic signaling pathway. Because IL-8 has been described to promote tumor cell survival 44,45,49,50 , we started by analyzing mitotic apoptosis in either control cells or cells, in which CXCL8 was silenced. Indeed, we observed a significant increase of mitotic apoptosis in CXCL8depleted cells (Fig.…”

Section: Wt1 Regulates Il-8 Transcription and Secretion In Mitosismentioning

confidence: 99%

Antagonistic activities of CDC14B and CDK1 on USP9X regulate WT1-dependent mitotic transcription and survival

et al. 2020

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Regulation of mitosis secures cellular integrity and its failure critically contributes to the development, maintenance, and treatment resistance of cancer. In yeast, the dual phosphatase Cdc14 controls mitotic progression by antagonizing Cdk1-mediated protein phosphorylation. By contrast, specific mitotic functions of the mammalian Cdc14 orthologue CDC14B have remained largely elusive. Here, we find that CDC14B antagonizes CDK1mediated activating mitotic phosphorylation of the deubiquitinase USP9X at serine residue 2563, which we show to be essential for USP9X to mediate mitotic survival. Starting from an unbiased proteome-wide screening approach, we specify Wilms' tumor protein 1 (WT1) as the relevant substrate that becomes deubiquitylated and stabilized by serine 2563phosphorylated USP9X in mitosis. We further demonstrate that WT1 functions as a mitotic transcription factor and specify CXCL8/IL-8 as a target gene of WT1 that conveys mitotic survival. Together, we describe a ubiquitin-dependent signaling pathway that directs a mitosis-specific transcription program to regulate mitotic survival.

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“…Interleukin-6, -8, and -1β are well-identified cytokines to promote the STAT3 signaling pathway [57][58][59]. After TGF-β1 treatment in LX-2 cells, expressions of interleukin-6, -8, and -1β were significantly increased in the mRNA level; however, down-regulation of interleukins was not observed by C7A treatment (data not shown).…”

Section: Discussionmentioning

confidence: 90%

(–)-Catechin-7-O-β-d-Apiofuranoside Inhibits Hepatic Stellate Cell Activation by Suppressing the STAT3 Signaling Pathway

Park

Kim

Jeong

et al. 2019

Cells

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Hepatic fibrosis is characterized by the abnormal deposition of extracellular matrix (ECM) proteins. During hepatic fibrogenesis, hepatic stellate cell (HSC) activation followed by chronic injuries is considered a key event in fibrogenesis, and activated HSCs are known to comprise approximately 90% of ECM-producing myofibroblasts. Here, we demonstrated that (-)-catechin-7-O-β-d-apiofuranoside (C7A) significantly inhibited HSC activation via blocking the signal transducer and activator of transcription 3 (STAT3) signaling pathway. This is the first study to show the hepatic protective effects of C7A with possible mechanisms in vitro and in vivo. In our bioactivity screening, we figured out that the EtOH extract of Ulmus davidiana var. japonica root barks, which have been used as a Korean traditional medicine, inhibited collagen synthesis in HSCs. Four catechins isolated from the EtOAc fraction of the EtOH extract were compared with each other in terms of reduction in collagen, which is considered as a marker of hepatic protective effects, and C7A showed the strongest inhibitory effects on HSC activation in protein and qPCR analyses. As a possible mechanism, we investigated the effects of C7A on the STAT3 signaling pathway, which is known to activate HSCs. We found that C7A inhibited phosphorylation of STAT3 and translocation of STAT3 to nucleus. C7A also inhibited expressions of MMP-2 and MMP-9, which are downstream genes of STAT3 signaling. Anti-fibrotic effects of C7A were evaluated in a thioacetamide (TAA)-induced liver fibrosis model, which indicated that C7A significantly inhibited ECM deposition through inhibiting STAT3 signaling. C7A decreased serum levels of aspartate amino transferase and alanine transaminase, which were markedly increased by TAA injection. Moreover, ECM-associated proteins and mRNA expression were strongly suppressed by C7A. Our study provides the experimental evidence that C7A has inhibitory effects on HSC activation after live injury and has preventive and therapeutic potentials for the management of hepatic fibrosis.

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IL-8 promotes proliferation and inhibition of apoptosis via STAT3/AKT/NF-κB pathway in prostate cancer

Cited by 49 publications

References 42 publications

Ethyl acetate extract from Inulaï¿½helenium L. inhibits the proliferation of pancreatic cancer cells by regulating the STAT3/AKT pathway

Ethyl acetate extract from Inulaï¿½helenium L. inhibits the proliferation of pancreatic cancer cells by regulating the STAT3/AKT pathway

Antagonistic activities of CDC14B and CDK1 on USP9X regulate WT1-dependent mitotic transcription and survival

(–)-Catechin-7-O-β-d-Apiofuranoside Inhibits Hepatic Stellate Cell Activation by Suppressing the STAT3 Signaling Pathway

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