STAT3-induced NCK1 elevation promotes migration of triple-negative breast cancer cells via regulating ERK1/2 signaling

He, Peina; Sheng, Jianyun; Qi, Jinxu; Bai, Xia; Li, Jiaxin; Wang, Fubao; Yuan, Yamin; Zheng, Xinhua

doi:10.1007/s11033-021-06868-y

Cited by 4 publications

(4 citation statements)

References 47 publications

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“…Thus, it is of great significance to explore the pathological mechanism to prevent and treat uRM. In recent years, studies have confirmed that NCK1 is highly expressed in some tumors, and is associated with enhanced tumor proliferation, migration and invasion ( Liu et al, 2020 ; He et al, 2022 ). The similarity between embryo implantation and tumor development is widely recognized ( Mor et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Reduced NCK1 participates in unexplained recurrent miscarriage by regulating trophoblast functions and macrophage proliferation at maternal-fetal interface

Ding,

Zhang,

Bao

et al. 2023

Genet. Mol. Biol.

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Recurrent miscarriage (RM) seriously affects the physical and mental health of women of childbearing age, and 50% of the causes are unknown. Thus, it is valuable to investigate the causes of unexplained recurrent miscarriage (uRM). Similarities between tumor development and embryo implantation make us realize that tumor studies are informative for uRM. The non-catalytic region of tyrosine kinase adaptor protein 1 (NCK1) is highly expressed in some tumors, and can promote tumor growth, invasion and migration. In this present paper, we firstly explore the role of NCK1 in uRM. We find that the NCK1 and PD-L1 are greatly reduced in peripheral blood mononuclear cells (PBMC) and decidua from patients with uRM. Next, we construct NCK1-knockdown HTR-8/SVneo cells, and find that NCK1-knockdown HTR-8/SVneo cells exhibit reduced proliferation and migration ability. Then we demonstrate that the expression of PD-L1 protein is decreased when the NCK1 is knocked down. In co-culture experiments with THP-1 and differently treated HTR-8/SVneo cells, we observe significantly increased proliferation of THP-1 in NCK1-knockdown group. In conclusion, NCK1 may be involved in RM by regulating trophoblast proliferation, migration, and regulating PD-L1mediated macrophage proliferation at the maternal-fetal interface. Moreover, NCK1 has the potential to be a new predictor and therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Reduced NCK1 participates in unexplained recurrent miscarriage by regulating trophoblast functions and macrophage proliferation at maternal-fetal interface

Ding,

Zhang,

Bao

et al. 2023

Genet. Mol. Biol.

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“…Emerging studies have discovered that STAT3, p300 and MMP19 are overexpressed in breast cancer [ 36 ], esophageal cancer [ 37 ], colorectal cancer (CRC) [ 38 ] or NSCLC [ 15 ] and so on [ 16 , 31 ], promoting cancer cell growth or metastasis. Therefore, we explored the role of p300, STAT3 and MMP19 in IL-17-induced H1299 cell migration and invasion as well as their relationship, and affirmed that the overexpression of these genes could augment the cell migration and invasion, but the knockdown of these genes had contrary effects.…”

Section: Discussionmentioning

confidence: 99%

IL-17 induces NSCLC cell migration and invasion by elevating MMP19 gene transcription and expression through the interaction of p300-dependent STAT3-K631 acetylation and its Y705-phosphorylation

GE,

LI,

RUAN

et al. 2024

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The cancer cell metastasis is a major death reason for patients with non-small cell lung cancer (NSCLC). Although researchers have disclosed that interleukin 17 (IL-17) can increase matrix metalloproteinases (MMPs) induction causing NSCLC cell metastasis, the underlying mechanism remains unclear. In the study, we found that IL-17 receptor A (IL-17RA), p300, p-STAT3, Ack-STAT3, and MMP19 were up-regulated both in NSCLC tissues and NSCLC cells stimulated with IL-17. p300, STAT3 and MMP19 overexpression or knockdown could raise or reduce IL-17-induced p-STAT3, Ack-STAT3 and MMP19 level as well as the cell migration and invasion. Mechanism investigation revealed that STAT3 and p300 bound to the same region (−544 to −389 nt) of MMP19 promoter, and p300 could acetylate STAT3-K631 elevating STAT3 transcriptional activity, p-STAT3 or MMP19 expression and the cell mobility exposed to IL-17. Meanwhile, p300-mediated STAT3-K631 acetylation and its Y705-phosphorylation could interact, synergistically facilitating MMP19 gene transcription and enhancing cell migration and invasion. Besides, the animal experiments exhibited that the nude mice inoculated with NSCLC cells by silencing p300, STAT3 or MMP19 gene plus IL-17 treatment, the nodule number, and MMP19, Ack-STAT3, or p-STAT3 production in the lung metastatic nodules were all alleviated. Collectively, these outcomes uncover that IL-17-triggered NSCLC metastasis involves up-regulating MMP19 expression via the interaction of STAT3-K631 acetylation by p300 and its Y705-phosphorylation, which provides a new mechanistic insight and potential strategy for NSCLC metastasis and therapy.

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“…Pirin signaling includes ( Table 1 ) Wiskott-Aldrich syndrome protein family member 2 (WASF2) and RAC1 which are associated with lamellipodia assembly ( Fig 5 ). Pirin also interacts with cytoplasmic protein NCK1, which mediates cancer metastasis [ 105 , 106 ] as well as functions as an intracellular messenger leading to angiogenesis in the ERBB signaling pathway (KEGG entry: hsa04012) [ 45 ]. RAC1, together with NCK, mediates activation of the Arp2/3 complex leading to polymerization of the actin cytoskeleton to form lamellipodia typical of mesenchymal movements as well as tumor metastasis and angiogenesis [ 107 , 108 ].…”

Section: Discussionmentioning

confidence: 99%

Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways

Ahsan,

Shoily,

Ahmed

et al. 2023

PLoS ONE

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Persistent cellular stress induced perpetuation and uncontrolled amplification of inflammatory response results in a shift from tissue repair toward collateral damage, significant alterations of tissue functions, and derangements of homeostasis which in turn can lead to a large number of acute and chronic pathological conditions, such as chronic heart failure, atherosclerosis, myocardial infarction, neurodegenerative diseases, diabetes, rheumatoid arthritis, and cancer. Keeping the vital role of balanced inflammation in maintaining tissue integrity in mind, the way to combating inflammatory diseases may be through identification and characterization of mediators of inflammation that can be targeted without hampering normal body function. Pirin (PIR) is a non-heme iron containing protein having two different conformations depending on the oxidation state of the iron. Through exploration of the Pirin interactome and using molecular docking approaches, we identified that the Fe2+-bound Pirin directly interacts with BCL3, NFKBIA, NFIX and SMAD9 with more resemblance to the native binding pose and higher affinity than the Fe3+-bound form. In addition, Pirin appears to have a function in the regulation of inflammation, the transition between the canonical and non-canonical NF-κB pathways, and the remodeling of the actin cytoskeleton. Moreover, Pirin signaling appears to have a critical role in tumor invasion and metastasis, as well as metabolic and neuro-pathological complications. There are regulatory variants in PIR that can influence expression of not only PIR but also other genes, including VEGFD and ACE2. Disparity exists between South Asian and European populations in the frequencies of variant alleles at some of these regulatory loci that may lead to differential occurrence of Pirin-mediated pathogenic conditions.

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STAT3-induced NCK1 elevation promotes migration of triple-negative breast cancer cells via regulating ERK1/2 signaling

Cited by 4 publications

References 47 publications

Reduced NCK1 participates in unexplained recurrent miscarriage by regulating trophoblast functions and macrophage proliferation at maternal-fetal interface

Reduced NCK1 participates in unexplained recurrent miscarriage by regulating trophoblast functions and macrophage proliferation at maternal-fetal interface

IL-17 induces NSCLC cell migration and invasion by elevating MMP19 gene transcription and expression through the interaction of p300-dependent STAT3-K631 acetylation and its Y705-phosphorylation

Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways

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