Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Li, Hui; Meng, Yuguang; Shang, Wen-Qing; Liu, Libing; Chen, Xuan; Yuan, Min‐Min; Jin, Liping; Li, Ming‐Qing; Li, Da‐Jin

doi:10.1530/rep-15-0119

Cited by 12 publications

(7 citation statements)

References 38 publications

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“…Co-culture systems comprising decidual fragments and trophoblasts have been widely used to explore their relationship. Li et al reported that DSCs promoted CCR3 levels of trophoblast cells (37). Our current result confirmed that DSCs significantly promoted CXCL5 and CXCR2 expression of trophoblast cells.…”

Section: Discussionsupporting

confidence: 89%

“…Wang et al pointed out that both exogenous and endogenous CXCL3 regulated trophoblast cells invasion (27,39). Similar results have been identified in CCL24, CXCL16, CXCL14, CCL14, and CCL17 (37,(40)(41)(42)(43). Chemokines have been widely reported in the field of cancer and are associated with angiogenesis, invasion, and metastatic potential of tumors.…”

Section: Discussionmentioning

confidence: 58%

“…Extensive evidence revealed that reproductive hormones and DSCs directly or indirectly affected chemokines expression (35)(36)(37). Therefore, to confirm their impacts on CXCL5 and CXCR2 expression of trophoblast cells, we cultured HTR-8 cells in the presence or absence of E, P, or HCG.…”

Section: Estrogen Progesterone Human Chorionic Gonadotropin and Decidual Stromal Cells Regulate Cxcl5/cxcr2 Expression Of Trophoblastmentioning

confidence: 99%

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CXCL5 Downregulation in Villous Tissue Is Correlated With Recurrent Spontaneous Abortion

et al. 2021

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Recurrent spontaneous abortion (RSA) affects 5% of childbearing-age women worldwide. Inadequate trophoblast invasion is one of the main reasons for the development of RSA; however, the underlying molecular mechanisms for RSA have not been fully understood, and further explanation is urgently needed. C-X-C motif chemokine ligand 5 (CXCL5) is reported to contribute to the invasion of cancer cells, and its aberrant expression is associated with the cellular process of tumor pathology. Considering the high behavioral similarity between trophoblast cells and cancer cells, we hypothesized that CXCL5 may influence trophoblast invasion, and its expression levels in villous tissue may be correlated with RSA. In this study, we firstly investigated the CXCL5 expression in placental villous tissues of 15 RSA patients and 13 control patients, and the results showed that CXCL5 levels were significantly lower in villous tissue from RSA patients than those of the controls. Further in vitro experiments presented that recombinant human CXCL5 can enhance trophoblast migration, invasion, and epithelial-to-mesenchymal transition (EMT) process. We also demonstrated that CXCL5 exerted these effects on trophoblast cells through PI3K/AKT/ERK1/2 signaling pathway. In conclusion, these data indicate that CXCL5 downregulation in human villous tissue is correlated with RSA. Additionally, we found that estrogen, progesterone, human chorionic gonadotropin, and decidual stromal cells can regulate CXCL5 and chemokine receptor 2 (CXCR2) expression of trophoblast in a cell manner.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 58%

Section: Estrogen Progesterone Human Chorionic Gonadotropin and Decidual Stromal Cells Regulate Cxcl5/cxcr2 Expression Of Trophoblastmentioning

confidence: 99%

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CXCL5 Downregulation in Villous Tissue Is Correlated With Recurrent Spontaneous Abortion

et al. 2021

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“…S3j). Second, given that the binding of CCL24 to its receptor CCR3 often leads to the activation of downstream signaling such as ERK and AKT 25,26 . Western blot assays were performed to show that gankyrin overexpression increased the expressions of p-ERK and p-AKT in ccRCC cells ( Supplementary Fig.…”

Section: Gankyrin Facilitates the Growth And Progression Of Ccrcc Celmentioning

confidence: 99%

Blocking the autocrine regulatory loop of Gankyrin/STAT3/CCL24/CCR3 impairs the progression and pazopanib resistance of clear cell renal cell carcinoma

Wang

Hong

et al. 2020

Cell Death Dis

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The poor prognosis of clear-cell renal cell carcinoma (ccRCC) patients is due to progression and targeted drug resistance, but the underlying molecular mechanisms need further elucidation. This study examined the biological function and related mechanisms of gankyrin in ccRCC based on the results of our previous study. To this end, in vitro functional experiments; in vivo models of subcutaneous tumor formation, lung metastasis, and orthotopic ccRCC; and antibody chip detection, co-IP, ChIP assays were performed to examine the biological role and molecular mechanisms of gankyrin in ccRCC. Two hundred fifty-six ccRCC patients were randomly divided into training and validation cohorts to examine the prognostic value of gankyrin and other markers through IHC and statistical analyses. We observed that the gankyrin-overexpressing ccRCC cell lines 786-O and 769-P exhibited increased proliferation, invasion, migration, tumorigenicity, and pazopanib resistance and decreased apoptosis, while gankyrin knockdown achieved the opposite results. Mechanistically, gankyrin recruited STAT3 via direct binding, and STAT3 binding to the CCL24 promoter promoted its expression. Reciprocally, an increase in autocrine CCL24 enhanced the expression of gankyrin and STAT3 activation via CCR3 in ccRCC, forming a positive autocrine-regulatory loop. Furthermore, in vivo experimental results revealed that blocking the positive loop through gankyrin knockdown or treatment with the CCR3 inhibitor SB328437 reversed the resistance to pazopanib and inhibited lung metastasis in ccRCC. Moreover, a positive correlation between gankyrin and STAT3 or CCL24 expression in ccRCC specimens was observed, and improved accuracy for ccRCC patient prognosis was achieved by combining gankyrin and STAT3 or CCL24 expression with existing clinical prognostic indicators, including the TNM stage and SSIGN score. In summary, targeting the gankyrin/STAT3/CCL24/CCR3 autocrine-regulatory loop may serve as a remedy for patients with advanced ccRCC, and combining gankyrin and STAT3 or CCL24 expression with the current clinical indicators better predicts ccRCC patient prognosis.

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“…We assessed the expression of a set of chemokines known to be strong modulators of innate immune responses [52,53]. The focus was set, in particular on DC biology (and other APC: CCl2, CCL3, CCl4 and CCL12; [54][55][56]) Th cells (CCL1, CCL20, CCL22 and CXCL10; [57][58][59][60]) or leukocytes and NK cells (CCL6, CCl24, CXCL3 and CXCL16; [61][62][63][64]). We could identify a significant effect of TBI (Two-way MANOVA: F = 4.494; Wilks λ = 0.357; p = 0.0001) and EI (F = 4.956; Wilks λ = 0.335; p = 0.0001), the interaction of the two parameters showed no significant effect in the Two-way MANOVA (F = 1.776; Wilks λ = 0.585; p = 0.099).…”

Section: Rapid Modulation Of the Splenic Chemokine Pattern By Tbi And By Ei/tbimentioning

confidence: 99%

Fast maturation of splenic dendritic cells upon TBI is associated with FLT3/FLT3L signaling

Zhang

Chandrasekar

et al. 2021

Preprint

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Systemic inflammatory consequences remain a significant burden after traumatic brain injury (TBI), with almost all organs affected. The spleen is connected with the brain by autonomic innervation and by soluble mediators, and the cross-talk between brain and spleen may be important to establish the systemic inflammatory response to TBI. Ethanol intoxication, the most common comorbidity of TBI, is posited to influence the peripheral inflammatory response either directly or through the brain-spleen cross-talk. Here we show that TBI causes a substantial change in transcription of genes associated with dendritic cells activation in the spleen, in particular a FLT3/FLT3L induction 3h after TBI, which was enhanced by EI. The FLT3L induction was associated with the phosphorylation of FLT3 receptor in CD11c+ dendritic cells, which enhanced the protein synthesis of a subset of mRNAs, as shown by the increase in pS6, peIF2A levels in dendritic cells. This corresponded to the upregulation of proteins associated with maturation process and immunostimulatory properties such MHC-II, LAMP1 and CD68, and of pro-inflammatory cytokines such as TNFα. Notably, EI enhanced the maturation of dendritic cells. However, whereas TBI decreases expression of the adrenergic 2b receptors on dendritic cells, EI increased it, thus augmenting the chances of cross-talk regulation of immune function by the autonomic system. In conclusion, this data indicates that TBI induces a fast maturation of the immunomodulatory functions of dendritic cells which is associated by FLT3/FLT3L signaling and which is enhanced by EI prior to TBI.

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Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Cited by 12 publications

References 38 publications

CXCL5 Downregulation in Villous Tissue Is Correlated With Recurrent Spontaneous Abortion

CXCL5 Downregulation in Villous Tissue Is Correlated With Recurrent Spontaneous Abortion

Blocking the autocrine regulatory loop of Gankyrin/STAT3/CCL24/CCR3 impairs the progression and pazopanib resistance of clear cell renal cell carcinoma

Fast maturation of splenic dendritic cells upon TBI is associated with FLT3/FLT3L signaling

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