CXCR4 and CXCR7 Mediate TFF3-Induced Cell Migration Independently From the ERK1/2 Signaling Pathway

Dieckow, Julia; Brandt, Wolfgang; Hattermann, Kirsten; Schob, Stefan; Schulze, Ute; Mentlein, Rolf; Ackermann, Philipp; Sel, Saadettin; Paulsen, Friedrich

doi:10.1167/iovs.15-18129

Cited by 39 publications

(61 citation statements)

References 51 publications

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“…These findings are similar to observations in hepatocellular and breast carcinoma models[8,24]. However, in thyroid cancer K1 cells and TFF3-dependent activation of cells, the overexpression of CXCR7 had no effect on cell proliferation[25,26]. Different studies have described that in different tumor cell types, depending on the differentiation status and environment, CXCR7 may play a different role.…”

Section: Discussionsupporting

confidence: 85%

“…The CXCR4-CXCR7 heterodimer complex recruits â-arrestin, resulting in the preferential activation of â-arrestin-linked signaling pathways[35]. In late neural progenitor cells (NPCs), CXCR7 mediates migration to CXCL12 in the absence of CXCR4 through extracellular signal-regulated kinases (ERK) 1/2[36] but TFF3 induced cell migration independently from the ERK1/2 signaling pathway[26]. …”

Section: Discussionmentioning

confidence: 99%

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CXCR7/CXCL12 axis is involved in lymph node and liver metastasis of gastric carcinoma

Zhang

et al. 2017

WJG

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AIMTo investigate the role of CXC chemokine receptor (CXCR)-7 and CXCL12 in lymph node and liver metastasis of gastric carcinoma.METHODSIn 160 cases of gastric cancer, the expression of CXCR7 and CXCL12 in tumor and matched tumor-adjacent non-cancer tissues, in the lymph nodes around the stomach and in the liver was detected using immunohistochemistry to analyze the relationship between CXCR7/CXCL12 expression and clinicopathological features and to determine whether CXCR7 and CXCL12 constitute a biological axis to promote lymph node and liver metastasis of gastric cancer. Furthermore, the CXCR7 gene was silenced and overexpressed in human gastric cancer SGC-7901 cells, and cell proliferation, migration and invasiveness were measured by the MTT, wound healing and Transwell assays, respectively.RESULTSCXCR7 expression was up-regulated in gastric cancer tissues (P = 0.011). CXCR7/CXCL12 expression was significantly related to high tumor stage and lymph node (r = 0.338, P = 0.000) and liver metastasis (r = 0.629, P = 0.000). The expression of CXCL12 in lymph node and liver metastasis was higher than that in primary gastric cancer tissues (χ2 = 6.669, P = 0.010; χ2 = 25379, P = 0.000), and the expression of CXCL12 in lymph node and liver metastasis of gastric cancer was consistent with the positive expression of CXCR7 in primary gastric cancer (r = 0.338, P = 0.000; r = 0.629, P = 0.000). Overexpression of the CXCR7 gene promoted cell proliferation, migration and invasion. Silencing of the CXCR7 gene suppressed SGC-7901 cell proliferation, migration and invasion. Human gastric cancer cell lines expressed CXCR7 and showed vigorous proliferation and migratory responses to CXCL12.CONCLUSIONThe CXCR7/CXCL12 axis is involved in lymph node and liver metastasis of gastric cancer. CXCR7 is considered a potential therapeutic target for the treatment of gastric cancer.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

CXCR7/CXCL12 axis is involved in lymph node and liver metastasis of gastric carcinoma

Zhang

et al. 2017

WJG

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“…2016 (cf. also in supplemental part) 52 . The corneal wound healing mouse model has been previously described (cf.…”

Section: Methods Summarymentioning

confidence: 99%

Plasma gelsolin promotes re-epithelialization

Wittmann

Dieckow

Hampel

et al. 2018

Sci Rep

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Woundhealing disorders characterized by impaired or delayed re-epithelialization are a serious medical problem that is painful and difficult to treat. Gelsolin (GSN), a known actin modulator, supports epithelial cell regeneration and apoptosis. The aim of this study was to estimate the potential of recombinant gelsolin (rhu-pGSN) for ocular surface regeneration to establish a novel therapy for delayed or complicated wound healing. We analyzed the influence of gelsolin on cell proliferation and wound healing in vitro, in vivo/ex vivo and by gene knockdown. Gelsolin is expressed in all tested tissues of the ocular system as shown by molecular analysis. The concentration of GSN is significantly increased in tear fluid samples of patients with dry eye disease. rhu-pGSN induces cell proliferation and faster wound healing in vitro as well as in vivo/ex vivo. TGF-β dependent transcription of SMA is significantly decreased after GSN gene knockdown. Gelsolin is an inherent protein of the ocular system and is secreted into the tear fluid. Our results show a positive effect on corneal cell proliferation and wound healing. Furthermore, GSN regulates the synthesis of SMA in myofibroblasts, which establishes GSN as a key protein of TGF-β dependent cell differentiation.

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“…It plays an essential role in the maintenance and protection of epithelial surface integrity by forming a protective barrier, and acting as a motogen to facilitate cell migration. Recent studies have described the important role of TFF3 in the occurrence, proliferation, invasion, migration and apoptosis of multiple human tumors [4,5]. Pandey et al assessed the value of TFF3 expression in predicting metastatic and poor survival outcome of ER+ mammary carcinoma, demonstrating that siRNA inhibition of TFF3 reduced the invasiveness of ER+ MC cells [6].…”

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confidence: 99%

Lentivirus-mediated shRNA interference of trefoil factor 3 blocks cell viability, migration and invasion in the papillary thyroid carcinoma cells

Wu¹,

Zhang²,

Zhang³

et al. 2018

neo

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Trefoil factor 3 (TFF3), a regulatory protein composed of 59 amino acids, has been suggested to be involved in pathogen- esis, proliferation, invasion, migration and apoptosis in multiple malignant tumors. However, the roles of TFF3 concerning the viability, migration and invasion in papillary thyroid carcinoma cells have not yet been studied. This study aimed to investigate the effect of TFF3 knockdown on a thyroid papillary carcinoma TPC-1 cell line both in vitro and in vivo. In the present study, lentivirus-mediated short hairpin RNA (shRNA) targeting TFF3 plasmids were first constructed and stable TPC-1 cells were obtained while their TFF3 gene was silenced with either shTFF3-TPC-1, or a scrambled shRNA control. TFF3 expression was detected using quantitative real-time PCR and western blot analyses. The TPC-1 cell viability was measured by CCK-8 assay and colony formation. The cell migration and invasion were assessed by wound scratch assay and transwell filters. AKT phosphorylation, MMP-9, and BCL-2 expression levels were detected by western blot analyses. Our results showed that TFF3 knockdown significantly inhibits TPC-1 cell viability, migration and invasion. AKT phosphoryla- tion, MMP-9, and BCL-2 levels were all remarkably depressed in TFF3 knockdown TPC-1 cells. Using a thyroid papillary carcinoma xenograft mouse model, we further investigated the effects of TFF3 knockdown in vivo. Significantly delayed xenograft emerging, slower growth rate and lower final tumor weights and volumes were observed in the shTFF3 group as compared to the control group. As expected, the expression levels of MMP-9 and BCL-2 in the xenograft are consistent with those of shTFF3-TPC-1 and shTFF3-TPC-1 cells in vitro. Our results suggest that TFF3 plays a vital role in the viability and oncogenesis of TPC-1 cells and may be a potential target for effective treatment of thyroid papillary carcinoma.

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CXCR4 and CXCR7 Mediate TFF3-Induced Cell Migration Independently From the ERK1/2 Signaling Pathway

Cited by 39 publications

References 51 publications

CXCR7/CXCL12 axis is involved in lymph node and liver metastasis of gastric carcinoma

CXCR7/CXCL12 axis is involved in lymph node and liver metastasis of gastric carcinoma

Plasma gelsolin promotes re-epithelialization

Lentivirus-mediated shRNA interference of trefoil factor 3 blocks cell viability, migration and invasion in the papillary thyroid carcinoma cells

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