Somatostatin and CXCR4 expression patterns in adenocarcinoma and squamous cell carcinoma of the lung relative to small cell lung cancer

Stumpf, Claudia; Kaemmerer, Daniel; Neubauer, Elisa; Sänger, Jörg; Schulz, Stefan; Lupp, Amelie

doi:10.1007/s00432-018-2722-5

Cited by 17 publications

(17 citation statements)

References 59 publications

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“…MMP-9 is one of the most important MMPs involved in tumor invasion and metastasis (Si et al 2018 ), whereas MMP-1 has also been reported to activate endothelial PAR-1 to facilitate endothelial permeability and transendothelial migration of tumor cells, and thus to promote metastatic dissemination (Andrae et al 2008 ). Both the PDGF/PDGFR and SDF-1/CXCR4 signaling pathways are involved in mediating EMT and angiogenesis, and thus, the regulation of tumor growth, invasion, and metastasis (Petit et al 2007 ; Stumpf et al 2018 ; Hu et al 2014 ; Lange et al 2018 ; Peng et al 2017 ), but this is the first time the secretion of PDGFR-α (by protein microarray and ELISA) from cancer cells has been detected. TGF-β is a key regulator of tumor progression, and high TGF-β expression has been observed in many cancer types (Vander Ark et al 2018 ; Watt et al 2018 ; Yang et al 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of VEGFR1+ hematopoietic progenitor cells on pre-metastatic niche formation and in vivo metastasis of breast cancer cells

Meng

Luo

et al. 2018

J Cancer Res Clin Oncol

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The pre-metastatic niche has been shown to play a critical role in tumor metastasis, and its formation is closely related to the tumor microenvironment. However, the underlying molecular mechanisms remain unclear. In the present study, we successfully established a mouse model of lung metastasis using luciferase-expressing MDA-MB-435s cells. In this model, recruitment of vascular endothelial growth factor receptor-1 (VEGFR1) + CD133 + hematopoietic progenitor cells (HPCs) was gradually increased in lung but gradually decreased after the formation of tumor colonies in lung. We also established a highly metastatic MDA-MB-435s (MDA-MB-435s-HM) cell line from the mouse model. Changes in protein profiles in different culture conditions were investigated by protein microarray analysis. The levels of CXC chemokine ligand 16, interleukin (IL)-2Rα, IL-2Rγ, matrix metalloproteinase (MMP)-1, MMP-9, platelet-derived growth factor receptor (PDGFR)-α, stromal cell-derived factor (SDF)-1α, transforming growth factor (TGF)-β, platelet endothelial cell adhesion molecule (PECAM)-1 and vascular endothelial (VE)-cadherin were significantly greater (> fivefold) in the culture medium from MDA-MB-435s-HM cells than in that from MDA-MB-435s cells. Moreover, the levels of MMP-9, PDGFR-α, and PECAM-1 were significantly greater in the co-culture medium of MDA-MB-435s-HM cells and CD133 + HPCs than in that from MDA-MB-435s-HM cells. Differentially expressed proteins were validated by enzyme-linked immunosorbent assay, and expression of their transcripts was confirmed by quantitative real-time polymerase chain reaction. Moreover, inhibition of MMP-9, PDGFR-α, and PECAM-1 by their specific inhibitors or antibodies significantly decreased cell migration, delayed lung metastasis, and decreased recruitment of VEGFR1 + CD133 + HPCs into lung. Intra-hepatic growth of HPCs enhanced the invasive growth of MDA-MB-435s-HM cells in the liver. Our data indicate that VEGFR1 + CD133 + HPCs contribute to lung metastasis. Electronic supplementary material The online version of this article (10.1007/s00432-018-2802-6) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Effects of VEGFR1+ hematopoietic progenitor cells on pre-metastatic niche formation and in vivo metastasis of breast cancer cells

Meng

Luo

et al. 2018

J Cancer Res Clin Oncol

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“…To date, only few solid tumor entities have shown pronounced overexpression of CXCR4, as assessed by PET/CT. For example, some studies have reported intense overexpression of CXCR4 in patients with SCLC [30][31][32], and Bluemel et al demonstrated feasibility of CXCR4-directed PET/CT imaging in patients with advanced adrenocortical cancer. In their initial patient cohort, about 70% of subjects demonstrated sufficient tumoral [ 68 Ga]Pentixafor uptake to qualify for potential CXCR4-directed radioligand therapy (RLT) [33].…”

Section: Cxcr4-targeted Theranostics In Cancer and Its Limitations 21 Cxcr4-targeted Pet Imagingmentioning

confidence: 99%

In Vivo Targeting of CXCR4—New Horizons

Schottelius

Herrmann

Lapa

2021

Cancers

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Given its pre-eminent role in the context of tumor cell growth as well as metastasis, the C-X-C motif chemokine receptor 4 (CXCR4) has attracted a lot of interest in the field of nuclear oncology, and clinical evidence on the high potential of CXCR4-targeted theranostics is constantly accumulating. Additionally, since CXCR4 also represents a key player in the orchestration of inflammatory responses to inflammatory stimuli, based on its expression on a variety of pro- and anti-inflammatory immune cells (e.g., macrophages and T-cells), CXCR4-targeted inflammation imaging has recently gained considerable attention. Therefore, after briefly summarizing the current clinical status quo of CXCR4-targeted theranostics in cancer, this review primarily focuses on imaging of a broad spectrum of inflammatory diseases via the quantification of tissue infiltration with CXCR4-expressing immune cells. An up-to-date overview of the ongoing preclinical and clinical efforts to visualize inflammation and its resolution over time is provided, and the predictive value of the CXCR4-associated imaging signal for disease outcome is discussed. Since the sensitivity and specificity of CXCR4-targeted immune cell imaging greatly relies on the availability of suitable, tailored imaging probes, recent developments in the field of CXCR4-targeted imaging agents for various applications are also addressed.

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“…Lung cancer can be divided into two subtypes, non-small cell lung cancer (NSCLC) and small cell lung cancer. NSCLC can be further divided into adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, accounting for about 80% of all lung cancer cases 2,3 . However, the main means of cancer treatment is still surgery combined with radiotherapy and chemotherapy 4 .…”

Section: Introductionmentioning

confidence: 99%

The mechanism of m6A methyltransferase METTL3-mediated autophagy in reversing gefitinib resistance in NSCLC cells by β-elemene

et al. 2020

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N6-methyladenosine (m6A) modification can alter gene expression by regulating RNA splicing, stability, translocation, and translation. Emerging evidence shows that m6A modification plays an important role in cancer development and progression, including cell proliferation, migration and invasion, cell apoptosis, autophagy, and drug resistance. Until now, the role of m6A modification mediated autophagy in cancer drug resistance is still unclear. In this study, we found that m6A methyltransferase METTL3-mediated autophagy played an important role in reversing gefitinib resistance by β-elemene in non-small cell lung cancer (NSCLC) cells. Mechanistically, in vitro and in vivo studies indicated that β-elemene could reverse gefitinib resistance in NSCLC cells by inhibiting cell autophagy process in a manner of chloroquine. β-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. Moreover, both β-elemene and gefitinib decreased the level of m6A methylation of gefitinib resistance cells. METTL3 was higher expressed in lung adenocarcinoma tissues than that of paired normal tissues, and was involved in the gefitinib resistance of NSCLC cells. Furthermore, METTL3 positively regulated autophagy by increasing the critical genes of autophagy pathway such as ATG5 and ATG7. In conclusion, our study unveiled the mechanism of METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by β-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance.

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Somatostatin and CXCR4 expression patterns in adenocarcinoma and squamous cell carcinoma of the lung relative to small cell lung cancer

Abstract: CXCR4 may be a promising target for diagnostics and therapy in both SCLC and NSCLC.

Cited by 17 publications

References 59 publications

Effects of VEGFR1+ hematopoietic progenitor cells on pre-metastatic niche formation and in vivo metastasis of breast cancer cells

Effects of VEGFR1+ hematopoietic progenitor cells on pre-metastatic niche formation and in vivo metastasis of breast cancer cells

In Vivo Targeting of CXCR4—New Horizons

The mechanism of m6A methyltransferase METTL3-mediated autophagy in reversing gefitinib resistance in NSCLC cells by β-elemene

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