G-CSF and G-CSFR are highly expressed in human gastric and colon cancers and promote carcinoma cell proliferation and migration

Morris, Katherine T.; Khan, Hamadhaider; Ahmad, Asmaa; Weston, Lea; Nofchissey, Robert A.; Pinchuk, Iryna V.; Beswick, Ellen J.

doi:10.1038/bjc.2013.822

Cited by 85 publications

(99 citation statements)

References 38 publications

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“…Although G-CSF behaves as a potent migratory stimulus for haematopoietic cells [48], just a moderate effect was observed in Swan 71 cells. In this regard, it should be considered that a wide range of G-CSF migratory potencies has been reported in non-haematopoietic tissues, being slight responses (up to 1.4-fold increase) induced in glioma cells [7] and head and neck squamous cell carcinomas [8], and more pronounced effects (up to 6-fold increase) observed in rat oval cells [49] and gastric and colon cancer cells [50]. In spite of the differences observed in the G-CSF-migratory potency, this cytokine might be considered as a promoting factor for cell migration, while other G-CSF-mediated biological effects, such as the proliferative and survival responses, seem to be more restricted to some cell types.…”

Section: Discussionmentioning

confidence: 99%

Granulocyte colony-stimulating factor (G-CSF) upregulates β1 integrin and increases migration of human trophoblast Swan 71 cells via PI3K and MAPK activation

Furmento

Marino

Blank

et al. 2016

Experimental Cell Research

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Multiple cytokines and growth factors expressed at the fetal-maternal interface are involved in the regulation of trophoblast functions and placental growth, but the role of G-CSF has not been completely established. Based on our previous study showing that G-CSF increases the activity of matrix metalloproteinase-2 and the release of vascular endothelial growth factor in Swan 71 human trophoblast cells, in this work we explore the possible contribution of G-CSF to cell migration and the G-CSF-triggered signaling pathway. We found that G-CSF induced morphological changes on actin cytoskeleton consistent with a migratory cell phenotype. G-CSF also up-regulated the expression levels of β1 integrin and promoted Swan 71 cell migration. By using selective pharmacological inhibitors and dominant negative mutants we showed that PI3K, Erk 1/2 and p38 pathways are required for promoting Swan 71 cell motility. It was also demonstrated that PI3K behaved as an upstream regulator of Erk 1/2 and p38 MAPK. In addition, the increase of β1 integrin expression was dependent on PI3K activation. In conclusion, our results indicate that G-CSF stimulates β1 integrin expression and Swan 71 cell migration by activating PI3K and MAPK signaling pathways, suggesting that G-CSF should be considered as an additional regulatory factor that contributes to a successful embryo implantation and to the placenta development.

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Section: Discussionmentioning

confidence: 99%

Granulocyte colony-stimulating factor (G-CSF) upregulates β1 integrin and increases migration of human trophoblast Swan 71 cells via PI3K and MAPK activation

Furmento

Marino

Blank

et al. 2016

Experimental Cell Research

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“…Tumor-related leukocytosis is observed in 10% of patients with solid tumors and is associated with poor clinical outcome (3). This condition is caused, in part, by granulocyte colony-stimulating factor (G-CSF) synthesized by neoplastic cells and has therefore been regarded as potentially indicative of the autocrine stimulation of tumor growth by G-CSF (4,5). However, little is known regarding the precise mechanisms of aggressive behavior and poor outcome in G-CSF-producing tumors.…”

Section: Introductionmentioning

confidence: 99%

Rapid progression of a granulocyte colony-stimulating factor-producing liver tumor metastasized from esophagogastric junction cancer: A case report and literature review

et al. 2018

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Abstract. The current study presents the case of a 72-year-old woman with a rapidly enlarged liver metastasis from esophagogastric junction (EGJ) cancer, accompanied by progressive leukocytosis (47,680/µl) and elevated serum granulocyte colony-stimulating factor (G-CSF; 779 pg/ml). The patient underwent right hemihepatectomy 26 months after a total gastrectomy. On the seventh post-operative day the patient's leukocyte count and serum G-CSF level decreased to 4,280/µl and ≤19.5 pg/ml, respectively. Histologically, the lesion was a well to moderately differentiated adenocarcinoma similar to the primary lesion. Therefore, this tumor was clinically diagnosed as a G-CSF-producing liver metastasis from EGJ cancer, although immunohistochemical staining for G-CSF was negative. A right pulmonary nodule detected simultaneously with the hepatic mass was resected four months following the hepatectomy and was diagnosed as a pulmonary metastasis. The patient's leukocyte count was normal at the time of her initial surgery for EGJ cancer, and her clinical course varied for different metastatic sites. The liver metastasis was accompanied by progressive leukocytosis and elevated serum G-CSF and demonstrated rapid tumor growth during a six-month period, whereas the non-G-CSF-producing pulmonary metastasis grew slowly during the same period. In addition 21 reported cases of G-CSF-producing upper gastrointestinal tract cancer were reviewed to elucidate the clinicopathological features of this disease.

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“…G-CSFR, a critical regulator of granulopoiesis, has been reported to play a pivotal role in tumorigenesis [80-82]. To this end, it has been shown that G-CSF/G-CSFR, though both autocrine and paracrine mechanism, enhanced cell survival and promoted cell growth in bladder cancer cells [83].…”

Section: Introductionmentioning

confidence: 99%

Aberrant regulation of FBW7 in cancer

Wang

Ye²,

Liu³

et al. 2014

Oncotarget

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FBW7 (F-box and WD repeat domain-containing 7) or Fbxw7 is a tumor suppressor, which promotes the ubiquitination and subsequent degradation of numerous oncoproteins including Mcl-1, Cyclin E, Notch, c- Jun, and c-Myc. In turn, FBW7 is regulated by multiple upstream factors including p53, C/EBP-δ, EBP2, Pin1, Hes-5 and Numb4 as well as by microRNAs such as miR-223, miR-27a, miR-25, and miR-129-5p. Given that the Fbw7 tumor suppressor is frequently inactivated or deleted in various human cancers, targeting FBW7 regulators is a promising anti-cancer therapeutic strategy.

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G-CSF and G-CSFR are highly expressed in human gastric and colon cancers and promote carcinoma cell proliferation and migration

Cited by 85 publications

References 38 publications

Granulocyte colony-stimulating factor (G-CSF) upregulates β1 integrin and increases migration of human trophoblast Swan 71 cells via PI3K and MAPK activation

Granulocyte colony-stimulating factor (G-CSF) upregulates β1 integrin and increases migration of human trophoblast Swan 71 cells via PI3K and MAPK activation

Rapid progression of a granulocyte colony-stimulating factor-producing liver tumor metastasized from esophagogastric junction cancer: A case report and literature review

Aberrant regulation of FBW7 in cancer

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