Tumor endothelial cells accelerate tumor metastasis

Maishi, Nako; Hida, Kyoko

doi:10.1111/cas.13336

Cited by 254 publications

(196 citation statements)

References 58 publications

(116 reference statements)

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“…During angiogenesis, tumor growth changes from slow to rapid; angiogenesis is the key step to facilitate this transformation. Inhibition of angiogenesis can obviously control tumor growth and metastasis . In this study, we found that miR‐873 suppression conspicuously enhanced the viability and growth of PC9 cells treated with gefitinib.…”

Section: Discussionmentioning

confidence: 57%

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MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

Jin

et al. 2018

Thoracic Cancer

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BackgroundThe five‐year survival rate of non‐small cell lung cancer (NSCLC) patients is very low. MiR‐873 is involved in the growth, metastasis, and differentiation of tumors. Herein, we determined the target gene and influence of miR‐873 in NSCLC.MethodsMiRanda and Targetscan websites were used to predict the target gene of miR‐873 in NSCLC. Luciferase activity was examined using a dual luciferase reporter gene assay kit. The viability, tube formation, and proliferation of cells were analyzed by cell counting kit‐8, angiogenic analysis, and flow cytometry, respectively. The levels of miR‐873 and GLI1 were evaluated using quantitative real‐time PCR and Western blot assays.ResultsLow levels of GLI1 and high levels of miR‐873 were observed in an NSCLC cell line (PC9) highly sensitive to EGFR‐tyrosine kinase inhibitors. There was a negative correlation between miR‐873 and GLI1 expression in PC9 and PC9/GR cells. The inhibition of miR‐873 enhanced GLI1 levels. MiR‐873 expression was inhibited by gefitinib. Gefitinib markedly reduced the viability, tube formation, and cell number in PC9 cells. However, suppression of miR‐873 enhanced the resistance and knockdown of GLI1 enhanced the sensitivity of PC9 cells to gefitinib.Conclusions GLI1 is a target gene of miR‐873 in NSCLC. The inhibition of miR‐873 increased gefitinib resistance of NSCLC cells via the upregulation of GLI1. These results indicate that miR‐873‐GLI1 signaling is involved in gefitinib resistance in NSCLC.

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Section: Discussionmentioning

confidence: 57%

“…Inhibition of angiogenesis can obviously control tumor growth and metastasis. [45][46][47][48][49] In this study, we found that miR-873 suppression conspicuously enhanced the viability and growth of PC9 cells treated with gefitinib. Moreover, the inhibition of miR-873 increased angiogenesis.…”

Section: Discussionmentioning

confidence: 97%

MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

Jin

et al. 2018

Thoracic Cancer

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“…While the ECs help in the formation of new blood vessels to assist tumour growth and metastasis [40], fibroblasts, CAFs secrete growth factors [41,42] and contribute to ECM remodelling. The presence of ECs as revealed by positivity to CD31 marker was identified in all the 12 RB tumours assessed, and these cells were majorly found localised in the blood vessels of RB tumours.…”

Section: Discussionmentioning

confidence: 99%

Evidence of Tumour Microenvironment and Stromal Cellular Components in Retinoblastoma

et al. 2018

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Background: The tumour microenvironment (TME) consisting of tumour cells and multiple stromal cell types regulate tumour growth, invasion and metastasis. While the concept of TME and presence of stromal cellular components is widely established in cancers, its significance in the paediatric intraocular malignancy, retinoblastoma (RB), remains unknown. Methods: The study qualitatively identified the presence of multiple stromal cellular subtypes in RB TME by immunohistochemistry. Results: Results of the study identified the presence of stromal cell types such as endothelial cells, tumour-associated macrophages, fibroblasts, cancer-associated fibroblasts, retinal astrocytes and glia in RB TME. The extent of stromal marker positivity, however, did not correlate with histopathological features of RB. Conclusions: The findings of the study convincingly suggest the presence of a stromal component in RB tumours. The interactions between stromal cells and tumour cells might be of profound importance in RB progression.

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“…Cancer metastasis involves a complex cascade of events: tumor cells i) invade the surrounding stroma and extracellular matrix; ii) intravasate into the bloodstream and survive in the blood circulation; iii) arrest at distant organ sites; and iv) extravasate and invade into the parenchyma of distant tissues [21,22]. Some enriched functional lists were found to be associated with these cascades during this process and to be present only in tumor-forming rats.…”

Section: Functional Analysismentioning

confidence: 99%

Early urinary protein changes in the tumor-forming process of the NuTu-19 lung metastasis

Wei

Meng

et al. 2019

Preprint

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The early detection of cancer is essential for effective intervention. Urine, which lacks homeostatic control, has been used to reflect early systemic changes in subcutaneous cancer models. However, urine has not been used to predict whether tumors will be formed in animal models. In this study, a cancer model was established by the tail-vein injection of 2 million NuTu-19 tumor cells. Approximately half of the rats formed lung metastatic carcinoma tumors. Urine samples were randomly selected from 4 tumor-forming rats and 4 non-tumor-forming rats on day 0/12/27/39/52 and analyzed by label-free proteomic quantitative analysis. Compared to day 0, a total of 180 and 118 urinary proteins in tumor-forming and non-tumor-forming rats, respectively, showed significant changes. Functional enrichment analysis of the differential proteins in tumor-forming rats revealed similar events during cancer metastasis cascades and tumor progression, such as the migration of tumor cell lines, coagulation system, TGF-β signaling, the STAT3 pathway and the adhesion of myeloid cells and alveolar macrophages. The differential proteins in non-tumor-forming rats were associated with agranulocyte/granulocyte adhesion and diapedesis, glutathione biosynthesis, IL-12 signaling and vitamin metabolism. After validation by parallel reaction monitoring (PRM) targeted proteomics quantitative analysis, a total of 22 urinary proteins showed significant changes in the early phase of the lung tumor formation process, 5 of which have been associated with the mechanisms of lung cancer, while 3 have been suggested as lung cancer biomarkers. Another 14 urinary proteins showed significant changes in the early phase in non-tumor-forming rats. Our results indicate that urine proteins could differentiate early tumor-forming and non-tumor-forming status.

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Tumor endothelial cells accelerate tumor metastasis

Cited by 254 publications

References 58 publications

MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

Evidence of Tumour Microenvironment and Stromal Cellular Components in Retinoblastoma

Early urinary protein changes in the tumor-forming process of the NuTu-19 lung metastasis

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