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      Ras‑related protein Rap2c promotes the migration and invasion of human osteosarcoma cells

      Author(s): 1 , 2 , 3 , 4 , 2 , 5 , 6 , 2
      Publication date Created:
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      Journal: Oncology Letters
      Publisher: Spandidos Publications

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          Abstract

          <p class="first" id="d15372118e214">Ras-related protein (Rap)2a and Rap2b are members of the GTP-binding protein family, and serve an important function in tumor progression. However, the associations between Rap2c and cancer cell functions have not yet been reported. Osteosarcoma is a type of bone cancer; its high degree of invasion is considered to be a major treatment challenge. The present study first investigated the biological role of Rap2c in human osteosarcoma cells and investigated the underlying mechanism of Rap2c on osteosarcoma cell migration and invasion. The results of the present study demonstrated that Rap2c overexpression promoted the migratory and invasive ability of cancer cells, and increased the activity of matrix metalloproteinase-2 (MMP2). Correspondingly, the knockdown of Rap2c inhibited tumor cell migration and invasion, whereas alterations to Rap2c had no effect on osteosarcoma cell proliferation or rate of apoptosis. Furthermore, Rap2c overexpression may decrease the protein level of tissue inhibitor of metalloproteinases 2 and increase the phosphorylation level of protein kinase B (Akt). Collectively, these results indicated that Rap2c has a key function in tumor migration and invasion, and the Akt signaling pathway may be involved in Rap2c-induced MMP2 expression. </p>

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          Changing views of the role of matrix metalloproteinases in metastasis.

          A Chambers, L M Matrisian (1997)
          Metastatic spread of cancer continues to be the greatest barrier to cancer cure. Understanding the molecular mechanisms of metastasis is crucial for the design and effective use of novel therapeutic strategies to combat metastases. One class of molecules that has been repeatedly implicated in metastasis is the matrix metalloproteinases (MMPs). In this review, we re-examine the evidence that MMPs are associated with metastasis and that they make a functional contribution to the process. Initially, it was believed that the major role of MMPs in metastasis was to facilitate the breakdown of physical barriers to metastasis, thus promoting invasion and entry into and out of blood or lymphatic vessels (intravasation, extravasation). However, recent evidence suggests that MMPs may have a more complex role in metastasis and that they may make important contributions at other steps in the metastatic process. Studies using intravital videomicroscopy, as well as experiments in which levels of MMPs or their inhibitors (tissue inhibitors of metalloproteinases [TIMPs]) are manipulated genetically or pharmacologically, suggest that MMPs are key regulators of growth of tumors, at both primary and metastatic sites. On the basis of this evidence, a new view of the functional role of MMPs in metastasis is presented, which suggests that MMPs are important in creating and maintaining an environment that supports the initiation and maintenance of growth of primary and metastatic tumors. Further clarification of the mechanisms by which MMPs regulate growth of primary and metastatic tumors will be important in the development of novel therapeutic strategies against metastases.
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            The role of RAS oncogene in survival of patients with lung cancer: a systematic review of the literature with meta-analysis

            C. Mascaux, N Iannino, B. Martin … (2004)
            The proto-oncogene RAS, coding for a 21 kDa protein (p21), is mutated in 20% of lung cancer. However, the literature remains controversial on its prognostic significance for survival in lung cancer. We performed a systematic review of the literature with meta-analysis to assess its possible prognostic value on survival. Published studies on lung cancer assessing prognostic value of RAS mutation or p21 overexpression on survival were identified by an electronic search. After a methodological assessment, we estimated individual hazard ratios (HR) estimating RAS protein alteration or RAS mutation effect on survival and combined them using meta-analytic methods. In total, 53 studies were found eligible, with 10 concerning the same cohorts of patients. Among the 43 remaining studies, the revelation method was immunohistochemistry (IHC) in nine and polymerase chain reaction (PCR) in 34. Results in terms of survival were significantly pejorative, significantly favourable, not significant and not conclusive in 9, 1, 31, 2, respectively. In total, 29 studies were evaluable for meta-analysis but we aggregated only the 28 dealing with non-small-cell lung cancer (NSCLC) and not the only one dealing with small-cell-lung cancer (SCLC). The quality scores were not statistically significantly different between studies with or without significant results in terms of survival, allowing us to perform a quantitative aggregation. The combined HR was 1.35 (95% CI: 1.16–1.56), showing a worse survival for NSCLC with KRAS2 mutations or p21 overexpression and, particularly, in adenocarcinomas (ADC) (HR 1.59; 95% CI 1.26–2.02) and in studies using PCR (HR 1.40; 95% CI 1.18–1.65) but not in studies using IHC (HR 1.08; 95% CI 0.86–1.34). RAS appears to be a pejorative prognostic factor in terms of survival in NSCLC globally, in ADC and when it is studied by PCR.
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              Is Open Access

              Tumor invasion after treatment of glioblastoma with bevacizumab: radiographic and pathologic correlation in humans and mice

              John de Groot, Gregory Fuller, Ashok J. Kumar … (2010)
              Patients with recurrent malignant glioma treated with bevacizumab, a monoclonal antibody to vascular endothelial growth factor (VEGF), alone or in combination with irinotecan have had impressive reductions in MRI contrast enhancement and vasogenic edema. Responses to this regimen, as defined by a decrease in contrast enhancement, have led to significant improvements in progression-free survival rates but not in overall survival duration. Some patients for whom this treatment regimen fails have an uncharacteristic pattern of tumor progression, which can be observed radiographically as an increase in hyperintensity on T2-weighted or fluid-attenuated inverse recovery (FLAIR) MRI. To date, there have been no reports of paired correlations between radiographic results and histopathologic findings describing the features of this aggressive tumor phenotype. In this study, we correlate such findings for 3 illustrative cases of gliomas that demonstrated an apparent phenotypic shift to a predominantly infiltrative pattern of tumor progression after treatment with bevacizumab. Pathologic examination of abnormal FLAIR areas on MRI revealed infiltrative tumor with areas of thin-walled blood vessels, suggesting vascular “normalization,” which was uncharacteristically adjacent to regions of necrosis. High levels of insulin-like growth factor binding protein-2 and matrix metalloprotease-2 expression were seen within the infiltrating tumor. In an attempt to better understand this infiltrative phenotype associated with anti-VEGF therapy, we forced a highly angiogenic, noninvasive orthotopic U87 xenograft tumor to become infiltrative by treating the mice with bevacizumab. This model mimicked many of the histopathologic findings from the human cases and will augment the discovery of alternative or additive therapies to prevent this type of tumor recurrence in clinical practice.
              Article 0 comments Cited 145 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Oncology Letters
                Abbreviated Title: Oncol Lett
                Publisher: Spandidos Publications
                ISSN (Print): 1792-1074
                ISSN (Electronic): 1792-1082
                Publication date Created: February 07 2018
                Publication date (Electronic): February 07 2018
                Affiliations
                [1 ]Department of Physiology, Xuzhou Medical University, Xuzhou, Jiangsu 221004, P.R. China
                [2 ]Jiangsu Key Laboratory of Biological Cancer Therapy, Xuzhou, Jiangsu 221002, P.R. China
                [3 ]Department of Neurosurgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China
                [4 ]Department of Pathology, Xuzhou Medical University, Xuzhou, Jiangsu 221004, P.R. China
                [5 ]Department of Radiation Oncology, The First People's Hospital of Xuzhou, Xuzhou, Jiangsu 221002, P.R. China
                [6 ]Department of Oncology, LinYi People's Hospital Affiliated to Shandong University, Jinan, Shandong 250012, P.R. China
                Article
                DOI: 10.3892/ol.2018.7987
                PMC ID: 5840554
                PubMed ID: 29552178
                SO-VID: 232462b2-596a-4473-a0ea-502cc0a1c31b
                Copyright © © 2018
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