Genetic gains and losses in oral squamous cell carcinoma: impact on clinical management

Ribeiro, Ilda Patrícia; Marques, Francisco Batel; Caramelo, Francisco; Pereira, João; Patrício, Miguel; Prazeres, Hugo; Ferrão, José; Julião, Maria José; Castelo‐Branco, Miguel; Melo, Joana Barbosa; Baptista, Isabel; Carreira, Isabel M.

doi:10.1007/s13402-013-0161-5

Cited by 47 publications

(25 citation statements)

References 46 publications

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“…After elimination of duplicate records, the title and abstract of 133 potentially eligible studies were screened, leading to the selection of 52 studies for evaluation of their full text. Among these articles, 18 met all eligibility criteria for inclusion in the qualitative study and quantitative meta‐analysis …”

Section: Resultsmentioning

confidence: 99%

“…Among these articles, 18 met all eligibility criteria for inclusion in the qualitative study and quantitative meta-analysis. [40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57] Table 1 summarizes the characteristics of the 18 selected studies, which include 1633 patients with HNSCC. The sample size of these studies ranges between 13 and 222 patients.…”

Section: Results Of the Search Of The Literaturementioning

confidence: 99%

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Prognostic and clinicopathological significance of CTTN/cortactin alterations in head and neck squamous cell carcinoma: Systematic review and meta‐analysis

et al. 2018

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Background To evaluate the prognostic significance of CTTN/cortactin alterations in head and neck squamous cell carcinoma (HNSCC). Material and methods We searched PubMed, Embase, Web of Science, and Scopus for studies published before May 2018. We conducted a meta‐analysis to quantify the impact of CTTN/cortactin alterations on clinicopathological and survival variables. Results Eighteen studies (1633 patients) met inclusion criteria. Quantitative evaluation revealed a strong association of CTTN/cortactin alterations with N+ status (P < .001), higher T status (P < .001), advanced clinical stage (P < .001), high histological grade (P = .001), and lower overall survival (OS) (P < .001). We found heterogeneity in T status, histological grade, and OS and observed small‐study effects on N status and OS. In subgroup analyses, a significant association of CTTN amplification and cortactin overexpression with the above variables was preserved. The strongest association between CTTN/cortactin alterations and a worse outcome was observed in the subgroups of Asian patients and pharyngolaryngeal squamous cell carcinomas. Conclusions CTTN/cortactin alterations should be evaluated to predict the HNSCC prognosis.

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Section: Resultsmentioning

confidence: 99%

Section: Results Of the Search Of The Literaturementioning

confidence: 99%

Prognostic and clinicopathological significance of CTTN/cortactin alterations in head and neck squamous cell carcinoma: Systematic review and meta‐analysis

et al. 2018

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“…The tumour suppressor candidate 3 ( TUSC3 ) is located in chromosomal region 8p22, in which allelic losses are frequent in a variety of epithelial malignancies . In CRC, an association of 8p allelic loss with poor outcome in CRC has been reported .…”

Section: Discussionmentioning

confidence: 99%

TUSC3 promotes colorectal cancer progression and epithelial-mesenchymal transition (EMT) through WNT/β-catenin and MAPK signalling

Wang

Guo

et al. 2016

J. Pathol.

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Colorectal cancer (CRC) is one of the most common malignancies and is the second leading cause of cancer death in humans. Tumour suppressor candidate 3 (TUSC3) plays an important role in embryogenesis and metabolism. Deletion of TUSC3 often causes non-syndromic mental retardation. Even though TUSC3 deregulation is frequently observed in epithelial cancers, the function of TUSC3 in CRC has remained unknown. In this study, we observed greater expression of TUSC3 at the mRNA and protein level in clinical colorectal tumour samples compared with paired normal tissues. Gain- and loss-of-function analyses were performed to evaluate the functional significance of TUSC3 in CRC initiation and progression. Immunoblotting, immunofluorescence, and co-immunoprecipitation analyses were used to identify potential pathways with which TUSC3 might be involved. Overexpression of TUSC3 in CRC cells induced epithelial-mesenchymal transition (EMT) in CRC cells, accompanied by down-regulation of the epithelial marker, E-cadherin, and up-regulation of the mesenchymal marker, vimentin. Increased proliferation, migration, and invasion, as well as accelerated xenograft tumour growth, were observed in TUSC3-overexpressing CRC cells, while opposite effects were achieved in TUSC3-silenced cells. In conclusion, our study demonstrated the oncogenic role of TUSC3 in CRC and showed that TUSC3 may be responsible for alternations in the proliferation ability, aggressiveness, and invasive/metastatic potential of CRC through regulating the MAPK, PI3K/Akt, and Wnt/β-catenin signalling pathways.

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“…NO has garnered our attention because it has been reported to regulate caveolin-1 through direct nitration [39], S-nitrosylation [29], or indirectly interfering with its ubiquitination [40]. Anoxia/reoxygenation increases iNOS-derived NO generation in hippocampal slices [41].…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Interacts with Caveolin-1 to Facilitate Autophagy-Lysosome-Mediated Claudin-5 Degradation in Oxygen-Glucose Deprivation-Treated Endothelial Cells

et al. 2015

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Using in vitro oxygen-glucose deprivation (OGD) model, we have previously demonstrated that 2-h OGD induces rapid, caveolin-1-mediated dissociation of claudin-5 from the cellular cytoskeletal framework and quick endothelial barrier disruption. In this study, we further investigated the fate of translocated claudin-5 and the mechanisms by which OGD promotes caveolin-1 translocation. Exposure of bEND3 cells to 4-h OGD, but not 2-h OGD plus 2-h reoxygenation, resulted in claudin-5 degradation. Inhibition of autophagy or the fusion of autophagosome with lysosome, but not proteasome, blocked OGD-induced claudin-5 degradation. Moreover, knockdown of caveolin-1 with siRNA blocked OGD-induced claudin-5 degradation. Western blot analysis showed a transient colocalization of caveolin-1, claudin-5, and LC3B in autolysosome or lipid raft fractions at 2-h OGD. Of note, inhibiting autophagosome and lysosome fusion sustained the colocalization of caveolin-1, claudin-5, and LC3B throughout the 4-h OGD exposure. EPR spin trapping showed increased nitric oxide (NO) generation in 2-h OGD-treated cells, and inhibiting NO with its scavenger C-PTIO or inducible nitric oxide synthase (iNOS) inhibitor 1400W prevented OGD-induced caveolin-1 translocation and claudin-5 degradation. Taken together, our data provide a novel mechanism underlying endothelial barrier disruption under prolonged ischemic conditions, in which NO promotes caveolin-1-mediated delivery of claudin-5 to the autophagosome for autophagy-lysosome-dependent degradation.

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Genetic gains and losses in oral squamous cell carcinoma: impact on clinical management

Abstract: Our results point towards relevance of the above mentioned cancer-related genes as putative genetic markers for oral cancer. For practical clinical purposes, these genetic markers should be validated in additional studies.

Cited by 47 publications

References 46 publications

Prognostic and clinicopathological significance of CTTN/cortactin alterations in head and neck squamous cell carcinoma: Systematic review and meta‐analysis

Prognostic and clinicopathological significance of CTTN/cortactin alterations in head and neck squamous cell carcinoma: Systematic review and meta‐analysis

TUSC3 promotes colorectal cancer progression and epithelial-mesenchymal transition (EMT) through WNT/β-catenin and MAPK signalling

Nitric Oxide Interacts with Caveolin-1 to Facilitate Autophagy-Lysosome-Mediated Claudin-5 Degradation in Oxygen-Glucose Deprivation-Treated Endothelial Cells

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