Modes of invasion during tumour dissemination

Pandya, Pahini; Orgaz, José L.; Sanz-Moreno, Victoria

doi:10.1002/1878-0261.12019

Cited by 164 publications

(185 citation statements)

References 197 publications

(357 reference statements)

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“…Ultimately, this process results in a gradual loss of epithelial features, and a concurrent acquisition of some mesenchymal traits. At this stage, a switch from collective to single-cell migration takes place, strikingly enhancing the efficiency of the invasion proces 12,13 . In other words, invasive cancer cells partly recapitulate an embryonic program known as epithelial-to-mesenchymal transition (EMT), through which epithelial cells dismantle cell-cell junctions, lose planar and apical-basal polarity, and eventually establish a front-rear axis, thus adopting an elongated, spindle-shaped morphology.…”

Section: Mechanisms Of Cancer Cell Invasivenessmentioning

confidence: 99%

“…Of course, the events described above merely represent a schematic depiction of a gradually evolving and highly dynamic process, during which cancer cells go through a wide spectrum of readily interconvertible phenotypic states, overall enabling the progression from non-motile to invasive carcinomas. EMT itself is a reversible process; indeed, metastatic colonies eventually tend to restore the expression of epithelial traits that are generally turned off throughout dissemination (e.g., cell-cell junctions), and to concomitantly lose the mesenchymal traits 12,13 .…”

Section: Mechanisms Of Cancer Cell Invasivenessmentioning

confidence: 99%

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Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview

et al. 2018

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The acquisition of invasive functions by tumor cells is a first and crucial step towards the development of metastasis, which nowadays represents the main cause of cancer-related death. Cholangiocarcinoma (CCA), a primary liver cancer originating from the biliary epithelium, typically develops intrahepatic or lymph node metastases at early stages, thus preventing the majority of patients from undergoing curative treatments, consistent with their very poor prognosis. As in most carcinomas, CCA cells gradually adopt a motile, mesenchymal-like phenotype, enabling them to cross the basement membrane, detach from the primary tumor, and invade the surrounding stroma. Unfortunately, little is known about the molecular mechanisms that synergistically orchestrate this pro-invasive phenotypic switch. Autocrine and paracrine signals (cyto/chemokines, growth factors, morphogens) permeating the tumor microenvironment undoubtedly play a prominent role in this context. Moreover, a number of recently identified signaling systems are currently drawing attention as putative mechanistic determinants of CCA cell invasion. They encompass transcription factors, protein kinases and phosphatases, ubiquitin ligases, adaptor proteins, and miRNAs, whose aberrant expression may result from either stochastic mutations or the abnormal activation of upstream pro-oncogenic pathways. Herein, we sought to summarize the most relevant molecules in this field, and to discuss their mechanism of action and potential prognostic relevance in CCA. Hopefully, a deeper knowledge of the molecular determinants of CCA invasiveness will help to identify clinically useful biomarkers and novel druggable targets, with the ultimate goal to develop innovative approaches to the management of this devastating malignancy.

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Section: Mechanisms Of Cancer Cell Invasivenessmentioning

confidence: 99%

Section: Mechanisms Of Cancer Cell Invasivenessmentioning

confidence: 99%

Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview

et al. 2018

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“…The role of epithelial to mesenchymal transformation (EMT) is unclear and plasticity of cells that metastasise and their relationship to the primary tumour cells, e.g. stem cells, remains the object of current research ( Pandya et al , 2017). Furthermore, cancers do not appear to disseminate randomly, but exhibit tropism for specific organs, especially lung, liver and bone ( Tarin, 2011).…”

Section: Introductionmentioning

confidence: 99%

Embryonic zebrafish xenograft assay of human cancer metastasis

et al. 2018

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Cancer metastasis is the most important prognostic factor determining patient survival, but currently there are very few drugs or therapies that specifically inhibit the invasion and metastasis of cancer cells. Currently, human cancer metastasis is largely studied using transgenic and immunocompromised mouse xenograft models, which are useful for analysing end-point tumour growth but are unable to accurately and reliably monitor in vivo invasion, intravasation, extravasation or secondary tumour formation of human cancer cells. Furthermore, limits in our ability to accurately monitor early stages of tumour growth and detect micro-metastases likely results in pain and suffering to the mice used for cancer xenograft experiments. Zebrafish ( Danio rerio) embryos, however, offer many advantages as a model system for studying the complex, multi-step processes involved during cancer metastasis. This article describes a detailed method for the analysis of human cancer cell invasion and metastasis in zebrafish embryos before they reach protected status at 5 days post fertilisation. Results demonstrate that human cancer cells actively invade within a zebrafish microenvironment, and form metastatic tumours at secondary tissue sites, suggesting that the mechanisms involved during the different stages of metastasis are conserved between humans and zebrafish, supporting the use of zebrafish embryos as a viable model of human cancer metastasis. We suggest that the embryonic zebrafish xenograft model of human cancer is a tractable laboratory model that can be used to understand cancer biology, and as a direct replacement of mice for the analysis of drugs that target cancer invasion and metastasis.

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“…Tumor invasion and migration are important indications for tumor progression because they are able to obtain information on the degree of malignancy and patient prognosis. 21 Tumor metastasis is a multistage process, which is regulated by several genes, including metastasis-associated genes and metastasis-suppressing genes. 22 A variety of circRNAs affect lung cancer invasion and migration by regulating related targets, such as hsa_circ_0007385, circ-BANP, and circPTK2.…”

Section: Discussionmentioning

confidence: 99%

Circ‐IGF1Rinhibits cell invasion and migration in non‐small cell lung cancer

Xiang

Chen

et al. 2020

Thoracic Cancer

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Background Circular RNA (circRNA) is a novel molecular marker and target candidate that is closely associated with tumor invasion and migration. The mechanism of action of hsa_circ_0005035 (circ‐IGF1R) in non‐small cell lung cancer remains unclear. In this study, we aimed to study the mechanism of action of circ‐IGF1R in lung cancer. Methods We screened circ‐IGF1R, one of the most notable differential expressions, from the Gene Expression Omnibus database, GSE104854, for further research. The expression level of circ‐IGF1R was examined using quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR) in five different lung cancer cell lines and 50 pairs of lung cancer and adjacent tissues. Wound‐healing and Transwell assays were used for verifying the biological function of circ‐IGF1R. The effect of overexpressing circ‐IGF1R on the transcriptome of whole lung cancer cells was explored in lung cancer cell lines using RNA‐seq. Results The expression level of circ‐IGF1R was notably lower in lung cancer tissues and lung cancer cell lines than in the adjacent normal tissues and cells (P < 0.0001). In addition, the expression level of circ‐IGF1R was associated with larger tumors (T2/T3/T4) and lymph node metastasis (N1/ N2/N3) (P < 0.05). The overexpression of circ‐IGF1R significantly inhibited the invasion and migration of the lung cancer cells. The potential network of circ‐IGF1R–miR‐1270–VANGL2 was preliminarily determined, and the expression patterns of miR‐1270 and VANGL2 were verified in lung cancer cell lines. Conclusion Circ‐IGF1R may inhibit lung cancer invasion and migration through a potential network of circ‐IGF1R–miR‐1270–VANGL2.

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Modes of invasion during tumour dissemination

Cited by 164 publications

References 197 publications

Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview

Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview

Embryonic zebrafish xenograft assay of human cancer metastasis

Circ‐IGF1Rinhibits cell invasion and migration in non‐small cell lung cancer

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