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Smith, Gary R.; Missailidis, Sotiris

doi:10.1186/1476-9255-1-3

Cited by 90 publications

(18 citation statements)

References 82 publications

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“…The involvement of the AT2R in the metastasis and progression of CRC is probably associated with the expression of various growth factors including EGFR [22], TGF-β [23], VEGF [18,24] and CD44 [25]. Further in vitro and in vivo experimental studies are needed to fully understand the underlying mechanisms and function of the AT2R in liver metastasis associated with CRC.…”

Section: Discussionmentioning

confidence: 99%

Role of Two Types of Angiotensin II Receptors in Colorectal Carcinoma Progression

et al. 2014

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Angiotensin II (Ang-II) is a bioactive peptide associated closely with the progression and metastasis of colorectal cancer (CRC). We examined the expression and role of 2 Ang-II receptor types in 20 cases of CRC. Ang-II type 1 receptor (AT1R) protein was localized to the plasma membrane, whereas Ang-II type 2 receptor (AT2R) protein was localized to the nuclei. AT1R expression showed a direct correlation with tumor stage and liver metastasis, whereas AT2R expression showed an inverse correlation. A knockdown study of the AT1R or AT2R with Ang-II treatment was performed to reveal their individual roles in a mouse rectal cell line CMT93, which expresses both Ang-II receptor types. AT2R knockdown showed that the AT1R was associated with tumor growth, survival, invasion and VEGF-A secretion in CMT93 cells in a dose-dependent manner. In contrast, AT1R knockdown showed that the AT2R was associated with increased VEGF-A secretion at low Ang-II concentrations, whereas high concentrations of Ang-II inhibited tumor growth, survival, invasion and VEGF-A secretion. Thus, the AT1R showed a monophasic protumoral effect, while the AT2R showed a biphasic amphitumoral effect. Our findings suggest that a high angiotensinogen condition in the liver might evoke the antitumoral role of the AT2R in CRC cells.

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Section: Discussionmentioning

confidence: 99%

Role of Two Types of Angiotensin II Receptors in Colorectal Carcinoma Progression

et al. 2014

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“…Oncogenic changes in cancer cells, including mutations in receptor tyrosine kinase or Wnt signalling pathways, render them especially responsive to EMT-inducing signals originating in the tumour stroma [38]. The tumour environment is often viewed as a "wound that never heals", with a chronic inflammatory environment that continually drives EMT of cancer cells at the tumour-stroma interface [39,40]. The induction of EMT is mediated by key transcription factors within the cell, including Slug, Snail and Twist.…”

Section: Cancer Stem Cells and Emtmentioning

confidence: 99%

Cancer stem cells and EMT in carcinoma

Biddle

Mackenzie

2012

Cancer Metastasis Rev

148

118

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The majority of deaths from carcinoma are caused by secondary growths that result from tumour invasion and metastasis. The importance of epithelial-to-mesenchymal transition (EMT) as a driver of invasion and metastasis is increasingly recognised, and recent evidence has highlighted a link between EMT and the cancer stem cells that initiate and maintain tumours and have also been implicated in invasion and metastasis. Here, we review cancer stem cells and their link with EMT, and explore the importance of this link in metastasis and therapeutic resistance of tumours. We also discuss new evidence from our laboratory demonstrating that cancer stem cells display a remarkable phenotypic plasticity that enables them to switch between an epithelial phenotype that drives tumour growth and an EMT phenotype that drives metastasis. As successful therapies must eradicate cancer stem cells in all their guises, the identification of sub-types of cancer stem cells that display therapeutic resistance and phenotypic plasticity has important implications for the future design of therapeutic strategies. The ability to assay the responses of different cancer stem cell phenotypes in vitro holds promise for the rapid development of a new generation of targeted therapies that fulfil this objective.

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“…Angiotensin II type 1 (AT1) receptors are regulated by oxidative stress and hypoxia, and are therefore important in cancer-related inflammation (97). AT1 receptor signaling activates fibroblasts, contributing to fibrosis.…”

Section: Targeting Inflammation To Prevent or Treat Cancermentioning

confidence: 99%

Cancer and inflammation

Munn

2016

WIREs Mechanisms of Disease

205

134

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The relationship between inflammation and cancer has been recognized since the 17th century (6), and we now know much about the cells, cytokines and physiological processes that are central to both inflammation and cancer (39, 62, 66–68, 86, 92, 125). Chronic inflammation can induce certain cancers (11, 14, 27, 59, 61, 76, 79, 82), and solid tumors, in turn, can initiate and perpetuate local inflammatory processes that foster tumor growth and dissemination (7, 17, 67, 96). Consequently, inflammatory pathways have been targeted in attempts to control cancer (22, 46, 47). Inflammation is a central aspect of the innate immune system’s response to tissue damage or infection, and also facilitates the recruitment of circulating cells and antibodies of the adaptive immune response to the tissue. Components of the innate immune response carry out a robust, but sometimes overly-conservative response, sacrificing specificity for the sake of preservation. Thus, when innate immunity goes awry, it can have profound implications. How the innate and adaptive immune systems cooperate to neutralize pathogens and repair damaged tissues is still an area of intense investigation. Further, how these systems can respond to cancer, which arises from normal “self” cells that undergo an oncogenic transformation, has profound implications for cancer therapy. Recently, immunotherapies that activate adaptive immunity have shown unprecedented promise in the clinic, producing durable responses and dramatic increases in survival rate in patients with advanced stage melanoma (84, 119, 121). Consequently, the relationship between cancer and inflammation has now returned to the forefront of clinical oncology.

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Cited by 90 publications

References 82 publications

Role of Two Types of Angiotensin II Receptors in Colorectal Carcinoma Progression

Role of Two Types of Angiotensin II Receptors in Colorectal Carcinoma Progression

Cancer stem cells and EMT in carcinoma

Cancer and inflammation

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