Downregulation of VEGF-C expression in lung and colon cancer cells decelerates tumor growth and inhibits metastasis via multiple mechanisms

Khromova, N.; Kopnin, Pavel; Rybko,; Bp, Kopnin

doi:10.1038/onc.2011.330

Cited by 69 publications

(54 citation statements)

References 36 publications

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“…Inhibition of tumoral lymphangiogenesis through neutralization of VEGFR3 or knockdown of VEGF-C expression blocks metastasis in vivo [101][102][103], indicating that this process is essential for metastasis in a variety of cancer models. Interestingly, this inhibition did not affect the normal lymphatic vasculature in adult mice, suggesting that alternative signaling mechanisms are employed after development, and targeting the VEGF-C/VEGFR3 signaling axis in adults may represent a potent means to target the tumor-associated lymphatics [104].…”

Section: Lymphangiogenesis and Cancermentioning

confidence: 99%

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

2011

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Angiogenesis, the formation of new blood vessels from preexisting vasculature, is essential for many physiological processes, and aberrant angiogenesis contributes to some of the most prevalent human diseases, including cancer. Angiogenesis is controlled by delicate balance between pro-and anti-angiogenic signals. While pro-angiogenic signaling has been extensively investigated, how developmentally regulated, naturally occurring anti-angiogenic molecules prevent the excessive growth of vascular and lymphatic vessels is still poorly understood. In this review, we summarize the current knowledge on how semaphorins and their receptors, plexins and neuropilins, control normal and pathological angiogenesis, with an emphasis on semaphorin-regulated anti-angiogenic signaling circuitries in vascular and lymphatic endothelial cells. This emerging body of information may afford the opportunity to develop novel anti-angiogenic therapeutic strategies.

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Section: Lymphangiogenesis and Cancermentioning

confidence: 99%

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

2011

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“…Inhibition of VEGF-C in lung cancer cells increased epithelial but decreased mesenchymal markers, as well as decreased side population (dye efflux property of putative cancer stem cell population) and tumorigenicity in vivo. 36 In breast cancer, VEGF-C level was enriched in a CD44þ/CD24-/low tumor initiating population isolated from breast cancer lesions 37 and inhibition of VEGF-C expression decreased aldehyde dehydrogenase positive population and tumor formation.…”

Section: Emerging Role Of Vegf-c In Cancer Stemnessmentioning

confidence: 99%

The non-canonical role of vascular endothelial growth factor-C axis in cancer progression

Wang

Tsai

2015

Exp Biol Med (Maywood)

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It has been shown in many clinical studies that the level of vascular endothelial growth factor-C (VEGF-C) positively correlates with lymph node metastasis. Nevertheless, beyond the canonical role of VEGF-C in stimulating lymphangiogenesis and thus promoting lymph node/distant metastasis, emerging evidence indicates that expression of VEGF-C contributes to various aspects of carcinogenicity via autocrine regulation. The newly identified functions of VEGF-C include but are not limited to proliferation, migration, invasion, and chemo-resistance. Besides tumor cell autocrine regulation, VEGF-C can also modulate the immune system such that tumor cells more easily escape immune surveillance. Therefore, understanding the functional roles and regulatory mechanisms related to the VEGF-C axis may lead to alternative strategies for cancer treatment. This mini-review will focus on summarizing recent discoveries regarding the unconventional functions of VEGF-C in cancer progression.

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“…Its suppression leads simultaneously both to reversion of EMT and to significant decrease in number of tumor cells in the population that could form colonies on semisolid medium [173]. It is important that cells as a result of EMT acquired typical features of tumor stem cells both on receptor levels and on the level of mor phology and behavior [3,4,174].…”

Section: Can Normal Cells Demonstrate Plasticity Of Migration Mechanimentioning

confidence: 99%

Plasticity of tumor cell migration: acquisition of new properties or return to the past?

Alexandrova¹

2014

Biochemistry Moscow

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During tumor development cancer cells pass through several stages when cell morphology and migration abilities change remarkably. These stages are named epithelial-mesenchymal and mesenchymal-amoeboid transitions. The molecular mechanisms underlying cell motility are changing during these transitions. As result of transitions the cells acquire new characteristics and modes of motility. Cell migration becomes more independent from the environmental conditions, and thus cell dissemination becomes more aggressive, which leads to formation of distant metastases. In this review we discuss the characteristics of each of the transitions, cell morphology, and the specificity of cellular structures responsible for different modes of cell motility as well as molecular mechanisms regulating each transition.

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Downregulation of VEGF-C expression in lung and colon cancer cells decelerates tumor growth and inhibits metastasis via multiple mechanisms

Cited by 69 publications

References 36 publications

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

The non-canonical role of vascular endothelial growth factor-C axis in cancer progression

Plasticity of tumor cell migration: acquisition of new properties or return to the past?

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