Expression of a novel endothelial marker, C-type lectin 14A, in epithelial ovarian cancer and its prognostic significance

Priya, Syama Krishna; Kumar, K. V. S. Hari; Hiran, K. R.; Bindhu, M R; Nagare, Rohit P.; Vijaykumar, D K; Ganesan, Trivadi S.

doi:10.1007/s10147-016-1033-6

Cited by 17 publications

(4 citation statements)

References 40 publications

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“…Clec14A expression is considered endothelial specific. Interestingly, the expression of Clec14A is barely detectable in healthy vessels but strongly upregulated in angiogenic tumor-associated blood vessels of non-small cell lung cancer and ovarian cancer tissues [ 15 , 16 ]. It has been found to regulate EC tube formation and migration in vitro as well as tumor angiogenesis in vivo.…”

Section: Introductionmentioning

confidence: 99%

A glimpse into the past: phylogenesis and protein domain analysis of the group XIV of C-type lectins in vertebrates

Barbera

Cucini

2022

BMC Genomics

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Background The group XIV of C-type lectin domain-containing proteins (CTLDcps) is one of the seventeen groups of CTLDcps discovered in mammals and composed by four members: CD93, Clec14A, CD248 and Thrombomodulin, which have shown to be important players in cancer and vascular biology. Although these proteins belong to the same family, their phylogenetic relationship has never been dissected. To resolve their evolution and characterize their protein domain composition we investigated CTLDcp genes in gnathostomes and cyclostomes and, by means of phylogenetic approaches as well as synteny analyses, we inferred an evolutionary scheme that attempts to unravel their evolution in modern vertebrates. Results Here, we evidenced the paralogy of the group XIV of CTLDcps in gnathostomes and discovered that a gene loss of CD248 and Clec14A occurred in different vertebrate groups, with CD248 being lost due to chromosome disruption in birds, while Clec14A loss in monotremes and marsupials did not involve chromosome rearrangements. Moreover, employing genome annotations of different lampreys as well as one hagfish species, we investigated the origin and evolution of modern group XIV of CTLDcps. Furthermore, we carefully retrieved and annotated gnathostome CTLDcp domains, pointed out important differences in domain composition between gnathostome classes, and assessed codon substitution rate of each domain by analyzing nonsynonymous (Ka) over synonymous (Ks) substitutions using one representative species per gnathostome order. Conclusions CTLDcps appeared with the advent of early vertebrates after a whole genome duplication followed by a sporadic tandem duplication. These duplication events gave rise to three CTLDcps in the ancestral vertebrate that underwent further duplications caused by the independent polyploidizations that characterized the evolution of cyclostomes and gnathostomes. Importantly, our analyses of CTLDcps in gnathostomes revealed critical inter-class differences in both extracellular and intracellular domains, which might help the interpretation of experimental results and the understanding of differences between animal models.

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Section: Introductionmentioning

confidence: 99%

A glimpse into the past: phylogenesis and protein domain analysis of the group XIV of C-type lectins in vertebrates

Barbera

Cucini

2022

BMC Genomics

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“…It was subsequently found to be upregulated at the protein level and increased with tumour progression in two different spontaneous mouse tumour models, namely cervical and pancreatic . More recently, CLEC14A overexpression on the vasculature in ovarian cancer has been reported but did not correlate with survival in this tumour type . The authors also demonstrated that CLEC14A expression was undetectable along with reductions in microvessel density in patients receiving neoadjuvant chemotherapy prior to surgery.…”

Section: Clec14amentioning

confidence: 98%

C‐type lectin domain group 14 proteins in vascular biology, cancer and inflammation

et al. 2019

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The C‐type lectin domain (CTLD) group 14 family of transmembrane glycoproteins consist of thrombomodulin, CD93, CLEC14A and CD248 (endosialin or tumour endothelial marker‐1). These cell surface proteins exhibit similar ectodomain architecture and yet mediate a diverse range of cellular functions, including but not restricted to angiogenesis, inflammation and cell adhesion. Thrombomodulin, CD93 and CLEC14A can be expressed by endothelial cells, whereas CD248 is expressed by vasculature associated pericytes, activated fibroblasts and tumour cells among other cell types. In this article, we review the current literature of these family members including their expression profiles, interacting partners, as well as established and speculated functions. We focus primarily on their roles in the vasculature and inflammation as well as their contributions to tumour immunology. The CTLD group 14 family shares several characteristic features including their ability to be proteolytically cleaved and engagement of some shared extracellular matrix ligands. Each family member has strong links to tumour development and in particular CD93, CLEC14A and CD248 have been proposed as attractive candidate targets for cancer therapy.

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“…Recently, Noy et al reported that tumor growth and vascularity was reduced in a CLEC14a-knockout syngeneic tumor mouse model, compared to wild-type mice [ 207 ]. More recently, Krishna et al, reported that microvessel density, detected using an anti-CLEC14a antibody, was significantly reduced in patients with epithelial ovarian cancer treated with chemotherapy, suggesting that CLEC14a may be a more specific endothelial marker to assess tumor angiogenesis [ 211 ]. Collectively, this evidence suggests that CLEC14a may be a novel tumor endothelial cell-specific marker of tumor angiogenesis and a central regulator of tumor angiogenesis.…”

Section: Clec14a Signalingmentioning

confidence: 99%

A Review of Anti-Angiogenic Targets for Monoclonal Antibody Cancer Therapy

Kong

Kim

Jang

et al. 2017

IJMS

133

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Tumor angiogenesis is a key event that governs tumor progression and metastasis. It is controlled by the complicated and coordinated actions of pro-angiogenic factors and their receptors that become upregulated during tumorigenesis. Over the past several decades, vascular endothelial growth factor (VEGF) signaling has been identified as a central axis in tumor angiogenesis. The remarkable advent of recombinant antibody technology has led to the development of bevacizumab, a humanized antibody that targets VEGF and is a leading clinical therapy to suppress tumor angiogenesis. However, despite the clinical efficacy of bevacizumab, its significant side effects and drug resistance have raised concerns necessitating the identification of novel drug targets and development of novel therapeutics to combat tumor angiogenesis. This review will highlight the role and relevance of VEGF and other potential therapeutic targets and their receptors in angiogenesis. Simultaneously, we will also cover the current status of monoclonal antibodies being developed to target these candidates for cancer therapy.

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Expression of a novel endothelial marker, C-type lectin 14A, in epithelial ovarian cancer and its prognostic significance

Abstract: This study demonstrates MVD as detected by CLEC14A in EOC. Treatment with chemotherapy reduces tumor blood vessels significantly. We suggest that CLEC14A may be a more specific endothelial marker to assess tumor angiogenesis.

Cited by 17 publications

References 40 publications

A glimpse into the past: phylogenesis and protein domain analysis of the group XIV of C-type lectins in vertebrates

A glimpse into the past: phylogenesis and protein domain analysis of the group XIV of C-type lectins in vertebrates

C‐type lectin domain group 14 proteins in vascular biology, cancer and inflammation

A Review of Anti-Angiogenic Targets for Monoclonal Antibody Cancer Therapy

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