Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.B1 (angiotensin-converting enzyme 2)
 1,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin-angiotensin system (RAS) is known mainly as a regulator of cardiovascular homeostasis. However, it has also been shown to mediate processes such as proliferation, apoptosis, angiogenesis, and carcinogenesis. Nonmelanoma skin cancers (NMSC) - including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) - are among the most common cancers. The aim of the present study was to determine the immunohistochemical expression of angiotensin-converting enzyme (ACE), angiotensin-converting enzyme 2 (ACE2), and Ki-67 antigen in archival samples of normal skin, actinic keratosis, and malignant skin lesions. Cytoplasmic-nuclear ACE immunoreactivity was observed in 99% of examined cases of both normal skin and cancers. Significantly higher ACE immunoreactivity occurred in normal skin, as compared with BCC and SCC (p < 0.01, p < 0.0001, respectively). Additionally, ACE immunoreactivity was also significantly higher in BCC, compared with SCC (p < 0.05). ACE2 immunoreactivity was noted in basal epidermal layers and in sebaceous gland cells in normal skin, though not in NMSC. These novel observations suggest that ACE and skin RAS may be involved in the pathogenesis of malignant skin lesions.
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PMID:ACE and ACE2 expression in normal and malignant skin lesions. 2420 30

Angiotensin II (Ang II) is the product of the proteolytic action of angiotensin-converting enzyme (ACE) on the precursor peptide, angiotensin I (Ang I). In addition to its vasoactive properties, Ang II is able to stimulate angiogenesis and act as a mitogen, promoting cellular proliferation. Recently, evidence has emerged that Ang II is also able to promote tumour invasion, a key step in the metastatic cascade, although the mechanisms by which it does so remain largely obscure. Here we show that Ang II is able to promote the invasion and migration of head and neck squamous cell carcinoma (HNSCC) cells both in an autocrine manner and by triggering stromal tumour-paracrine interactions. The effects of Ang II on autocrine and paracrine signalling pathways are mediated by angiotensin receptor 1 (AT1 R) and inhibited by angiotensin 1-7 (Ang 1-7), a peptide produced from Ang II by the action of angiotensin-converting enzyme 2 (ACE2). These data are the first to demonstrate a role for the renin-angiotensin system in oral carcinogenesis and raise the possibility of utilizing AT1 R receptor antagonists and/or Ang 1-7 as novel therapeutic agents for HNSCC.
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PMID:Angiotensin 1-7 inhibits angiotensin II-stimulated head and neck cancer progression. 2865 23

Transmembrane serine protease 2 is encoded by the TMPRSS2 gene. The gene is widely conserved and has two isoforms, both being autocatalytically activated from the inactive zymogen form. A fusion gene between the TMPRSS2 gene and ERG (erythroblast-specific-related gene), an oncogenic transcription factor, is the most common chromosomal aberration detected in prostate cancer, responsible for driving carcinogenesis. The other key role of TMPRSS2 is in priming the viral spike protein which facilitates viral entry essential for viral infectivity. The protease activates a diverse range of viruses. Both SARS-CoV and SARS-CoV-2 (COVID-19) use angiotensin-converting enzyme 2 (ACE2) and TMPRSS2 to facilitate entry to cells, but with SARS-CoV-2 human-to-human transmission is much higher than SARS-CoV. As TMPRSS2 is expressed outside of the lung, and can therefore contribute to extrapulmonary spread of viruses, it warrants further exploration as a potential target for limiting viral spread and infectivity.
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PMID:Gene of the month: TMPRSS2 (transmembrane serine protease 2). 3287