About: Pre-treatment with angiotensin-(1–7) inhibits tumor growth via autophagy by downregulating PI3K/Akt/mTOR signaling in human nasopharyngeal carcinoma xenografts

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About: Pre-treatment with angiotensin-(1–7) inhibits tumor growth via autophagy by downregulating PI3K/Akt/mTOR signaling in human nasopharyngeal carcinoma xenografts Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Pre-treatment with angiotensin-(1–7) inhibits tumor growth via autophagy by downregulating PI3K/Akt/mTOR signaling in human nasopharyngeal carcinoma xenografts
Creator	Chien, Chih-Yen Chuang, Hui-Ching Hsu, Yi-Chiang Lin, Yu-Tsai Wang, Hung-Chen Yang, Ming-Yu
Source	PMC
abstract	ABSTRACT: The highest incidence of nasopharyngeal carcinoma (NPC) is in southeast China, including Taiwan. Many side effects have been observed following radiation therapy with chemotherapy; hence, exploring new treatment modalities for NPC is an important future direction. Angiotensin-(1–7) [Ang-(1–7)] is an endogenous heptapeptide hormone and important component of the renin–angiotensin system that acts through both the Mas receptor and AT2 receptor, exhibiting anti-proliferative and anti-angiogenic properties in cancer cells. However, the anti-cancer activity of Ang-(1–7) related to autophagy in NPC remains largely debated. The effects and signaling pathway(s) involved in the Ang-(1–7)/Mas receptor axis in NPC were investigated both in vitro and in vivo. Ang-(1–7) inhibited cell proliferation, migration, and invasion in NPC-TW01 cells. Ang-(1–7) induced autophagy by increasing the levels of the autophagy marker LC3-II and by enhancing p62 degradation via activation of the Beclin-1/Bcl-2 signaling pathway with involvement of the PI3K/Akt/mTOR and p38 pathways in vitro study. In addition, pre-treatment with Ang-(1–7) inhibited tumor growth in NPC xenografts by inducing autophagy, suggesting a correlation between PI3K/Akt/mTOR pathway inhibition and the abovementioned anti-cancer activities. However, no autophagy was observed following Ang-(1–7) post-treatment. Taken together, these data indicate that Ang-(1–7) plays a novel role in autophagy downstream signaling pathways in NPC, supporting its potential as a therapeutic agent for alleviation the incidence of NPC and preventive treatment of recurrent NPC. KEY MESSAGES: Ang-(1–7) inhibits cell proliferation, migration, and invasion by activating autophagy. Ang-(1–7)pre-treatment inhibits tumor growth via autophagy by suppressing PI3K/Akt/mTOR pathway. Ang-(1–7) may provide a novel preventative treatment for NPC and recurrent NPC. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s00109-018-1704-z) contains supplementary material, which is available to authorized users.
has issue date	2018-10-29(xsd:dateTime)
bibo:doi	10.1007/s00109-018-1704-z
bibo:pmid	30374682
has license	no-cc
sha1sum (hex)	a54c5264dc9b37bbb9a6549cf7fc9a96564c9d6d
schema:url	https://doi.org/10.1007/s00109-018-1704-z
resource representing a document's title	Pre-treatment with angiotensin-(1–7) inhibits tumor growth via autophagy by downregulating PI3K/Akt/mTOR signaling in human nasopharyngeal carcinoma xenografts
has PubMed Central identifier	PMC7095977
has PubMed identifier	30374682
schema:publication	J Mol Med (Berl)
resource representing a document's body	covid:a54c5264dc9b37bbb9a6549cf7fc9a96564c9d6d#body_text
is schema:about of	named entity 'EXHIBITING' named entity 'RELATED' named entity 'PROPERTIES' named entity 'INVESTIGATED' named entity 'RECEPTOR' named entity 'DIRECTION' named entity 'HIGHEST' named entity 'ANG' named entity 'ACTIVATION' named entity 'RENIN-ANGIOTENSIN SYSTEM' named entity 'POST-TREATMENT' named entity 'signaling pathways' named entity 'LC3' named entity 'autophagy' named entity 'preventive treatment' named entity 'cancer cells' named entity 'Angiotensin' named entity 'Beclin-1' named entity 'therapeutic agent' named entity 'anti-cancer' named entity 'hormone' named entity 'antiproliferative' named entity 'autophagic' named entity 'nude mice' named entity 'Sigma-Aldrich' named entity 'Autophagy' named entity 'transfection' named entity 'cell proliferation' named entity 'siRNA' named entity 'nasopharyngeal' named entity 'Bcl-2' named entity 'standard deviation' named entity 'autophagy' named entity 'siRNA' named entity 'treatment group' named entity 'AKT' named entity 'type II' named entity 'phosphorylation' named entity 'lung carcinoma' named entity 'serum' named entity 'Taiwan' named entity 'p38' named entity 'autophagosome' named entity 'alternative medicines' named entity 'mice' named entity 'Radiotherapy' named entity 'analysis of variance' named entity 'Basement Membrane' named entity 'Tumor' named entity 'Germany' named entity 'JNK' named entity 'Bcl-2' named entity 'angiotensin II' named entity 'BD Biosciences' named entity 'organelles' named entity 'caspase-3' named entity 'PBS' named entity 'cell apoptosis' named entity 'Wound healing' named entity 'protein' named entity 'lysis buffer' named entity 'immunohistochemistry' named entity 'angiotensin-converting enzyme 2' named entity 'control group' named entity 'blood pressure' named entity 'tumor' named entity 'protein' named entity 'mTOR' named entity 'protein' named entity 'PBS' named entity 'mucositis' named entity 'mounting medium' named entity 'angiotensin-converting enzyme 2' named entity 'treatment of patients' named entity 'citrate' named entity 'ribosomal protein'

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