https://transhumanist.ru/index.php?action=history&feed=atom&title=LPAR3 2026-06-08T06:08:37Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=LPAR3&diff=4646&oldid=prev 2021-04-29T19:27:59Z

<p>Новая страница: «Lysophosphatidic acid receptor 3 (LPA receptor 3) (LPA-3) (Lysophosphatidic acid receptor Edg-7) [EDG7] [LPA3] ==Publications== {{medline-entry |title=Upregulat...»</p> <p><b>Новая страница</b></p><div>Lysophosphatidic acid receptor 3 (LPA receptor 3) (LPA-3) (Lysophosphatidic acid receptor Edg-7) [EDG7] [LPA3]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Upregulated microRNA-15b alleviates ovarian cancer through inhitbition of the PI3K/Akt pathway by targeting [[LPAR3]].<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31140597<br /> |abstract=Ovarian cancer characterizes as the fourth leading consequence of death associated with cancer for women. Accumulating evidence underscores the vital roles of microRNAs (miRNAs) in preventing ovarian cancer development. Besides, induction of the phosphatidylinositol-3 kinase/serine/threonine kinase (PI3K/Akt) pathway associated with the ovarian cancer cell migration and invasion. The study aims to examine the effects of miR-15b on the proliferation, apoptosis, and senescence of human ovarian cancer cells by binding to lysophosphatidic acid receptor 3 ([[LPAR3]]) with the involvement of the PI3K/Akt pathway. The positive expression of [[LPAR3]] protein was detected by immunohistochemistry. Then the interaction between miR-15b and [[LPAR3]] was examined. The possible role of miR-15b in ovarian cancer was explored using gain- and loss-of-function experiments. Subsequently, the functions of miR-15b on PI3K/Akt pathway, proliferation, migration, invasion, senescence and apoptosis of ovarian cancer cells were assessed. Furthermore, in vivo tumorigenicity assay in nude mice was performed. [[LPAR3]] was overexpressed, whereas miR-15b was poorly expressed in ovarian cancer tissues. [[LPAR3]] is a direct target of miR-15b. Restored miR-15b promoted Bax expression, apoptosis, and senescence, inhibited expression of [[LPAR3]] and Bcl-2, the extent of PI3K and Akt phosphorylation, as well as ovarian cancer cell proliferation, migration, and invasion. Further, tumor growth was observed to be prevented by miR-15b overexpression. Collectively, our study demonstrates that miR-15b represses the proliferation and drives the senescence and apoptosis of ovarian cancer cells through the suppression of [[LPAR3]] and the PI3K/Akt pathway, highlighting an antitumorigenic role of miR-15b.<br /> |mesh-terms=* Adult<br /> * Aged<br /> * Animals<br /> * Cell Line, Tumor<br /> * Cell Movement<br /> * Cell Proliferation<br /> * Female<br /> * Gene Expression Regulation, Neoplastic<br /> * Humans<br /> * Mice, Nude<br /> * MicroRNAs<br /> * Middle Aged<br /> * Neoplasm Invasiveness<br /> * Ovarian Neoplasms<br /> * Phosphatidylinositol 3-Kinases<br /> * Proto-Oncogene Proteins c-akt<br /> * Proto-Oncogene Proteins c-bcl-2<br /> * Receptors, Lysophosphatidic Acid<br /> * Signal Transduction<br /> * Up-Regulation<br /> |keywords=* LPAR3<br /> * PI3K/Akt pathway<br /> * apoptosis<br /> * microRNA-15b<br /> * ovarian cancer<br /> * proliferation<br /> * senescence<br /> |full-text-url=https://sci-hub.do/10.1002/jcp.28799<br /> }}</div>

OdysseusBot