https://transhumanist.ru/index.php?action=history&feed=atom&title=ABI3BPABI3BP - История изменений2026-08-17T18:11:49ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=ABI3BP&diff=5782&oldid=prevOdysseusBot: Новая страница: «Target of Nesh-SH3 precursor (Tarsh) (ABI gene family member 3-binding protein) (Nesh-binding protein) (NeshBP) [NESHBP] [TARSH] ==Publications== {{medline-entr...»2021-05-12T14:51:19Z<p>Новая страница: «Target of Nesh-SH3 precursor (Tarsh) (ABI gene family member 3-binding protein) (Nesh-binding protein) (NeshBP) [NESHBP] [TARSH] ==Publications== {{medline-entr...»</p>
<p><b>Новая страница</b></p><div>Target of Nesh-SH3 precursor (Tarsh) (ABI gene family member 3-binding protein) (Nesh-binding protein) (NeshBP) [NESHBP] [TARSH]<br />
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==Publications==<br />
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{{medline-entry<br />
|title=Long noncoding RNA MALAT1 potentiates growth and inhibits senescence by antagonizing [[ABI3BP]] in gallbladder cancer cells.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31174563<br />
|abstract=Gallbladder cancer (GBC) is the most malignant cancer occurring in the biliary tract cancer featured with undesirable prognosis, in which most patients die within a year of cholecystectomy. Long noncoding RNAs (lncRNAs) function as critical regulators of multiple stages of cancers. Herein, the mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in GBC is investigated. Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up-regulated while that of the ABI family member 3 binding protein ([[ABI3BP]]) was down-regulated in GBC tissues and cell lines. Kaplan-Meier method was then adopted to analyze the relationship between the MALAT1 expression and overall survival and disease-free survival of patients with GBC. A set of in vitro and in vivo experiments were conducted by transducing [[ABI3BP]]-vector or sh-MALAT1 into GBC cells. The results confirmed that the cancer prevention effects triggered by restored [[ABI3BP]] and depleted MALAT1 as evidenced by suppressed cell growth and enhanced cell senescence. MALAT1 was observed to down-regulate [[ABI3BP]] expression through recruitment of the enhancer of zeste homolog 2 ([[EZH2]]) to the [[ABI3BP]] promoter region while the silencing of MALAT1 or suppression of H3K27 methylation was observed to promote the expression of [[ABI3BP]]. Furthermore, GBC patients with high expression of MALAT1 indicated poor prognosis. The current study clarifies that MALAT1 silencing and [[ABI3BP]] elevation impede the GBC development through the H3K27 methylation suppression induced by [[EZH2]], highlighting a promising competitive paradigm for therapeutic approaches of GBC.<br />
|mesh-terms=* Adult<br />
* Animals<br />
* Carrier Proteins<br />
* Cell Line, Tumor<br />
* Cell Movement<br />
* Cell Proliferation<br />
* Cell Transformation, Neoplastic<br />
* Cellular Senescence<br />
* Disease Models, Animal<br />
* Female<br />
* Gallbladder Neoplasms<br />
* Gene Expression Regulation, Neoplastic<br />
* Heterografts<br />
* Histones<br />
* Humans<br />
* Male<br />
* Methylation<br />
* Mice<br />
* Middle Aged<br />
* Models, Biological<br />
* Prognosis<br />
* RNA Interference<br />
* RNA, Long Noncoding<br />
* Young Adult<br />
|keywords=* ABI family member 3 binding protein<br />
* Enhancer of zeste homolog 2<br />
* Gallbladder cancer<br />
* Growth<br />
* Histone<br />
* Metastasis associated lung adenocarcinoma transcript 1<br />
* Methylation<br />
* Senescence<br />
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6555920<br />
}}</div>OdysseusBot