About: Transdifferentiation of MALME-3M and MCF-7 Cells toward Adipocyte-like Cells is Dependent on Clathrin-mediated Endocytosis

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About: Transdifferentiation of MALME-3M and MCF-7 Cells toward Adipocyte-like Cells is Dependent on Clathrin-mediated Endocytosis 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	Transdifferentiation of MALME-3M and MCF-7 Cells toward Adipocyte-like Cells is Dependent on Clathrin-mediated Endocytosis
Creator	Aguilar-Gallardo, Cristóbal Carcel-Trullols, Jaime Conesa, Ana Dopazo, Joaquin Garcia-Alcalde, Fernando Simón, Carlos Pardo-Cea, Miguel
Source	Medline; PMC
abstract	ABSTRACT: Enforced cell transdifferentiation of human cancer cells is a promising alternative to conventional chemotherapy. We previously identified albumin-associated lipid- and, more specifically, saturated fatty acid-induced transdifferentiation programs in human cancer cells (HCCLs). In this study, we further characterized the adipocyte-like cells, resulting from the transdifferentiation of human cancer cell lines MCF-7 and MALME-3M, and proposed a common mechanistic approach for these transdifferentiating programs. We showed the loss of pigmentation in MALME-3M cells treated with albumin-associated lipids, based on electron microscopic analysis, and the overexpression of perilipin 2 (PLIN2) by western blotting in MALME-3M and MCF-7 cells treated with unsaturated fatty acids. Comparing the gene expression profiles of naive melanoma MALME-3M cells and albumin-associated lipid-treated cells, based on RNA sequencing, we confirmed the transcriptional upregulation of some key adipogenic gene markers and also an alternative splicing of the adipogenic master regulator PPARG, that is probably related to the reported up regulated expression of the protein. Most importantly, these results also showed the upregulation of genes responsible for Clathrin (CLTC) and other adaptor-related proteins. An increase in CLTC expression in the transdifferentiated cells was confirmed by western blotting. Inactivation of CLTC by chlorpromazine (CHP), an inhibitor of CTLC mediated endocytosis (CME), and gene silencing by siRNAs, partially reversed the accumulation of neutral lipids observed in the transdifferentiated cells. These findings give a deeper insight into the phenotypic changes observed in HCCL to adipocyte-like transdifferentiation and point towards CME as a key pathway in distinct transdifferentiation programs. DISCLOSURES: Simon C and Aguilar-Gallardo C are co-inventors of the International Patent Application No. PCT/EP2011/004941 entitled “Methods for tumor treatment and adipogenesis differentiation”. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/2193-1801-1-44) contains supplementary material, which is available to authorized users.
has issue date	2012-10-30(xsd:dateTime)
bibo:doi	10.1186/2193-1801-1-44
bibo:pmid	23961369
has license	cc-by
sha1sum (hex)	fc29089acf4b70c64a5a5e4ea64a318e8d52edbb
schema:url	https://doi.org/10.1186/2193-1801-1-44
resource representing a document's title	Transdifferentiation of MALME-3M and MCF-7 Cells toward Adipocyte-like Cells is Dependent on Clathrin-mediated Endocytosis
has PubMed Central identifier	PMC3725915
has PubMed identifier	23961369
schema:publication	Springerplus
resource representing a document's body	covid:fc29089acf4b70c64a5a5e4ea64a318e8d52edbb#body_text
is schema:about of	named entity 'confirmed' named entity 'PPARG' named entity 'master regulator' named entity 'upregulation' named entity 'gene' named entity 'programs' named entity 'PROBABLY RELATED' named entity 'GENES' named entity 'MCF-7 CELLS' named entity 'LIPID' named entity 'PERILIPIN 2' named entity 'RESULTS' named entity 'TRANSDIFFERENTIATION' named entity 'PPARG' named entity 'MCF-7 CELLS' named entity 'CELLS' named entity 'CELLS' named entity 'PREVIOUSLY' named entity 'APPROACH' named entity 'MCF-7' named entity 'WESTERN BLOTTING' named entity 'RESPONSIBLE' named entity 'A COMMON' covid:arg/fc29089acf4b70c64a5a5e4ea64a318e8d52edbb named entity 'IS A' named entity 'ELECTRON' named entity 'MASTER' named entity 'INSIGHT' named entity 'CONVENTIONAL' named entity 'CHARACTERIZED' named entity 'MELANOMA' named entity 'DEPENDENT' named entity 'LIKE' named entity 'CONFIRMED BY' named entity 'PROTEINS' named entity 'PROGRAMS' named entity 'GENE' named entity 'PATHWAY' named entity 'REGULATED' named entity 'CLATHRIN-MEDIATED ENDOCYTOSIS' named entity 'TRANSDIFFERENTIATION' named entity 'ADIPOCYTE' named entity 'PIGMENTATION' named entity 'UPREGULATION' named entity 'SIRNAS' named entity 'CELL TRANSDIFFERENTIATION' named entity 'ENDOCYTOSIS' named entity 'HUMAN' named entity 'PARTIALLY' named entity 'CHEMOTHERAPY' named entity 'EXPRESSION' named entity 'ALBUMIN' named entity 'RELATED' named entity 'BASED' named entity 'REVERSED' named entity 'CHLORPROMAZINE' named entity 'PROTEIN' named entity 'IDENTIFIED' named entity 'MALME-3M' named entity 'CME' named entity 'STUDY' named entity 'DISTINCT' named entity 'INHIBITOR' named entity 'TRANSDIFFERENTIATING' named entity 'PROPOSED' named entity 'REPORTED' named entity 'OBSERVED' named entity 'ANALYSIS' named entity 'CLATHRIN' named entity 'GENE EXPRESSION PROFILES' named entity 'LIKE' named entity 'RESULTING FROM' named entity 'RNA SEQUENCING' named entity 'POINT' named entity 'COMPARING'

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