Adipose-derived stromal cell secretome disrupts autophagy in glioblastoma.
Onzi GR., Faccioni JL., Pereira LC., Thomé MP., Bertoni APS., Buss JH.
Prospective Study, published in J Mol Med (Berl) (2019) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- J Mol Med (Berl) (2019)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31401659
- DOI
- 10.1007/s00109-019-01829-2
Abstract (original English)
Mesenchymal stromal cells (MSCs) are frequently recruited to tumor sites to play a part in the tumor microenvironment (TME). However, their real impact on cancer cell behavior remains obscure. Here we investigated the effects of human adipose-derived stromal cell (hADSC) secretome in autophagy of glioblastoma (GBM), as a way to better comprehend how hADSCs influence the TME. GBM U-87 MG cells were treated with conditioned medium (CM) from hADSCs and autophagic flux was evaluated. hADSC CM treatment blocked the autophagic flux in tumor cells, as indicated by the accumulation of autophagosomes in the cytosol, the high LC3-II and p62/SQSTM1 protein levels, and the lack of increase in the amount of acidic vesicular organelles. These effects were further detected in other GBM cell lines tested and also in co-cultures of hADSCs and U-87 MG. hADSC CM did not compromise lysosomal acidification; however, it was able to activate mTORC1 signaling and, as a consequence, led to a decrease in the nuclear translocation of TFEB, a master transcriptional regulator of lysosomal biogenesis and autophagy, thereby contributing to a defective autophagic process. hADSCs secrete transforming growth factor beta 1 (TGFβ1) and this cytokine is an important mediator of CM effects on autophagy. A comprehensive knowledge of MSC roles in tumor biology is of great importance to shed light on the complex dialo
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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