Expression of interleukin-12 by adipose-derived mesenchymal stem cells for treatment of lung adenocarcinoma.
Li X., Zhang P., Liu X., Lv P.
Laboratory Study, published in Thorac Cancer (2015) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- 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
- Laboratory Study
- Journal
- Thorac Cancer (2015)
- Country
- Singapore
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 26273339
- PMCID
- PMC4448467
- DOI
- 10.1111/1759-7714.12151
- Citations
- 16
Abstract (original English)
Studies have revealed mesenchymal cells tend to directionally migrate toward tumor cells and inhibit tumor growth. However, there have been rare reports about adipose-derived mesenchymal stem cells (AMSCs), which achieved stable expression of interleukin (IL)-12 to inhibit lung adenocarcinoma cell migration and invasion. We aimed to achieve stable expression of IL-12 in AMSCs through transgenic technology and utilize the paracrine effect of IL-12 to inhibit lung adenocarcinoma cell migration and invasion. Adipose-derived AMSCs were transduced with lentivirus encoding IL-12. IL-12/AMSCs and lung adenocarcinoma A549 cells were co-cultured using a cylinder column to assess cellular attraction, and expression of Ki67 was detected. Dual-chamber transwell experiments were used to assess migration and invasiveness of A549 cells exposed to conditioned media from IL-12/AMSCs. When A549 cells were co-cultured with lentivirus vectors (LV)-IL-12-green fluorescent protein (GFP)/AMSCs, the intercellular distance was great (346.44 ± 41.07 μm vs. 201.58 ± 27.96 μm vs. 191.45 ± 24.07 μm) (F = 25.414, P < 0.05); the Ki67-positive rate was low (59.13 ± 17.21% vs. 92.31 ± 6.11% vs. 94.25 ± 5.27%) (F = 21.426, P < 0.05). When the lower Transwell chamber contained culture medium from LV-IL-12-GFP/AMSCs, the percentage of the invasive A549 cells was low (31.55 ± 6.21% vs. 70.65 ± 10.46% vs. 68.65 ± 9
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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