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Expression of interleukin‐12 by adipose‐derived mesenchymal stem cells for treatment of lung adenocarcinoma
Author(s) -
Li Xin,
Zhang Peng,
Liu Xiaozhi,
Lv Peng
Publication year - 2015
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.12151
Subject(s) - medicine , mesenchymal stem cell , adipose tissue , lung , adenocarcinoma , cancer research , interleukin , pathology , cytokine , cancer
Background S tudies 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 ( AMSC s), 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 AMSC s through transgenic technology and utilize the paracrine effect of IL ‐12 to inhibit lung adenocarcinoma cell migration and invasion. Methods Adipose‐derived AMSC s were transduced with lentivirus encoding IL ‐12. IL ‐12/ AMSC s and lung adenocarcinoma A 549 cells were co‐cultured using a cylinder column to assess cellular attraction, and expression of K i67 was detected. Dual‐chamber transwell experiments were used to assess migration and invasiveness of A 549 cells exposed to conditioned media from IL ‐12/ AMSC s. Results When A 549 cells were co‐cultured with lentivirus vectors ( LV )‐ IL ‐12‐green fluorescent protein ( GFP )/ AMSC s, 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 K i67‐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 / AMSC s, the percentage of the invasive A 549 cells was low (31.55 ± 6.21% vs. 70.65 ± 10.46% vs. 68.65 ± 9.50%) ( F = 27.494, P < 0.05). The percentages of colonized A549 cells that invaded the culture media of LV ‐ IL ‐12‐ GFP / AMSC s were low (4.46 ± 1.21 vs. 10.11 ± 2.07 vs. 9.48 ± 1.4) ( F = 23.219, P < 0.05). Conclusions AMSC s could target lung carcinoma and mediate stable expression of IL ‐12, to play a role in tumor treatment.

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