Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 20, Issue 14, Pages -Publisher
MDPI
DOI: 10.3390/ijms20143568
Keywords
TGF-beta; ovarian cancer; EMT; SKOV3; 3D models
Funding
- Weill Cornell Medicine and Qatar Foundation (BMRP)
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Transcriptome profiling of 3D models compared to 2D models in various cancer cell lines shows differential expression of TGF-beta-mediated and cell adhesion pathways. Presence of TGF-beta in these cell lines shows an increased invasion potential which is specific to cell type. In the present study, we identified exogenous addition of TGF-beta can induce Epithelial to Mesenchymal Transition (EMT) in a few cancer cell lines. RNA sequencing and real time PCR were carried out in different ovarian cancer cell lines to identify molecular profiling and metabolic profiling. Since EMT induction by TGF- beta is cell-type specific, we decided to select two promising ovarian cancer cell lines as model systems to study EMT. TGF-beta modulation in EMT and cancer invasion were successfully depicted in both 2D and 3D models of SKOV3 and CAOV3 cell lines. Functional evaluation in 3D and 2D models demonstrates that the addition of the exogenous TGF- beta can induce EMT and invasion in cancer cells by turning them into aggressive phenotypes. TGF-beta receptor kinase I inhibitor (LY364947) can revert the TGF-beta effect in these cells. In a nutshell, TGF-beta can induce EMT and migration, increase aggressiveness, increase cell survival, alter cell characteristics, remodel the Extracellular Matrix (ECM) and increase cell metabolism favorable for tumor invasion and metastasis. We concluded that transcriptomic and phenotypic effect of TGF-beta and its inhibitor is cell-type specific and not cancer specific.
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