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Showing 2 results for Cancer Cells

Reyhaneh Khoshchehreh, Mehdi Totonchi, Hossein Baharvand, Marzieh Ebrahimi,
Volume 22, Issue 3 (8-2019)
Abstract

Background and Aim: There is increasing evidence that cancer cells in addition to multiple genetic mutations, also acquire epigenetic abnormalities during development, maintenance, and progression. By utilizing the reprogramming technology as a tool to introduce the ‘pressure’ to alter epigenetic regulations, we might be able to clarify the epigenetic behavior that is unique to cancer cells. So far, iPSCs have been generated from normal primary cells, but it is unclear whether human primary cancer cell can be reprogrammed. We investigated the production of the iPS cells from the pancreatic adenocarcinoma cells using defined transcription factors.
Materials and Methods: We sought to reprogram patient derived xenograft from human PDAC, by introducing lentiviral mediated induction of Yamanaka Factors (OSKM) and characterized of induced cells by Alkaline Phosphatase staining, Real-Time PCR and immunostaining.
Ethical Considerations: This study with research ethics code EC/93/1025 has been approved by research ethics committee at Royan Institute.
Findings: Alkaline Phosphatase staining, Real-Time PCR and immunostaining showed that induction with the OSKM results in generating iPS cell line from fibroblast cells but not from PDAC PDX cells .We showed that, PDAC cells could not fully reprogrammed by the expression of 4 transcription factors.
Conclusion: This study demonstrated that the PDAC-PDX cancer cells were distinct from PDAC induced cells with regard to their epigenetic modifier genes expression pattern, although the expression of pluripotency genes did not increased significantly in the induced PDAC cells.

Marjan Hajimoradi Javarsiani, Javad Sajedianfard, Shagayegh Haghjooy Javanmard,
Volume 24, Issue 3 (8-2021)
Abstract

Background and Aim: Cancer cannot be explained only by genetic alterations but involves epigenetic processes. Modifying histones by acetylation plays a key role in epigenetic regulation of gene expression and is controlled by the balance between Histone Deacetylases (HDAC) and Histone Acetyltransferases (HAT). The HDACs expression and activity could be involved in several tumorigenesis mechanisms, so their inhibition induces cancer cell cycle arrest and migration.
Methods & Materials: Quisinostat is a novel promising second-generation HDAC inhibitor class of hydroxamic acid with high cellular potency towards classes I and II HDACs. Therefore, its low IC50 (<0.5nM) and bioavailability have been chosen to carry out our studies. Cancer cells were treated with Quiznos at nM200, and cell migration was measured by fluorescent microscopy.
Ethical Considerations: This study was the result of a preliminary study of Shiraz University (Code: 96GCU3M1293).
Results: The data showed that treatment of cancer cells with Quiznos significantly (P<0.05) reduced cell migration. DMSO did not affect reducing cell migration.
Conclusion: In this project try to explore the possible therapeutic application of this HDAC inhibitor against colon cancer. This study showed Quisinostat exerts broad-spectrum antiproliferative activity and migration.

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