Recent experiments have shown that cells with different genetic mutations can give rise to cancer transformation, both in vitro and in vivo, supported by the crosstalk between cancer cells and stroma. The stroma and the complex set of involved cells make up the tumor microenvironment that supports the engraftment of metastatic cells. In fact, environmental factors support colorectal cancer arise by formation and maintenance of cancer stem cells (CSCs). In this review, we discuss interactions between CSCs and their microenvironment that can provide better therapeutic opportunities in the metastatic cancer.

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Background: Melanoma, also known as malignant melanoma, is a type of skin cancer that develops from the pigment-producing cells known as melanocytes. Melanomas typically occur in the skin but may rarely occur in the mouth, intestines or, eye. The study aimed to examine the expression of the mammalian target of rapamycin (mTOR)/70S6K signaling pathway in melanoma cancer. Methods: The B16F10 cell line treated with dacarbazine IC50 and different concentrations of metformin (0.5, 2, and 8 mM) for 24 hr and mTOR and 70S6k proteins expression was examined by western blotting. Cell viability was measured by MTT assay. Results: Western blot analysis showed that after different concentra¬tions of metformin and dacarbazine treatments, the mTOR and 70S6K protein expression significantly (P<0.05) decreased. Conclusion: Metformin-induced repression of mTOR/70S6k axis activity disrupts B16F10 growth. Thus, we believe that combination therapy may be a suitable potential therapeutic target for melanoma cancer.

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.