Cancer stem cells (CSCs) are a subpopulation of tumour cells that possess the stem cell properties of self-renewal and differentiation. Stem cells might be the target cells responsible for malignant transformation, and tumour formation may be a disorder of stem cell self-renewal pathway. Epigenetic alterations and mutations of genes involved in signal transmissions may promote the formation of CSCs. These cells have been identified in many solid tumours including breast, brain, lung, prostate, testis, ovary, colon, skin, liver, and also in acute myeloid leukaemia. The CSC theory clarifies not only the issue of tumour initiation, development, metastasis and relapse, but also the ineffectiveness of conventional cancer therapies. Treatments directed against the bulk of the cancer cells may produce striking responses but they are unlikely to result in long-term remissions if the rare CSCs are not targeted. In this review, we consider the properties of CSCs and possible strategies for controlling the viability and tumourigenecity of these cells, including therapeutic models for selective elimination of CSCs and induction of their proper differentiation.

BORIS (CTCFL) is a DNA binding protein which is involved in tumorigenesis. Although, there are different opinions on the level of gene expression and function of BORIS in normal and cancer tissues, the results of many studies have classified BORIS as a protein belonging to cancer/testis (CT) genes, which are identified as a group of genes that are expressed normally in testis, and abnormally in various types of cancers. In testis, BORIS induces the expression of some male germ cell/testis specific genes, and plays crucial roles during spermatogenesis and production of sperm. In tumorigenesis, the role of BORIS in the expression induction of some CT genes and oncogenes, as well as increasing proliferation/viability of cancer cells has been demonstrated in many researches. In addition to cancer cells, some believe that BORIS is also expressed in normal conditions and plays a universal function in cell division and regulation of genes. The following is a comprehensive review on contradictory views on the expression pattern and biological function of BORIS in normal, as well as cancer cells/tissues, and presents some evidence that support the expression of BORIS in cancer stem cells (CSCs) and advanced stage/poorer differentiation grade of cancers. Boris is involved in the regulation of CSC cellular and molecular features such as self-renewal, chemo-resistance, tumorigenicity, sphere-forming ability, and migration capacity. Finally, the role of BORIS in regulating two important signaling pathways including Wnt/β-catenin and Notch in CSCs, and its ability in recruiting transcription factors or chromatin-remodeling proteins to induce tumorigenesis is discussed.

Directed cell migration is a crucial mobility phase of cancer stem cells having stemness and tumorigenic characteristics. It is known that CXCR4 plays key roles in the perception of chemotactic gradients throughout the directed migration of CSCs. There are a number of complex signaling pathways and transcription factors that coordinate with CXCR4/CXCL12 axis during directed migration. In this review, we focus on some transcription factors such as Nanog, NF-κB, and Bmi-1 that cooperate with CXCR4/CXCL12 for the maintenance of stemness and induction of metastasis behavior in cancer stem cells.

The present study reports the synthesis of ZnO-NPs using Acantholimon serotinum extracts followed by characterization and evaluation of biological activities. Field emission scanning electron microscope revealed irregular spherical morphology with a size in the range of 20–80 nm. The X-ray diffraction analysis confirmed the synthesis of highly pure ZnO NPs with a hexagonal shape and a crystalline size of 16.3 nm. The UV-Vis spectroscopy indicates the synthesis of ZnO-NPs. FT-IR confirmed the presence of phytocomponents in the plant extract, which was responsible for nanoparticle synthesis. According to MTT results, the biosynthesized ZnO-NPs showed cytotoxic effects on human colon cancer Caco-2 (IC50: 61 µg/mL), neuroblastoma SH-SY5Y (IC50: 42 µg/mL), breast cancer MDA-MB-231 (IC50: 24 µg/mL), and embryonic kidney HEK-293 (IC50: 60 µg/mL) cell lines. Significant reactive oxygen species (ROS) generation was measured by the DCFH-DA assay after 24 h incubation with ZnO-NPs (200 µg/mL). ZnO-NPs caused apoptotic and necrotic effects on cells, which was confirmed by Annexin V-PE/7-AAD staining and 6.8-fold increase in pro-apoptosis gene Bax and 178-fold decrease in anti-apoptosis gene Bcl-2. The well diffusion method did not show effective growth inhibition activities of the ZnO-NPs against bacteria. In conclusion, the ZnO-NPs induce cytotoxicity in cell lines through ROS generation and oxidative stress.

No abstract