Background: There is a great deal of interest in using adipose tissue-derived mesenchymal stem cells (AT-MSCs) for clinical applications. However, the important limitations of clinical application of stem cells are the small number of cells and their differentiation into undesirable lineage in vitro. To overcome this problem, various growth factors are studied extensively. Objectives: The current study aimed at using 3 different doses of epidermal growth factor (EGF), glial cell line-derived neurotrophic (GDNF), and leukemia inhibitory factor (LIF) to culture AT-MSCs and evaluating their effects on proliferation, viability, differentiation potential, and maintenance of the stemness state of cells. Methods: The current experimental study was conducted on 8 -10 male NMRI (Naval medical research institute) mice provided from research center and experimental animal house of Jundishapur University of Ahvaz, Iran, from September 2016 to April 2017. AT-MSCs were isolated from mice adipose tissue. The cells were cultured with three different doses of EGF, LIF, and GDNF. The morphology and cell proliferation of the AT-MSCs were studied on the days 5, 7, and 11 by an inverted microscope and MTT assay, respectively. To evaluate the stemness state of the cells, Oct4 expression was measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Also, differentiation potential of AT-MSCs toward adipogenic and osteogenic lineages was assessed. All tests were done in triplicate.
Cancers with a high capability for angiogenesis are frequently regarded as being difficult to treat. Anti-angiogenesis drugs are considered the primary therapy for these types of cancers. Due to intrinsic or acquired anti-angiogenesis resistance, therapies result in moderate clinical consequences, despite some hopeful findings. The importance of non-coding RNAs (ncRNAs) such as microRNAs (miRNAs), long non-coding (lncRNAs), and circular RNAs (circRNAs) in drug resistance mechanisms in cancer treatment has been discovered in the previous decade. Anti-angiogenic drug resistance can be influenced by ncRNA dysregulation. Hence, ncRNAs are potential drug resistance targets for new anti-angiogenic drugs in the inhibition of angiogenesis in tumors. Furthermore, some ncRNAs can be employed as biomarkers for anti-angiogenic drug responses and can be used to monitor cancer non-invasively. Combination treatment approaches, combined with routine anti-angiogenesis and some drugs that target the ncRNAs causing resistance, can be potential ways to overcome anti-angiogenesis resistance. For the first time, we explain the mechanisms of anti-angiogenic drug resistance and the related miRNAs and lncRNAs and their signaling pathways in commonly used anti-angiogenic drugs implicated in this review article. These ncRNAs could be suggestions for targeting and reducing anti-angiogenic drugs in the future.
Cancer stem cells (CSCs) are cancer-initiating cells found in most tumors and hematological cancers. CSCs are involved in cells progression, recurrence of tumors, and drug resistance. Current therapies have been focused on treating the mass of tumor cells and cannot eradicate the CSCs. CSCs drug-specific targeting is considered as an approach to precisely target these cells. Clustered regularly interspaced short palindromic repeats (CRISPR/Cas9) gene-editing systems are making progress and showing promise in the cancer research field. One of the attractive applications of CRISPR/Cas9 as one approach of gene therapy is targeting the critical genes involved in drug resistance and maintenance of CSCs. The synergistic effects of gene editing as a novel gene therapy approach and traditional therapeutic methods, including chemotherapy, can resolve drug resistance challenges and regression of the cancers. This review article considers different aspects of CRISPR/Cas9 ability in the study and targeting of CSCs with the intention to investigate their application in drug resistance.
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