فهرست مطالب foruzan moradi

Tamoxifen (TAM) is routinely used for the treatment of estrogen-positive breast carcinoma. Approximately 40% of patients with metastatic breast cancer will develop resistance to TAM. TAM therapeutic failure has been a major challenge in the treatment of TAM-resistant breast cancer cells. Therefore, finding a way to eliminate TAM resistance is very valuable. Curcumin is a polyphenol extracted from the rhizomes of Curcuma longa and has extensive biological and pharmacological effects on many cancers. The purpose of this study was to look into the effects of dendrosomal nano-curcumin (DNC) on cell growth and apoptosis, as well as the effects of DNC on the expression levels of long non-coding RNA CCAT2 in TAM-resistant MCF-7 cells (TAM-R). TAM-R cells were created, and CCAT2 expression was evaluated in TAM-R compared to TAM-sensitive MCF-7 cells (TAM-S). Forty eighth hours after TAM-R treatment with 20 μM of DNC, Q-RT-PCR, and flow cytometry cell cycle and Annexin V-PI assays were performed. P-value < 0.05 was defined as statistical significance. CCAT2 was significantly upregulated in TAM-R compared to TAM-S. DNC administration downregulated CCAT2 expression, and markedly suppressed cell cycle and induced apoptosis in TAM-R. Furthermore, DNC decreased the anti-apoptosis gene (BCL-2) and increased the apoptotic gene (BAX) expression levels respectively in TAM-R. DNC promoted cell cycle arrest and apoptosis, eventually by CCAT2 downregulation in TAM-R. However, the probable mechanisms of how DNC affects CCAT2 expression levels are unknown and need future studies.

Tamoxifen (TAM) is routinely used for the treatment of estrogen-positive breast carcinoma. Approximately 40% of patients with metastatic breast cancer will develop resistance to TAM. TAM therapeutic failure has been a major challenge in the treatment of TAM-resistant breast cancer cells. Therefore, finding a way to eliminate TAM resistance is very valuable. Curcumin is a polyphenol extracted from the rhizomes of Curcuma longa and has extensive biological and pharmacological effects on many cancers. The purpose of this study was to look into the effects of dendrosomal nano-curcumin (DNC) on cell growth and apoptosis, as well as the effects of DNC on the expression levels of long non-coding RNA CCAT2 in TAM-resistant MCF-7 cells (TAM-R). TAM-R cells were created, and CCAT2 expression was evaluated in TAM-R compared to TAM-sensitive MCF-7 cells (TAM-S). Forty eighth hours after TAM-R treatment with 20 μM of DNC, Q-RT-PCR, and flow cytometry cell cycle and Annexin V-PI assays were performed. P-value < 0.05 was defined as statistical significance. CCAT2 was significantly upregulated in TAM-R compared to TAM-S. DNC administration downregulated CCAT2 expression, and markedly suppressed cell cycle and induced apoptosis in TAM-R. Furthermore, DNC decreased the anti-apoptosis gene (BCL-2) and increased the apoptotic gene (BAX) expression levels respectively in TAM-R. DNC promoted cell cycle arrest and apoptosis, eventually by CCAT2 downregulation in TAM-R. However, the probable mechanisms of how DNC affects CCAT2 expression levels are unknown and need future studies.

Chronic myeloid leukemia (CML) is a myeloid clonal proliferation disease defining by the presence of the Philadelphia chromosome that shows the movement of BCR-ABL1. In this study, the critical role of the Musashi2-Numb axis in determining cell fate and relationship of the axis to important signaling pathways such as Hedgehog and Notch that are essential for self-renewal pathways in CML stem cells will be reviewed meticulously. In this review, a PubMed search using the keywords of Leukemia, signaling pathways, Musashi2-Numb was performed, and then we summarized different research works. Although tyrosine kinase inhibitors such as Imatinib significantly kill and remove the cell with BCR-ABL1 translocation, they are unable to target BCR-ABL1 leukemia stem cells. The main problem is stem cells resistance to Imatinib therapy. Therefore, the identification and control of downstream molecules/ signaling route of the BCR-ABL1 that are involved in the survival and self-renewal of leukemia stem cells can be an effective treatment strategy to eliminate leukemia stem cells, which supposed to be cured by Musashi2-Numb signaling pathway. The control of molecules /pathways downstream of the BCR-ABL1 and targeting Musashi2-Numb can be an effective therapeutic strategy for treatment of chronic leukemia stem cells. While Musashi2 is a poor prognostic marker in leukemia, in treatment and strategy, it has significant diagnostic value.