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    Cancer stem cell-mediated drug resistance: A comprehensive gene expression profile analysis in breast cancer
    (Elsevier Gmbh, 2023) Torabian, Pedram; Yousefi, Hassan; Fallah, Aysan; Moradi, Zahra; Naderi, Tohid; Delavar, Mahsa Rostamian; Ertas, Yavuz Nuri
    Breast cancer is the most frequently diagnosed malignancy in women and a major public health concern. In the current report, differential expression of the breast cancer resistance promoting genes with a focus on breast cancer stem cell related elements as well as the correlation of their mRNAs with various clinicopathologic characteristics, including molecular subtypes, tumor grade/stage, and methylation status, have been investigated using METABRIC and TCGA datasets. To achieve this goal, we downloaded gene expression data of breast cancer patients from TCGA and METABRIC. Then, statistical analyses were used to assess the correlation between the expression levels of stem cell related drug resistant genes and methylation status, tumor grades, various molecular subtypes, and some cancer hallmark gene sets such as immune evasion, metastasis, and angiogenesis. According to the results of this study, a number of stem cell related drug resistant genes are deregulated in breast cancer patients. Furthermore, we observe negative correlations between methylation of resistance genes and mRNA expression. There is a significant difference in the expression of resistance-promoting genes between different molecular subtypes. As mRNA expression and DNA methylation are clearly related, DNA methylation might be a mechanism that regulates these genes in breast cancer cells. As indicated by the differential expression of resistance-promoting genes among various breast cancer molecular subtypes, these genes may function differently in different subtypes of breast cancer. In conclusion, significant deregulation of resistance-promoting factors indicates that these genes may play a significant role in the development of breast cancer.
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    Noncoding RNAs and their therapeutics in paclitaxel chemotherapy: Mechanisms of initiation, progression, and drug sensitivity
    (Wiley, 2022) Mahabady, Mahmood K.; Mirzaei, Sepideh; Saebfar, Hamidreza; Gholami, Mohammad H.; Zabolian, Amirhossein; Hushmandi, Kiavash; Hashemi, Farid; Tajik, Fatemeh; Hashemi, Mehrdad; Kumar, Alan P.; Aref, Amir R.; Zarrabi, Ali; Khan, Haroon; Hamblin, Michael R.; Ertas, Yavuz Nuri; Samarghandian, Saeed
    The identification of agents that can reverse drug resistance in cancer chemotherapy, andenhance the overall efficacy is of great interest. Paclitaxel (PTX) belongs to taxane family hat exerts an antitumor effect by stabilizing microtubules and inhibiting cell cycleprogression. However, PTX resistance often develops in tumors due to the over-expression of drug transporters and tumor?promoting pathways. Noncoding RNAs(ncRNAs) are modulators of many processes in cancer cells, such as apoptosis, migration,differentiation, and angiogenesis. In the present study, we summarize the effects ofncRNAs on PTX chemotherapy. MicroRNAs (miRNAs) can have opposite effects on PTXresistance (stimulation or inhibition) via influencing YES1, SK2, MRP1, and STAT3.Moreover, miRNAs modulate the growth and migration rates of tumor cells in regulatingPTX efficacy. PIWI?interacting RNAs, small interfering RNAs, and short?hairpin RNAs areother members of ncRNAs regulating PTX sensitivity of cancer cells. Long noncodingRNAs (LncRNAs) are similar to miRNAs and can modulate PTX resistance/sensitivity bytheir influence on miRNAs and drug efflux transport. The cytotoxicity of PTX againsttumor cells can also be affected by circular RNAs (circRNAs) and limitation is thatoncogenic circRNAs have been emphasized and experiments should also focus on onco?suppressor circRNAs.
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    Targeting AMPK signaling in ischemic/reperfusion injury: From molecular mechanism to pharmacological interventions
    (2022) Paskeh, Mahshid Deldar Abad; Asadi, Ava; Mirzaei, Sepideh; Hashemi, Mehrdad; Entezari, Maliheh; Raesi, Rasoul; Hushmandi, Kiavash; Zarrabi, Ali; Ertas, Yavuz Nuri; Aref, Amir Reza; Samarghandian, Saeed; Reiter, Russel J; Ren, Jun
    Ischemia is a pathological process in which blood supply to a particular organ is temporarily interrupted resulting in disturbed biological function and homeostasis of local tissues. Following ischemia, reperfusion and reoxygenation may occur which further worsens oxidative stress-mediated damage in cells and tissues. The combined processes are referred to as ischemia/reperfusion (I/R) injury. Immediate management and treatment of I/R is of utmost importance for preventing irreversible and extensive cellular damage. Apoptosis, inflammation and oxidative stress are the most validated pathologies associated with I/R. AMP-activated protein kinase (AMPK) modulates energy metabolism in cells and its activation occurs in response to elevated AMP and ADP levels. Aberrant levels of AMPK are noted in various pathological settings such as diabetes mellitus, cancer and neurological diseases. This review emphasizes AMPK signaling, its related molecular pathways and therapeutic utility during I/R. Activation of AMPK through phosphorylation prevents apoptosis and reduces oxidative stress and inflammation upon I/R. Inducing AMPK signaling normalizes mitochondrial function to inhibit cell death. Autophagy as a cytoprotective mechanism undergoes activation by AMPK/mTOR and AMPK/ULK1 pathways. AMPK reinforces the antioxidant defense capacity via Nrf2 signaling to counteract oxidative stress in I/R. Protective compounds including phytochemicals activate AMPK to alleviate I/R injury.