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Öğe Advances in understanding the role of P-gp in doxorubicin resistance: molecular pathways, therapeutic strategies, and prospects(Elsevier, 2022) Mirzaei, Sepideh; Gholami, Mohammad Hossein; Hashemi, Farid; Zabolian, Amirhossein; Zarrabi, AliP-glycoprotein (P-gp) is a drug efflux transporter that triggers doxorubicin (DOX) resistance. In this review, we highlight the molecular avenues regulating P-gp, such as Nrf2, HIF-1?, miRNAs, and long noncoding (lnc)RNAs, to reveal their participation in DOX resistance. These antitumor compounds and genetic tools synergistically reduce P-gp expression. Furthermore, ATP depletion impairs P-gp activity to enhance the antitumor activity of DOX. Nanoarchitectures, including liposomes, micelles, polymeric nanoparticles (NPs), and solid lipid nanocarriers, have been developed for the co-delivery of DOX with anticancer compounds and genes enhancing DOX cytotoxicity. Surface modification of nanocarriers, for instance with hyaluronic acid (HA), can promote selectivity toward cancer cells. We discuss these aspects with a focus on P-gp expression and activity. © 2021 The Author(s)Öğe Correction: The long and short non-coding RNAs modulating EZH2 signaling in cancer (Journal of Hematology & Oncology, (2022), 15, 1, (18), 10.1186/s13045-022-01235-1)(BioMed Central Ltd, 2022) Mirzaei, Sepideh; Gholami, Mohammad Hossein; Hushmandi, Kiavash; Hashemi, Farid; Zabolian, Amirhossein; Canadas, Israel; Zarrabi, Ali; Nabavi, Noushin; Aref, Amir Reza; Crea, Francesco; Wang, Yuzhuo; Ashrafizadeh, Milad; Kumar, Alan PremThe original article [1] contained an error in co-author, Farid Hashemi’s name which has since been corrected. © 2022, The Author(s).Öğe Curcumin and its derivatives in cancer therapy: potentiating antitumor activity of cisplatin and reducing side effects(WILEY, 2021) Abadi, Asal Jalal; Mirzaei, Sepideh; Mahabady, Mahmood Khaksary; Hashemi, Farid; Zabolian, Amirhossein; Hashemi, Fardin; Raee, Pourya; Zarrabi, AliCurcumin is a phytochemical isolated from Curcuma longa with potent tumor-suppressor activity, which has shown significant efficacy in pre-clinical and clinical studies. Curcumin stimulates cell death, triggers cycle arrest, and suppresses oncogenic pathways, thereby suppressing cancer progression. Cisplatin (CP) stimulates DNA damage and apoptosis in cancer chemotherapy. However, CP has adverse effects on several organs of the body, and drug resistance is frequently observed. The purpose of the present review is to show the function of curcumin in decreasing CP's adverse impacts and improving its antitumor activity. Curcumin administration reduces ROS levels to prevent apoptosis in normal cells. Furthermore, curcumin can inhibit inflammation via down-regulation of NF-kappa B to maintain the normal function of organs. Curcumin and its nanoformulations can reduce the hepatoxicity, neurotoxicity, renal toxicity, ototoxicity, and cardiotoxicity caused by CP. Notably, curcumin potentiates CP cytotoxicity via mediating cell death and cycle arrest. Besides, curcumin suppresses the STAT3 and NF-kappa B as tumor-promoting pathways, to enhance CP sensitivity and prevent drug resistance. The targeted delivery of curcumin and CP to tumor cells can be mediated nanostructures. In addition, curcumin derivatives are also able to reduce CP-mediated side effects, and increase CP cytotoxicity against various cancer types.Öğe Nanoliposomes as nonviral vectors in cancer gene therapy(John Wiley and Sons Inc, 2024) Yıldız, Safiye Nur; Entezari, Maliheh; Paskeh, Mahshid Deldar Abad; Mirzaei, Sepideh; Kalbasi, Alireza; Zabolian, Amirhossein; Hashemi, Farid; Hushmandi, Kiavash; Hashemi, Mehrdad; Raei, Mehdi; Goharrizi, Mohammad Ali Sheikh Beig; Aref, Amir Reza; Zarrabi, Ali; Ren, Jun; Orive, Gorka; Rabiee, Navid; Ertaş, Yavuz NuriNonviral vectors, such as liposomes, offer potential for targeted gene delivery in cancer therapy. Liposomes, composed of phospholipid vesicles, have demonstrated efficacy as nanocarriers for genetic tools, addressing the limitations of off-targeting and degradation commonly associated with traditional gene therapy approaches. Due to their biocompatibility, stability, and tunable physicochemical properties, they offer potential in overcoming the challenges associated with gene therapy, such as low transfection efficiency and poor stability in biological fluids. Despite these advancements, there remains a gap in understanding the optimal utilization of nanoliposomes for enhanced gene delivery in cancer treatment. This review delves into the present state of nanoliposomes as carriers for genetic tools in cancer therapy, sheds light on their potential to safeguard genetic payloads and facilitate cell internalization alongside the evolution of smart nanocarriers for targeted delivery. The challenges linked to their biocompatibility and the factors that restrict their effectiveness in gene delivery are also discussed along with exploring the potential of nanoliposomes in cancer gene therapy strategies by analyzing recent advancements and offering future directions. © 2024 The Author(s). MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.Öğe 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, SaeedThe 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.