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Article ; Online: Biomedical application of metal-organic frameworks (MOFs) in cancer therapy: Stimuli-responsive and biomimetic nanocomposites in targeted delivery, phototherapy and diagnosis.

Li, Beixu / Ashrafizadeh, Milad / Jiao, Taiwei

International journal of biological macromolecules

2024 Volume 260, Issue Pt 2, Page(s) 129391

Abstract: The nanotechnology is an interdisciplinary field that has become a hot topic in cancer therapy. Metal-organic frameworks (MOFs) are porous materials and hybrid composites consisted of organic linkers and metal cations. Despite the wide application of ... ...

Abstract	The nanotechnology is an interdisciplinary field that has become a hot topic in cancer therapy. Metal-organic frameworks (MOFs) are porous materials and hybrid composites consisted of organic linkers and metal cations. Despite the wide application of MOFs in other fields, the potential of MOFs for purpose of cancer therapy has been revealed by the recent studies. High surface area and porosity, significant drug loading and encapsulation efficiency are among the benefits of using MOFs in drug delivery. MOFs can deliver genes/drugs with selective targeting of tumor cells that can be achieved through functionalization with ligands. The photosensitizers and photo-responsive nanostructures including carbon dots and gold nanoparticles can be loaded in/on MOFs to cause phototherapy-mediated tumor ablation. The immunogenic cell death induction and increased infiltration of cytotoxic CD
MeSH term(s)	Humans ; Metal-Organic Frameworks/chemistry ; Gold ; Biomimetics ; Metal Nanoparticles ; Phototherapy ; Drug Delivery Systems ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Nanocomposites/therapeutic use
Chemical Substances	Metal-Organic Frameworks ; Gold (7440-57-5)
Language	English
Publishing date	2024-01-17
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	282732-3
ISSN	1879-0003 ; 0141-8130
ISSN (online)	1879-0003
ISSN	0141-8130
DOI	10.1016/j.ijbiomac.2024.129391
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Article ; Online: Wnt/β-catenin-driven EMT regulation in human cancers.

Xue, Wenhua / Yang, Lin / Chen, Chengxin / Ashrafizadeh, Milad / Tian, Yu / Sun, Ranran

Cellular and molecular life sciences : CMLS

2024 Volume 81, Issue 1, Page(s) 79

Abstract: Metastasis accounts for 90% of cancer-related deaths among the patients. The transformation of epithelial cells into mesenchymal cells with molecular alterations can occur during epithelial-mesenchymal transition (EMT). The EMT mechanism accelerates the ... ...

Abstract	Metastasis accounts for 90% of cancer-related deaths among the patients. The transformation of epithelial cells into mesenchymal cells with molecular alterations can occur during epithelial-mesenchymal transition (EMT). The EMT mechanism accelerates the cancer metastasis and drug resistance ability in human cancers. Among the different regulators of EMT, Wnt/β-catenin axis has been emerged as a versatile modulator. Wnt is in active form in physiological condition due to the function of GSK-3β that destructs β-catenin, while ligand-receptor interaction impairs GSK-3β function to increase β-catenin stability and promote its nuclear transfer. Regarding the oncogenic function of Wnt/β-catenin, its upregulation occurs in human cancers and it can accelerate EMT-mediated metastasis and drug resistance. The stimulation of Wnt by binding Wnt ligands into Frizzled receptors can enhance β-catenin accumulation in cytoplasm that stimulates EMT and related genes upon nuclear translocation. Wnt/β-catenin/EMT axis has been implicated in augmenting metastasis of both solid and hematological tumors. The Wnt/EMT-mediated cancer metastasis promotes the malignant behavior of tumor cells, causing therapy resistance. The Wnt/β-catenin/EMT axis can be modulated by upstream mediators in which non-coding RNAs are main regulators. Moreover, pharmacological intervention, mainly using phytochemicals, suppresses Wnt/EMT axis in metastasis suppression.
MeSH term(s)	Humans ; beta Catenin/genetics ; beta Catenin/metabolism ; Glycogen Synthase Kinase 3 beta/metabolism ; Wnt Signaling Pathway ; Cell Line, Tumor ; Cell Movement ; Epithelial-Mesenchymal Transition/physiology ; Gene Expression Regulation, Neoplastic ; Neoplasms/genetics
Chemical Substances	beta Catenin ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
Language	English
Publishing date	2024-02-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-05099-7
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Zs.A 195: Show issues

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Article ; Online: Molecular panorama of therapy resistance in prostate cancer: a pre-clinical and bioinformatics analysis for clinical translation.

Ashrafizadeh, Milad / Zhang, Wei / Tian, Yu / Sethi, Gautam / Zhang, Xianbin / Qiu, Aiming

Cancer metastasis reviews

2024 Volume 43, Issue 1, Page(s) 229–260

Abstract: Prostate cancer (PCa) is a malignant disorder of prostate gland being asymptomatic in early stages and high metastatic potential in advanced stages. The chemotherapy and surgical resection have provided favourable prognosis of PCa patients, but advanced ... ...

Abstract	Prostate cancer (PCa) is a malignant disorder of prostate gland being asymptomatic in early stages and high metastatic potential in advanced stages. The chemotherapy and surgical resection have provided favourable prognosis of PCa patients, but advanced and aggressive forms of PCa including CRPC and AVPC lack response to therapy properly, and therefore, prognosis of patients is deteriorated. At the advanced stages, PCa cells do not respond to chemotherapy and radiotherapy in a satisfactory level, and therefore, therapy resistance is emerged. Molecular profile analysis of PCa cells reveals the apoptosis suppression, pro-survival autophagy induction, and EMT induction as factors in escalating malignant of cancer cells and development of therapy resistance. The dysregulation in molecular profile of PCa including upregulation of STAT3 and PI3K/Akt, downregulation of STAT3, and aberrant expression of non-coding RNAs are determining factor for response of cancer cells to chemotherapy. Because of prevalence of drug resistance in PCa, combination therapy including co-utilization of anti-cancer drugs and nanotherapeutic approaches has been suggested in PCa therapy. As a result of increase in DNA damage repair, PCa cells induce radioresistance and RelB overexpression prevents irradiation-mediated cell death. Similar to chemotherapy, nanomaterials are promising for promoting radiosensitivity through delivery of cargo, improving accumulation in PCa cells, and targeting survival-related pathways. In respect to emergence of immunotherapy as a new tool in PCa suppression, tumour cells are able to increase PD-L1 expression and inactivate NK cells in mediating immune evasion. The bioinformatics analysis for evaluation of drug resistance-related genes has been performed.
MeSH term(s)	Male ; Humans ; Phosphatidylinositol 3-Kinases/metabolism ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Antineoplastic Agents/therapeutic use ; Apoptosis ; Radiation Tolerance ; Cell Line, Tumor
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Antineoplastic Agents
Language	English
Publishing date	2024-02-19
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-024-10168-9
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Zs.A 1812: Show issues

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Article ; Online: Natural product/diet-based regulation of macrophage polarization: Implications in treatment of inflammatory-related diseases and cancer.

Ashrafizadeh, Milad / Aref, Amir Reza / Sethi, Gautam / Ertas, Yavuz Nuri / Wang, Lu

The Journal of nutritional biochemistry

2024 , Page(s) 109647

Abstract: Macrophages are phagocytic cells with important physiological functions, including the digestion of cellular debris, foreign substances, and microbes, as well as tissue development and homeostasis. The tumor microenvironment (TME) shapes the ... ...

Abstract	Macrophages are phagocytic cells with important physiological functions, including the digestion of cellular debris, foreign substances, and microbes, as well as tissue development and homeostasis. The tumor microenvironment (TME) shapes the aggressiveness of cancer, and the biological and cellular interactions in this complicated space can determine carcinogenesis. The TME can determine the progression, biological behavior, and therapy resistance of human cancers. The macrophages are among the most abundant cells in the TME, and their functions and secretions can determine tumor progression. The education of macrophages to M2 polarization can accelerate cancer progression, and therefore, the re-education and reprogramming of these cells is promising. Moreover, macrophages can cause inflammation in aggravating pathological events, including cardiovascular diseases, diabetes, and neurological disorders. The natural products are pleiotropic and broad-spectrum functional compounds that have been deployed as ideal alternatives to conventional drugs in the treatment of cancer. The biological and cellular interactions in the TME can be regulated by natural products, and for this purpose, they enhance the M1 polarization of macrophages, and in addition to inhibiting proliferation and invasion, they impair the chemoresistance. Moreover, since macrophages and changes in the molecular pathways in these cells can cause inflammation, the natural products impair the pro-inflammatory function of macrophages to prevent the pathogenesis and progression of diseases. Even a reduction in macrophage-mediated inflammation can prevent organ fibrosis. Therefore, natural product-mediated macrophage targeting can alleviate both cancerous and non-cancerous diseases.
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1014929-6
ISSN	1873-4847 ; 0955-2863
ISSN (online)	1873-4847
ISSN	0955-2863
DOI	10.1016/j.jnutbio.2024.109647
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Zs.A 2838: Show issues

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Article ; Online: Peptide-functionalized, -assembled and -loaded nanoparticles in cancer therapy.

Dai, Jingyuan / Ashrafizadeh, Milad / Aref, Amir Reza / Sethi, Gautam / Ertas, Yavuz Nuri

Drug discovery today

2024 , Page(s) 103981

Abstract: The combination of peptides and nanoparticles in cancer therapy has shown synergistic results. Nanoparticle functionalization with peptides can increase their targeting ability towards tumor cells. In some cases, the peptides can develop self-assembled ... ...

Abstract	The combination of peptides and nanoparticles in cancer therapy has shown synergistic results. Nanoparticle functionalization with peptides can increase their targeting ability towards tumor cells. In some cases, the peptides can develop self-assembled nanoparticles, in combination with drugs, for targeted cancer therapy. The peptides can be loaded into nanoparticles and can be delivered by other drugs for synergistic cancer removal. Multifunctional types of peptide-based nanoparticles, including pH- and redox-sensitive classes, have been introduced in cancer therapy. The tumor microenvironment remolds, and the acceleration of immunotherapy and vaccines can be provided by peptide nanoparticles. Moreover, the bioimaging and labeling of cancers can be mediated by peptide nanoparticles. Therefore, peptides can functionalize nanoparticles in targeted cancer therapy.
Language	English
Publishing date	2024-04-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2024.103981
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Zs.A 4725: Show issues

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Article: Naturally Occurring SGLT2 Inhibitors: A Review.

Yaribeygi, Habib / Ashrafizadeh, Milad / Sathyapalan, Thozhukat / Jamialahmadi, Tannaz / Sahebkar, Amirhossein

Advances in experimental medicine and biology

2022 Volume 1328, Page(s) 523–530

Abstract: With an increasing incidence of diabetes mellitus globally due to various factors, including unhealthy lifestyle, there is a need for developing novel drugs for the management of diabetes. This chronic metabolic disorder results in high blood glucose ... ...

Abstract	With an increasing incidence of diabetes mellitus globally due to various factors, including unhealthy lifestyle, there is a need for developing novel drugs for the management of diabetes. This chronic metabolic disorder results in high blood glucose levels due to the body's inability to reduce the concentration of glucose. The decreased secretion of insulin and increased resistance to insulin action contribute to the development of diabetes mellitus. There have been efforts to target pathways involved in the metabolism of blood glucose. It seems that most of the currently applied antidiabetic medications are associated with unwanted side effects. Hence, it appears that plant-derived chemicals can be considered as potential candidates in the management of diabetes. Sodium-glucose cotransporter inhibitors (SGLT2i) are synthetic hypoglycemic medications approved for managing patients with diabetes in lowering blood glucose. SGLT2i reduces blood glucose concentration by enhancing its urinary excretion and inhibition of its absorption through the kidney. It has been demonstrated that some of the naturally occurring nutraceutical agents can imitate the action of SGLT2i and, consequently, diminish the level of blood glucose. At the present review, we have discussed the phytochemicals that act like SGLT2i to decrease blood glucose level.
MeSH term(s)	Blood Glucose ; Diabetes Mellitus, Type 2/drug therapy ; Humans ; Hypoglycemic Agents/therapeutic use ; Insulin ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Blood Glucose ; Hypoglycemic Agents ; Insulin ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2022-01-04
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-73234-9_37
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Article ; Online: Chitosan-functionalized bioplatforms and hydrogels in breast cancer: immunotherapy, phototherapy and clinical perspectives.

Li, Tianfeng / Ashrafizadeh, Milad / Shang, Yuru / Nuri Ertas, Yavuz / Orive, Gorka

Drug discovery today

2023 Volume 29, Issue 1, Page(s) 103851

Abstract: Breast cancer is the most common and malignant tumor among women. Chitosan (CS)-based nanoparticles have been introduced into breast cancer therapy as a way to increase the targeted delivery of drugs and genes to the tumor site. CS nanostructures ... ...

Abstract	Breast cancer is the most common and malignant tumor among women. Chitosan (CS)-based nanoparticles have been introduced into breast cancer therapy as a way to increase the targeted delivery of drugs and genes to the tumor site. CS nanostructures suppress tumorigenesis by enhancing both the targeted delivery of cargo (drug and gene) and its accumulation in tumor cells. The tumor cells internalize CS-based nanoparticles through endocytosis. Moreover, chitosan nanocarriers can also induce phototherapy-mediated tumor ablation. Smart and multifunctional types of CS nanoparticles, including pH-, light- and redox-responsive nanoparticles, can be used to improve the potential for breast cancer removal. In addition, the acceleration of immunotherapy by CS nanoparticles has also been achieved, and there is potential to develop CS-nanoparticle hydrogels that can be used to suppress tumorigenesis.
MeSH term(s)	Female ; Humans ; Breast Neoplasms/drug therapy ; Chitosan/chemistry ; Drug Delivery Systems ; Phototherapy ; Nanoparticles/chemistry ; Carcinogenesis ; Immunotherapy ; Hydrogen-Ion Concentration
Chemical Substances	Chitosan (9012-76-4)
Language	English
Publishing date	2023-12-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2023.103851
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Article ; Online: A bioinformatics analysis, pre-clinical and clinical conception of autophagy in pancreatic cancer: Complexity and simplicity in crosstalk.

Ashrafizadeh, Milad / Zhang, Wei / Zou, Rongjun / Sethi, Gautam / Klionsky, Daniel J / Zhang, Xianbin

Pharmacological research

2023 Volume 194, Page(s) 106822

Abstract: Pancreatic cancer (PC) is a serious gastrointestinal tract disease for which the 5-year survival rate is less than 10%, even in developed countries such as the USA. The genomic profile alterations and dysregulated biological mechanisms commonly occur in ... ...

Abstract	Pancreatic cancer (PC) is a serious gastrointestinal tract disease for which the 5-year survival rate is less than 10%, even in developed countries such as the USA. The genomic profile alterations and dysregulated biological mechanisms commonly occur in PC. Macroautophagy/autophagy is a cell death process that is maintained at a basal level in physiological conditions, whereas its level often changes during tumorigenesis. The function of autophagy in human cancers is dual and can be oncogenic and onco-suppressor. Autophagy is a potent controller of tumorigenesis in PC. The supportive autophagy in PC escalates the growth rate of PC cells and its suppression can mediate cell death. Autophagy also determines the metastasis of PC cells, and it can control the EMT in affecting migration. Moreover, starvation and hypoxia can stimulate glycolysis, and glycolysis induction can be mediated by autophagy in enhancing tumorigenesis in PC. Furthermore, protective autophagy stimulates drug resistance and gemcitabine resistance in PC cells, and its inhibition can enhance radiosensitivity. Autophagy can degrade MHC-I to mediate immune evasion and also regulates polarization of macrophages in the tumor microenvironment. Modulation of autophagy activity is provided by silibinin, ursolic acid, chrysin and huaier in the treatment of PC. Non-coding RNAs are also controllers of autophagy in PC and its inhibition can improve therapy response in patients. Moreover, mitophagy shows dysregulation in PC, which can enhance the proliferation of PC cells. Therefore, a bioinformatics analysis demonstrates the dysregulation of autophagy-related proteins and genes in PC as biomarkers.
MeSH term(s)	Humans ; Cell Line, Tumor ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Autophagy ; Carcinogenesis ; Tumor Microenvironment ; Pancreatic Neoplasms
Language	English
Publishing date	2023-06-17
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2023.106822
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Zs.A 721: Show issues

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Article ; Online: Melatonin as a potential modulator of Nrf2.

Ahmadi, Zahra / Ashrafizadeh, Milad

Fundamental & clinical pharmacology

2019 Volume 34, Issue 1, Page(s) 11–19

Abstract: Nuclear factor erythroid 2-related factor 2 (Nrf2) is considered as the sensor of oxidative stress, and the main aim of this signaling pathway is to maintain physiological condition by induction of redox balance. Also, this pathway exerts anti- ... ...

Abstract	Nuclear factor erythroid 2-related factor 2 (Nrf2) is considered as the sensor of oxidative stress, and the main aim of this signaling pathway is to maintain physiological condition by induction of redox balance. Also, this pathway exerts anti-inflammatory effects via antioxidant response element. Oxidative stress is a key factor in a variety of pathological conditions and high level of oxidative stress is associated with damages in lipids, proteins, genetic material, and cell membrane. Multiple drugs have been developed in order to diminish oxidative stress. However, synthetic drugs suffer from various drawbacks such as high cost and side effects. On the other hand, naturally occurring compounds are of interest due to their minimal side effects and valuable biological activities. Melatonin is a hormone of pineal gland which is found in different plants. This compound has a variety of favorable biological and therapeutic activities such as antioxidant, anti-inflammatory, anti-tumor, anti-diabetic, and cardioprotection. At the present review, we demonstrate that Nrf2 signaling pathway explains some of the therapeutic and biological effects of melatonin.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Antioxidant Response Elements ; Antioxidants/pharmacology ; Humans ; Melatonin/pharmacology ; NF-E2-Related Factor 2/drug effects ; NF-E2-Related Factor 2/metabolism ; Oxidation-Reduction/drug effects ; Oxidative Stress/drug effects ; Signal Transduction/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Antioxidants ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2019-07-31
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639134-5
ISSN	1472-8206 ; 0767-3981
ISSN (online)	1472-8206
ISSN	0767-3981
DOI	10.1111/fcp.12498
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Zs.A 2247: Show issues

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Article ; Online: Acquired and intrinsic gemcitabine resistance in pancreatic cancer therapy: Environmental factors, molecular profile and drug/nanotherapeutic approaches.

Ashrafizadeh, Milad / Luo, Kuo / Zhang, Wei / Reza Aref, Amir / Zhang, Xianbin

Environmental research

2023 Volume 240, Issue Pt 2, Page(s) 117443

Abstract: A high number of cancer patients around the world rely on gemcitabine (GEM) for chemotherapy. During local metastasis of cancers, surgery is beneficial for therapy, but dissemination in distant organs leads to using chemotherapy alone or in combination ... ...

Abstract	A high number of cancer patients around the world rely on gemcitabine (GEM) for chemotherapy. During local metastasis of cancers, surgery is beneficial for therapy, but dissemination in distant organs leads to using chemotherapy alone or in combination with surgery to prevent cancer recurrence. Therapy failure can be observed as a result of GEM resistance, threatening life of pancreatic cancer (PC) patients. The mortality and morbidity of PC in contrast to other tumors are increasing. GEM chemotherapy is widely utilized for PC suppression, but resistance has encountered its therapeutic impacts. The purpose of current review is to bring a broad concept about role of biological mechanisms and pathways in the development of GEM resistance in PC and then, therapeutic strategies based on using drugs or nanostructures for overcoming chemoresistance. Dysregulation of the epigenetic factors especially non-coding RNA transcripts can cause development of GEM resistance in PC and miRNA transfection or using genetic tools such as siRNA for modulating expression level of these factors for changing GEM resistance are suggested. The overexpression of anti-apoptotic proteins and survival genes can contribute to GEM resistance in PC. Moreover, supportive autophagy inhibits apoptosis and stimulates GEM resistance in PC cells. Increase in metabolism, glycolysis induction and epithelial-mesenchymal transition (EMT) stimulation are considered as other factors participating in GEM resistance in PC. Drugs can suppress tumorigenesis in PC and inhibit survival factors and pathways in increasing GEM sensitivity in PC. More importantly, nanoparticles can increase pharmacokinetic profile of GEM and promote its blood circulation and accumulation in cancer site. Nanoparticles mediate delivery of GEM with genes and drugs to suppress tumorigenesis in PC and increase drug sensitivity. The basic research displays significant connection among dysregulated pathways and GEM resistance, but the lack of clinical application is a drawback that can be responded in future.
MeSH term(s)	Humans ; Gemcitabine ; Pharmaceutical Preparations ; Neoplasm Recurrence, Local ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Carcinogenesis ; Cell Transformation, Neoplastic ; Pancreatic Neoplasms
Chemical Substances	Gemcitabine ; Pharmaceutical Preparations
Language	English
Publishing date	2023-10-18
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	205699-9
ISSN	1096-0953 ; 0013-9351
ISSN (online)	1096-0953
ISSN	0013-9351
DOI	10.1016/j.envres.2023.117443
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