Hamidreza Zalpoor

Mr. Hamidreza Zalpoor

orcid

Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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9 April 2022 in Cellular & Molecular Biology Letters
Verified
Journal Article
Open access
PDF file
MFMohsen Karami Fath
Mohsen Karami Fath
KBKimiya Babakhaniyan
Kimiya Babakhaniyan
MZMaryam Zokaei
Maryam Zokaei
AYAzadeh Yaghoubian
Azadeh Yaghoubian
SASadaf Akbari
Sadaf Akbari
ABArmina Alagheband Bahrami
Armina Alagheband Bahrami
Background: Nowadays, conventional medical treatments such as surgery, radiotherapy, and chemotherapy cannot cure all types of cancer. A promising approach to treat solid tumors is the use of tumor-targeting peptides to deliver drugs or active agents selectively. Result: Introducing beneficial therapeutic approaches, such as therapeutic peptides and their varied methods of action against tumor cells, can aid researchers in the discovery of novel peptides for cancer treatment. The biomedical applications of therapeutic peptides are highly interesting. These peptides, owing to their high selectivity, specificity, small dimensions, high biocompatibility, and easy modification, provide good opportunities for targeted drug delivery. In recent years, peptides have shown considerable promise as therapeutics or targeting ligands in cancer research and nanotechnology. Conclusion: This study reviews a variety of therapeutic peptides and targeting ligands in cancer therapy. Initially, three types of tumor-homing and cell-penetrating peptides (CPPs) are described, and then their applications in breast, glioma, colorectal, and melanoma cancer research are discussed.

28 June 2022 in Cellular & Molecular Biology Letters
Verified
Journal Article
Open access
PDF file
MFMohsen Karami Fath
Mohsen Karami Fath
AAAli Azargoonjahromi
Ali Azargoonjahromi
AKArash Kiani
Arash Kiani
FJFateme Jalalifar
Fateme Jalalifar
POParisa Osati
Parisa Osati
ZPZahra Payandeh
Zahra Payandeh
Background: Breast cancer is defined as a biological and molecular heterogeneous disorder that originates from breast cells. Genetic predisposition is the most important factor giving rise to this malignancy. The most notable mutations in breast cancer occur in the BRCA1 and BRCA2 genes. Owing to disease heterogeneity, lack of therapeutic target, anti-cancer drug resistance, residual disease, and recurrence, researchers are faced with challenges in developing strategies to treat patients with breast cancer. Results: It has recently been reported that epigenetic processes such as DNA methylation and histone modification, as well as microRNAs (miRNAs), have potently contributed to the pathophysiology, diagnosis, and treatment of breast cancer. These observations have persuaded researchers to move their therapeutic approaches beyond the genetic framework toward the epigenetic concept. Conclusion: Herein we discuss the molecular and epigenetic mechanisms underlying breast cancer progression and resistance as well as various aspects of epigenetic-based therapies as monotherapy and combined with immunotherapy.

15 May 2023 in Cell Communication and Signaling
Verified
Journal Article
Open access
PDF file
SKSareh Kakavandi
Sareh Kakavandi
IZIman Zare
Iman Zare
MVMaryam VaezJalali
Maryam VaezJalali
MDMasoud Dadashi
Masoud Dadashi
MAMaryam Azarian
Maryam Azarian
BHBahareh Hajikhani
Bahareh Hajikhani
Coronavirus disease 2019 (COVID-19) is caused by a new member of the Coronaviridae family known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). There are structural and non-structural proteins (NSPs) in the genome of this virus. S, M, H, and E proteins are structural proteins, and NSPs include accessory and replicase proteins. The structural and NSP components of SARS-CoV-2 play an important role in its infectivity, and some of them may be important in the pathogenesis of chronic diseases, including cancer, coagulation disorders, neurodegenerative disorders, and cardiovascular diseases. The SARS-CoV-2 proteins interact with targets such as angiotensin-converting enzyme 2 (ACE2) receptor. In addition, SARS-CoV-2 can stimulate pathological intracellular signaling pathways by triggering transcription factor hypoxia-inducible factor-1 (HIF-1), neuropilin-1 (NRP-1), CD147, and Eph receptors, which play important roles in the progression of neurodegenerative diseases like Alzheimer's disease, epilepsy, and multiple sclerosis, and multiple cancers such as glioblastoma, lung malignancies, and leukemias. Several compounds such as polyphenols, doxazosin, baricitinib, and ruxolitinib could inhibit these interactions. It has been demonstrated that the SARS-CoV-2 spike protein has a stronger affinity for human ACE2 than the spike protein of SARS-CoV, leading the current study to hypothesize that the newly produced variant Omicron receptor-binding domain (RBD) binds to human ACE2 more strongly than the primary strain. SARS and Middle East respiratory syndrome (MERS) viruses against structural and NSPs have become resistant to previous vaccines. Therefore, the review of recent studies and the performance of current vaccines and their effects on COVID-19 and related diseases has become a vital need to deal with the current conditions. This review examines the potential role of these SARS-CoV-2 proteins in the initiation of chronic diseases, and it is anticipated that these proteins could serve as components of an effective vaccine or treatment for COVID-19 and related diseases.

21 September 2023 in Cell Communication and Signaling
Verified
Journal Article
Open access
PDF file
MBMaryam Bakhtiyari
Maryam Bakhtiyari
MLMahsa Liaghat
Mahsa Liaghat
FAFatemeh Aziziyan
Fatemeh Aziziyan
HSHooriyeh Shapourian
Hooriyeh Shapourian
SYSheida Yahyazadeh
Sheida Yahyazadeh
MPMajid Pornour
Majid Pornour
Acute myeloid leukemia (AML) comprises a multifarious and heterogeneous array of illnesses characterized by the anomalous proliferation of myeloid cells in the bone marrow microenvironment (BMM). The BMM plays a pivotal role in promoting AML progression, angiogenesis, and metastasis. The immune checkpoints (ICs) and metabolic processes are the key players in this process. In this review, we delineate the metabolic and immune checkpoint characteristics of the AML BMM, with a focus on the roles of BMM cells e.g. tumor-associated macrophages, natural killer cells, dendritic cells, metabolic profiles and related signaling pathways. We also discuss the signaling pathways stimulated in AML cells by BMM factors that lead to AML progression. We then delve into the roles of immune checkpoints in AML angiogenesis, metastasis, and cell proliferation, including co-stimulatory and inhibitory ICs. Lastly, we discuss the potential therapeutic approaches and future directions for AML treatment, emphasizing the potential of targeting metabolic and immune checkpoints in AML BMM as prognostic and therapeutic targets. In conclusion, the modulation of these processes through the use of directed drugs opens up new promising avenues in combating AML. Thereby, a comprehensive elucidation of the significance of these AML BMM cells' metabolic and immune checkpoints and signaling pathways on leukemic cells can be undertaken in the future investigations. Additionally, these checkpoints and cells should be considered plausible multi-targeted therapies for AML in combination with other conventional treatments in AML.

2 December 2024 in Cell Communication and Signaling
Verified
Journal Article
Open access
PDF file
MLMahsa Liaghat
Mahsa Liaghat
SFSaeid Ferdousmakan
Saeid Ferdousmakan
SMSeyedeh Haniyeh Mortazavi
Seyedeh Haniyeh Mortazavi
SYSheida Yahyazadeh
Sheida Yahyazadeh
AIAsrin Irani
Asrin Irani
MNMohsen Nabi-Afjadi
Mohsen Nabi-Afjadi
The intricate cellular process, known as the epithelial-mesenchymal transition (EMT), significantly influences solid tumors development. Changes in cell shape, metabolism, and gene expression linked to EMT facilitate tumor cell invasion, metastasis, drug resistance, and recurrence. So, a better understanding of the intricate processes underlying EMT and its role in tumor growth may lead to the development of novel therapeutic approaches for the treatment of solid tumors. This review article focuses on the signals that promote EMT and metabolism, the intracellular signaling pathways leading to EMT, and the network of interactions between EMT and cancer cell metabolism. Furthermore, the functions of EMT in treatment resistance, recurrence, and metastasis of solid cancers are covered. Lastly, treatment approaches that focus on intracellular signaling networks and metabolic alterations brought on by EMT will be discussed.

23 November 2022 in Cell Communication and Signaling
Verified
Journal Article
Open access
PDF file
HZHamidreza Zalpoor
Hamidreza Zalpoor
FAFatemeh Aziziyan
Fatemeh Aziziyan
MLMahsa Liaghat
Mahsa Liaghat
MBMaryam Bakhtiyari
Maryam Bakhtiyari
AAAbdullatif Akbari
Abdullatif Akbari
NRNima Rezaei
Nima Rezaei
Innate and adaptive immune cells patrol and survey throughout the human body and sometimes reside in the tumor microenvironment (TME) with a variety of cell types and nutrients that may differ from those in which they developed. The metabolic pathways and metabolites of immune cells are rooted in cell physiology, and not only provide nutrients and energy for cell growth and survival but also influencing cell differentiation and effector functions. Nowadays, there is a growing awareness that metabolic processes occurring in cancer cells can affect immune cell function and lead to tumor immune evasion and angiogenesis. In order to safely treat cancer patients and prevent immune checkpoint blockade-induced toxicities and autoimmunity, we suggest using anti-angiogenic drugs solely or combined with Immune checkpoint blockers (ICBs) to boost the safety and effectiveness of cancer therapy. As a consequence, there is significant and escalating attention to discovering techniques that target metabolism as a new method of cancer therapy. In this review, a summary of immune-metabolic processes and their potential role in the stimulation of intracellular signaling in TME cells that lead to tumor angiogenesis, and therapeutic applications is provided.