Cancer Research, Molecular Medicine, Molecular Biology, General Biochemistry, Genetics and Molecular Biology
26
Scopus Publications
945
Scholar Citations
12
Scholar h-index
13
Scholar i10-index
Scopus Publications
PP2A activation targets MYCN in neuroblastoma Nazia Nazam, Shamza Manzoor, Maryam Shaikh, Morgan L. Brown, Janet R. Julson, Colin H. Quinn, Swatika Butey, Sorina N. Shirley, Jamie M. Aye, Karina Yoon, Jianmei W. Leavenworth, Michael Ohlmeyer, Elizabeth A. Beierle Cell Death and Disease, 2026 Neuroblastoma (NBL) is the most common extracranial solid tumor of childhood, accounting for 7-10% of all children cancers, but leading to 15% of childhood cancer related deaths. Children with high-risk neuroblastoma (HR-NBL) lack effective treatments that achieve durable outcomes. While multiple factors stratify NBL patients into the high- risk category, MYCN amplification is a crucial determinant for that group. Thus far, efforts towards directly targeting MYCN have proven unsuccessful. Serine/threonine protein phosphatase 2 A (PP2A) functions as a tumor suppressor across cancers through its epigenetic effects, and its activity and tumor suppressor function are inhibited in NBL. We hypothesized that MYCN may be a target for PP2A, and that reactivation of PP2A may have a tumor suppressive effect on NBL. We employed studies to document the phenotypic, epigenetic, and in vivo effects of pharmacologic PP2A activation. Novel PP2A activators, ATUX-1215 or ATUX-5800, reduced MYCN mRNA abundance and MYCN phosphorylation and protein expression. PP2A activation decreased the acetylation of H3K27 (H3K27ac) as well as the enrichment of H3K27ac at the MYCN promoter. ATUX-1215 and ATUX-5800 treatment led to hypophosphorylation of RNA Pol II carboxy-terminal domain (CTD) and BRD4, transcriptional and epigenetic regulators respectively, coinciding with decreased MYCN expression and gene regulator acetylation. Tumor growth decreased in animals treated with ATUX-1215, and analysis of tumor specimens confirmed decreased MYCN expression. We conclude that pharmacologic PP2A reactivation may be a relevant therapeutic component in NBL treatment through its targeting of MYCN.
Upregulation of the lncRNA MEG3 in Metastatic Hepatoblastoma Morgan L. Brown, Maryam G. Shaikh, Nazia Nazam, Ali M. Eakes, Pranava Nande, Abdulraheem Kaimari, Joel C. Opara, Jamie M. Aye, Karina J. Yoon, Elizabeth A. Beierle Cells, 2026 Hepatoblastoma is the predominant primary liver malignancy in children, and outcomes remain poor for patients with metastatic disease. Long non-coding RNAs (lncRNAs) regulate tumor behavior, but their role in metastatic hepatoblastoma is not well defined. This study investigates the expression and functional significance of the lncRNA, maternally expressed gene 3 (MEG3), in a metastatic hepatoblastoma model. RNA sequencing comparing the metastatic hepatoblastoma cell line, HLM_2, with its parental HuH6 cell line identified MEG3 as being significantly upregulated in metastatic cells. MEG3 expression was examined using hepatoblastoma patient datasets and validated using qPCR in cell lines, orthotopic tumors, and COA67 patient-derived xenografts. The effects of siRNA MEG3 knockdown in HLM_2 cells on clonogenicity, migration, and invasion were evaluated. The effects of MEG3 overexpression on migration and invasion were assessed in HuH6 cells. MEG3 was significantly upregulated in metastatic cells and orthotopic tumors compared with controls. MEG3 silencing reduced clonogenicity, tumorsphere formation, migration, and invasion. MEG3 overexpression increased migration and invasion. These findings indicate that MEG3 contributes to an aggressive tumor phenotype, highlighting the need for further examination into its mechanistic role in hepatoblastoma and its potential as a biomarker or therapeutic target.
Deciphering Pharmacological Targets of Plumbagin in Cisplatin-resistant Ovarian Cancer Model using in vitro and in silico Approaches Nazia Nazam, Iftikhar Ahmad, Nasimudeen R. Jabir, Torki A. Zughaibi, Pallavi Agarwal, Ahdab Alsaieedi, Mohd Shahnawaz Khan, Shams Tabrez Current Pharmaceutical Design, 2026 Introduction: Ovarian cancer (OC) is a malignancy of the female reproductive system for which cisplatin chemotherapy is one of the first-line treatments. Despite the initial response to chemotherapy, such patients eventually develop resistance, which poses a major obstacle to treatment, along with potential side effects. Phytochemicals function as chemosensitizers, offering novel therapies in OC patients by targeting drug resistance, and are perceived to be less toxic. Plumbagin has emerged as an anticancer compound, with some findings suggesting its anti-ovarian cancer activity. However, there is no study on the potential of plumbagin to target cisplatin resistance in non-high-grade OC. The current study aimed to determine the antitumor activity of plumbagin for cisplatin resistance in OC cells in vitro, and to identify its potential molecular target for therapeutic benefit using in silico studies. Methods: Plumbagin was used for in vitro cytotoxic effects on cisplatin-resistant (A2780-CR) and sensitive (A2780-CS) isogenic cell lines using a crystal violet cell viability assay. The binding of plumbagin to the nine selected molecular targets was estimated by molecular docking, and their binding energies were compared. The stabilities of the selected docked complexes were confirmed by molecular dynamics simulation (MDS) and molecular mechanics generalized born surface area (MM-GBSA) calculations, and conclusions were drawn to predict the inhibition potential of plumbagin to its best targets. Results: Plumbagin demonstrated the potential to kill A2780-CR cells, and, expectedly, the cell death effect on A2780-CS ovarian cancer cells demonstrated its anti-tumor activity in vitro. It was found to be noneffective in killing normal non-tumorigenic RPE cells, even at higher doses. Docking analysis suggested that it potentially inhibits ovarian cancer cells through various pharmacological targets with high affinity for binding to Chk1 (PDB ID=1ia8) and Aurora Kinase (PDB ID=5ORL). Molecular dynamic simulation data revealed strong and stable protein-ligand complex formation, which was measured in terms of root mean square deviation (RMSD), root mean square fluctuation (RMSF), and radius of gyration (Rg). On the other hand, the MM-GBSA study revealed that the binding free energy of the CT1019-1ia8 complex (-84.26 ± 2.99 Kcal/mol) and CT1019-5ORL (-67.04 ± 2.63 Kcal/mol) was better when compared to other complexes. Discussion: Plumbagin showed the anti-ovarian cancer benefits of plumbagin in cisplatin-resistant ovarian cells, and the potential pharmacological targets identified were Chk1 and Aurora kinase. Conclusion: Our study offers promising insights into plumbagin, particularly in combating cisplatin-resistant OC. However, further in vivo and mechanistic studies are required to validate plumbagin';s potential as a therapeutic candidate for OC.
A Novel Rexinoid Agonist, UAB116, Decreases Metastatic Phenotype in Hepatoblastoma by Inhibiting the Wnt/β-Catenin Pathway via Upregulation of TRIM29 Swatika Butey, Morgan L. Brown, Janet R. Julson, Raoud Marayati, Venkatram R. Atigadda, Maryam G. Shaikh, Nazia Nazam, Colin H. Quinn, Sorina Shirley, Laura L. Stafman, Elizabeth A. Beierle International Journal of Molecular Sciences, 2025 Hepatoblastoma (HB) is the most common pediatric primary liver tumor. About 20% of affected children have pulmonary metastasis at presentation. Survival rates for these children are dismal, not exceeding 25%. To study this subset of patients, we sequenced a metastatic HB cell line, HLM_2, and identified downregulation of the Liver X Receptor (LXR)/Retinoid X Receptor (RXR) pathway. LXR/RXRs function as transcriptional regulators that influence genes implicated in HB development, including the Wnt/β-catenin signaling pathway. We assessed the effects of a novel LXR/RXR agonist, UAB116, on metastatic HB, hypothesizing that this compound would affect genes governing the Wnt/β-catenin pathway, decreasing the metastatic phenotype of HLM_2 metastatic HB cells. We evaluated its effects on viability, proliferation, stemness, clonogenicity, and motility, and performed RNA sequencing to study differential gene regulation. Treatment with UAB116 for 72 h decreased HLM_2 proliferation, stemness, clonogenicity, and invasion. RNA sequencing identified an eight-fold increase in TRIM29, a gene known to inhibit β-catenin, in cells treated with UAB116. Administration of the LXR/RXR agonist, UAB116, reduces proliferation, stemness, and invasiveness of metastatic HB cells, potentially by upregulation of TRIM29, a known modulator of the Wnt/β-catenin pathway, providing support for further exploration of LXR/RXR agonism as a therapeutic strategy for metastatic HB.
Oncolytic virotherapy augments self-maintaining natural killer cell line cytotoxicity against neuroblastoma Colin H. Quinn, Janet R. Julson, Hooper R. Markert, Nazia Nazam, Swatika Butey, Jerry E. Stewart, Jennifer C. Coleman, James M. Markert, Jianmei W. Leavenworth, Elizabeth A. Beierle Cancer Immunology Immunotherapy, 2024 BACKGROUND: Neuroblastoma is the most common extracranial solid tumor in children and accounts for 15% of pediatric cancer related deaths. Targeting neuroblastoma with immunotherapies has proven challenging due to a paucity of immune cells in the tumor microenvironment and the release of immunosuppressive cytokines by neuroblastoma tumor cells. We hypothesized that combining an oncolytic Herpes Simplex Virus (oHSV) with natural killer (NK) cells might overcome these barriers and incite tumor cell death. METHODS: We utilized MYCN amplified and non-amplified neuroblastoma cell lines, the IL-12 expressing oHSV, M002, and the human NK cell line, NK-92 MI. We assessed the cytotoxicity of NK cells against neuroblastoma with and without M002 infection, the effects of M002 on NK cell priming, and the impact of M002 and priming on the migratory capacity and CD107a expression of NK cells. To test clinical applicability, we then investigated the effects of M002 and NK cells on neuroblastoma in vivo. RESULTS: NK cells were more attracted to neuroblastoma cells that were infected with M002. There was an increase in neuroblastoma cell death with the combination treatment of M002 and NK cells both in vitro and in vivo. Priming the NK cells enhanced their cytotoxicity, migratory capacity and CD107a expression. CONCLUSIONS: To the best of our knowledge, these investigations are the first to demonstrate the effects of an oncolytic virus combined with self-maintaining NK cells in neuroblastoma and the priming effect of neuroblastoma on NK cells. The current studies provide a deeper understanding of the relation between NK cells and neuroblastoma and these data suggest that oHSV increases NK cell cytotoxicity towards neuroblastoma.
PP2A activation overcomes leptomeningeal dissemination in group 3 medulloblastoma Nazia Nazam, Michael H. Erwin, Janet R. Julson, Colin H. Quinn, Andee M. Beierle, Laura V. Bownes, Jerry E. Stewart, Kyung-Don Kang, Swatika Butey, Elizabeth Mroczek-Musulman, Michael Ohlmeyer, Elizabeth A. Beierle Journal of Biological Chemistry, 2024 Leptomeningeal dissemination (LMD) is the primary cause of treatment failure in children with group 3 medulloblastoma (MB). Building on our previous work on protein phosphatase 2A (PP2A) activation in MB, here we present preclinical and molecular data on the effects of two novel classes of PP2A activators on disease processes of LMD in group 3 MB. The PP2A activators used in this study are ATUX-6156 and ATUX-6954 (diarylmethylcycloamine sulfonylureas), and ATUX-1215 and ATUX-5800 (diarylmethyl-4-aminotetrahydropyran-sulfonamides). Treatment with these compounds led to suppression of the endogenous PP2A inhibitor, cancerous inhibitor of PP2A (CIP2A), enhanced phosphatase activity (10-60%), and reduced MB viability, migration, and invasion, prerequisites for MB cells to access the cerebrospinal fluid, affecting the initiation stage of LMD. PP2A activator treatment of MB cells led to apoptosis mediated via caspase 9/PARP signaling due to decreased phosphorylation of Bad, impeding the dispersal stage of LMD. Cell proliferation and LMD-driving cellular traits and molecules pertinent to the third stage, colonization, were also affected. Treatment with ATUX-1215 or ATUX-5800 prevented LMD in an intraventricular murine model of MB, possibly mediated by disruption of the CCL2-CCR2 axis by altered NF-kB phosphorylation via disrupted AKT signaling. The present investigation offers proof-of-principle data for PP2A-based reactivation therapy for Group 3 MB and provides the first indications that PP2A reactivation may challenge the current paradigm in targeting the 3-stage process of MB LMD. Further investigations of PP2A activators are warranted as these compounds may prove beneficial as therapeutics for MB.
Novel PP2A-Activating Compounds in Neuroblastoma Nazia Nazam, Laura V. Bownes, Janet R. Julson, Colin H. Quinn, Michael H. Erwin, Raoud Marayati, Hooper R. Markert, Sorina Shirley, Jerry E. Stewart, Karina J. Yoon, Jamie Aye, Michael Ohlmeyer, Elizabeth A. Beierle Cancers, 2024 Background: Neuroblastoma (NB) remains one of the deadliest pediatric solid tumors. Recent advancements aimed at improving outcomes have been insufficient, and patients with high-risk NB continue to have a poor prognosis. Protein phosphatase 2A (PP2A) is a tumor suppressor protein downregulated in many cancers, including NB. PP2A activation has been shown to affect the malignant phenotype in other solid tumors. The present studies aim to investigate the effects of two novel PP2A activators as a NB therapeutic. Methods: Four established NB cell lines and a patient-derived xenoline were utilized to study the effect on cell viability, proliferation, motility, and in vivo tumor growth using two novel tricyclic sulfonamide PP2A activators, ATUX-3364 and ATUX-8385. Results: ATUX-3364 and ATUX-8385 increased PP2A activity. These PP2A activators led to decreased viability, proliferation, and motility of NB cells. Treatment of animals bearing NB tumors with ATUX-3364 or ATUX-8385 resulted in decreased tumor growth in MYCN-amplified SK-N-BE(2) tumors. At the molecular level, PP2A-based reactivation led to dephosphorylation of MYCN-S62 and decreased MYCN protein expression. Conclusions: PP2A activators decreased NB cell viability, proliferation, and motility. In vivo experiments show that PP2A activators have more significant effects on tumorigenesis in MYCN-amplified tumors. Finally, phosphorylation of MYCN protein was decreased following treatment with novel sulfonamide PP2A activators. These data and mechanistic insights may be useful for developing new PP2A-based therapies that target MYCN for the treatment of NB.
PIM Kinase Inhibition Attenuates the Malignant Progression of Metastatic Hepatoblastoma Janet R. Julson, Colin H. Quinn, Swatika Butey, Michael H. Erwin, Raoud Marayati, Nazia Nazam, Jerry E. Stewart, Elizabeth A. Beierle International Journal of Molecular Sciences, 2024 Hepatoblastoma is the most common primary pediatric liver tumor. Children with pulmonary metastases at diagnosis experience survival rates as low as 25%. We have shown PIM kinases play a role in hepatoblastoma tumorigenesis. In this study, we assessed the role of PIM kinases in metastatic hepatoblastoma. We employed the metastatic hepatoblastoma cell line, HLM_2. PIM kinase inhibition was attained using PIM3 siRNA and the pan-PIM inhibitor, AZD1208. Effects of PIM inhibition on proliferation were evaluated via growth curve. Flow cytometry determined changes in cell cycle. AlamarBlue assay assessed effects of PIM kinase inhibition and cisplatin treatment on viability. The lethal dose 50% (LD50) of each drug and combination indices (CI) were calculated and isobolograms constructed to determine synergy. PIM kinase inhibition resulted in decreased HLM_2 proliferation, likely through cell cycle arrest mediated by p21. Combination therapy with AZD1208 and cisplatin resulted in synergy, potentially through downregulation of the ataxia-telangiectasia mutated (ATM) kinase DNA damage response pathway. When assessing the combined effects of pharmacologic PIM kinase inhibition with cisplatin on HLM_2 cells, we found the agents to be synergistic, potentially through inhibition of the ATM pathway. These findings support further exploration of PIM kinase inhibition as a therapeutic strategy for metastatic hepatoblastoma.
Gold Nanoparticles Inhibit PMA-Induced MMP-9 Expression via microRNA-204-5p Upregulation and Deactivation of NF-κBp65 in Breast Cancer Cells Aisha Farhana, Abdullah Alsrhani, Nazia Nazam, Muhammad Ikram Ullah, Yusuf Saleem Khan, Zafar Rasheed Biology, 2023 Objective: Breast cancer (BC) is the most common malignancy in females globally. Matrix metalloproteinase-9 (MMP-9) is crucial to the invasion, progression and spread of BC. Gold nanoparticles (AuNPs) have an anti-tumorigenic role, but their therapeutic role in microRNAs (miRNAs) regulation has not been explored. This study determined the potential of AuNPs against MMP-9 overexpression/production and miRNA-204-5p regulation in BC cells. Methods: AuNPs were newly engineered, and their stability was analyzed using the zeta potential, polydispersity index, surface-plasmon-resonance peak and transmission electron microscopy. A bioinformatics algorithm was used to predict the pairing of miRNA in the 3′untranslated-region (3′UTR) of MMP-9 mRNA. TaqMan assays were carried out to quantify miRNA and mRNA, whereas MMP-9-specific immunoassays and gelatin zymography were used to determine protein secretion and activity. The binding of miRNA in MMP-9 mRNA 3′UTR was verified by luciferase reporter clone assays and transfection with anti-miRNAs. In addition, NF-κBp65 activity was determined and confirmed with parthenolide treatment. Results: Engineered AuNPs were highly stable and spherical in shape, with a mean size of 28.3 nm. Tested in MCF-7 BC cells, microRNA-204-5p directly regulates MMP-9. AuNPs inhibit PMA-induced MMP-9 mRNA and protein via hsa-miR-204-5p upregulation. Anti-miR-204 transfected MCF-7 cells demonstrated enhanced MMP-9 expression (p < 0.001), while AuNPs treatment attenuated MMP-9 expression in a dose-dependent manner (p < 0.05). Moreover, AuNPs also inhibit PMA-induced NF-κBp65 activation in anti-hsa-miR-204 transfected MCF-7 cells. Conclusion: Engineered AuNPs were stable and non-toxic to BC cells. AuNPs inhibit PMA-induced MMP-9 expression, production and activation via NF-κBp65 deactivation and hsa-miR-204-5p upregulation. These novel therapeutic potentials of AuNPs on stimulated BC cells provide novel suggestions that AuNPs inhibit carcinogenic activity via inverse regulation of microRNAs.
Genotoxicity and immunotoxic effects of 1,2-dichloroethane in Wistar rats Mohammad Iqbal Lone, Nazia Nazam, Aashiq Hussain, Shashank K Singh, Abid Hamid Dar, Rauf Ahmad Najar, Mohammed Hussein Al-Qahtani, Waseem Ahmad Journal of Environmental Science and Health Part C Environmental Carcinogenesis and Ecotoxicology Reviews, 2016
Oncolytic herpes simplex virus, M002, increases the antitumor radiation response by decreasing the G2/M arrest in murine rhabdomyosarcoma orthotopic allograft cells MG Shaikh, N Nazam, ML Brown, P Nande, AM Eakes, S Manzoor, ... Cancer Research 86 (7_Supplement), 4638-4638 , 2026 2026
PP2A reactivation upregulates FGA gene in neuroblastoma. N Nazam, S Manzoor, M Ghufran, ML Brown, AM Eakes, P Nande, ... Cancer Research 86 (7_Supplement), 648-648 , 2026 2026
Abstract B059: A small molecule activator of the tumor suppressor phosphatase PP2A overcomes leptomeningeal dissemination in group 3 medulloblastoma N Nazam, MH Erwin, JR Julson, KD Kang, S Butey, CH Quinn, AM Beierle, ... Cancer Research 86 (6_Supplement), B059-B059 , 2026 2026
Upregulation of the lncRNA MEG3 in Metastatic Hepatoblastoma ML Brown, MG Shaikh, N Nazam, AM Eakes, P Nande, A Kaimari, ... Cells 15 (4), 361 , 2026 2026
PP2A activation targets MYCN in neuroblastoma N Nazam, S Manzoor, M Shaikh, ML Brown, JR Julson, CH Quinn, ... Cell Death & Disease 17 (1), 42 , 2026 2026
Deciphering Pharmacological Targets of Plumbagin in Cisplatin-resistant Ovarian Cancer Model using in vitro and in silico Approaches ST Nazia Nazam, Iftikhar Ahmad, Nasimudeen R Jabir, Torki A Zughaibi ... Current Pharmaceutical Design , 2025 2025 Citations: 1
Abstract LB478: Oncolytic herpes simplex virus enhances the anti-tumor response to radiation in human fusion-positive rhabdomyosarcoma patient derived xenografts MG Shaikh, ML Brown, N Nazam, S Shirley, L Markert, J Markert, JM Aye, ... Cancer Research 85 (8_Supplement_2), LB478-LB478 , 2025 2025
A Novel Rexinoid Agonist, UAB116, Decreases Metastatic Phenotype in Hepatoblastoma by Inhibiting the Wnt/β-Catenin Pathway via Upregulation of TRIM29 S Butey, ML Brown, JR Julson, R Marayati, VR Atigadda, MG Shaikh, ... International Journal of Molecular Sciences 26 (9), 3933 , 2025 2025 Citations: 1
PP2A activation targets PAI-1/CCL2 to suppress therapy-induced senescence in neuroblastoma N Nazam, M Ghufran, ML Brown, S Shirley, JE Stewart, M Ohlmeyer, ... Cancer Research 85 (8_Supplement_1), 6444-6444 , 2025 2025
Oncolytic herpes simplex virus enhances the anti-tumor response to radiation in human fusion-positive rhabdomyosarcoma patient derived xenografts Free MG Shaikh, ML Brown, N Nazam, S Shirley, L Markert, J Markert, JM Aye, ... CANCER RESEARCH 85 (8) , 2025 2025
Novel PP2A-activating compounds in neuroblastoma N Nazam, LV Bownes, JR Julson, CH Quinn, MH Erwin, R Marayati, ... Cancers 16 (22), 3836 , 2024 2024 Citations: 5
PP2a Activating Compound Sensitizes Group 3 Medulloblastoma Cells to Irradiation M Erwin, MG Shaikh, N Nazam, S Butey, TL Schanel, JE Stewart, ... JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 239 (5), S358-S358 , 2024 2024
Novel Rexinoid Agonist Inhibits Hepatoblastoma Motility by Inhibiting Wnt/beta-catenin Pathway via Upregulation of TRIM29 S Butey, MG Shaikh, N Nazam, M Erwin, JE Stewart, VR Atigadda, ... JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 239 (5), S356-S356 , 2024 2024
PP2A activation overcomes leptomeningeal dissemination in group 3 medulloblastoma N Nazam, MH Erwin, JR Julson, CH Quinn, AM Beierle, LV Bownes, ... Journal of Biological Chemistry 300 (11) , 2024 2024 Citations: 2
Oncolytic virotherapy augments self-maintaining natural killer cell line cytotoxicity against neuroblastoma CH Quinn, JR Julson, HR Markert, N Nazam, S Butey, JE Stewart, ... Cancer Immunology, Immunotherapy 73 (11), 221 , 2024 2024 Citations: 3
PIM kinase inhibition sensitizes neuroblastoma to doxorubicin JR Julson, CH Quinn, N Nazam, LV Bownes, JE Stewart, EA Beierle Journal of pediatric surgery 59 (7), 1334-1341 , 2024 2024 Citations: 3
Effect of oncolytic herpes simplex virus on fusion-positive rhabdomyosarcoma to radiotherapy. MG Shaikh, N Nazam, S Butey, MH Erwin, JE Stewart, J Aye, EA Beierle Journal of Clinical Oncology 42 (16_suppl), 10063-10063 , 2024 2024
PP2A activation as a new therapeutic strategy in neuroblastoma: Making sense out of senescence. N Nazam, MG Shaikh, S Butey, MH Erwin, JE Stewart, M Ohlmeyer, ... Journal of Clinical Oncology 42 (16_suppl), 10055-10055 , 2024 2024
PIM kinase inhibition attenuates the malignant progression of metastatic hepatoblastoma JR Julson, CH Quinn, S Butey, MH Erwin, R Marayati, N Nazam, ... International Journal of Molecular Sciences 25 (1), 427 , 2023 2023 Citations: 2
PIM Kinase Inhibition Halts the Malignant Progression of Metastatic Hepatoblastoma J Julson, CH Quinn, R Marayati, N Nazam, J Stewart, EA Beierle JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 237 (5), S360-S360 , 2023 2023
MOST CITED SCHOLAR PUBLICATIONS
Mechanistic insights into the antimicrobial actions of metallic nanoparticles and their implications for multidrug resistance S Shaikh, N Nazam, SMD Rizvi, K Ahmad, MH Baig, EJ Lee, I Choi International journal of molecular sciences 20 (10), 2468 , 2019 2019 Citations: 597
Brain-derived neurotrophic factor: a connecting link between nutrition, lifestyle, and Alzheimer’s disease B Xue, SMA Waseem, Z Zhu, MA Alshahrani, N Nazam, F Anjum, ... Frontiers in Neuroscience 16, 925991 , 2022 2022 Citations: 57
Phenolic acids-mediated regulation of molecular targets in ovarian cancer: current understanding and future perspectives N Nazam, NR Jabir, I Ahmad, SA Alharthy, MS Khan, R Ayub, S Tabrez Pharmaceuticals 16 (2), 274 , 2023 2023 Citations: 32
Dimethoate induces DNA Damage and Mitochondrial Dysfunction Triggering Apoptosis in Rat Bone-Marrow and Peripheral Blood Cells N Nazia, MI Lone, A Hamid, T Qadah, A Banjar, Q Alam, M Saeed, ... Toxics 8 (4), 80 , 2020 2020 Citations: 29
Mechanistic insights into the pathogenesis of neurodegenerative diseases: towards the development of effective therapy F Nazam, S Shaikh, N Nazam, AS Alshahrani, GM Hasan, MI Hassan Molecular and Cellular Biochemistry 476 (7), 2739-2752 , 2021 2021 Citations: 24
Abstracts from the 3rd International Genomic Medicine Conference (3rd IGMC 2015) Jeddah, Kingdom of Saudi Arabia. 30 November-3 December 2015 JW Shay, N Homma, R Zhou, MI Naseer, AG Chaudhary, M Al-Qahtani, ... BMC genomics 17 (Suppl 6), 487 , 2016 2016 Citations: 24
Toxicogenetic evaluation of dichlorophene in peripheral blood and in the cells of the immune system using molecular and flow cytometric approaches MI Lone, A Nabi, NJ Dar, A Hussain, N Nazam, A Hamid, W Ahmad Chemosphere 167, 520-529 , 2017 2017 Citations: 21
Genotoxicity and immunotoxic effects of 1, 2-dichloroethane in Wistar rats MI Lone, N Nazam, A Hussain, SK Singh, AH Dar, RA Najar, ... Journal of Environmental Science and Health, Part C 34 (3), 169-186 , 2016 2016 Citations: 18
Assessment of genotoxic potential of the insecticide Dichlorvos using cytogenetic assay N Nazam, MI Lone, S Shaikh, W Ahmad Interdisciplinary Toxicology 6 (2), 77 , 2013 2013 Citations: 17
Gold nanoparticles inhibit PMA-induced MMP-9 expression via microRNA-204-5p upregulation and deactivation of NF-κBp65 in breast cancer cells A Farhana, A Alsrhani, N Nazam, MI Ullah, YS Khan, Z Rasheed Biology 12 (6), 777 , 2023 2023 Citations: 16
Genotoxicity of an organochlorine pesticide dichlorophene by micronucleus and chromosomal aberration assays using bone marrow cells of Rattus norvegicus M Iqbal Lone, N Nazam, S Shaikh, W Ahmad Caryologia 66 (4), 296-303 , 2013 2013 Citations: 16
Dichlorophene and dichlorvos mediated genotoxic and cytotoxic assessment on root meristem cells of Allium cepa S Shaikh, N Nazam, MI Lone, W Ahmad Science Diliman 1, 13-22 , 2012 2012 Citations: 13
Evidence of apoptosis in some cell types due to pentachlorophenol (PCP) in Heteropneustes fossilis MN Ali, N Nazam, MI Lone, S Shaikh, W Ahmad Saudi Journal of Biological Sciences 20 (1), 45-49 , 2013 2013 Citations: 10
Anti-Amyloid Aggregating Gold Nanoparticles: Can they Really be Translated from Bench to Bedside for Alzheimer's Disease Treatment? S Shaikh, N Nazam, SM Danish Rizvi, T Hussain, A Farhana, I Choi Current Protein and Peptide Science 21 (12), 1184-1192 , 2020 2020 Citations: 9
Protective effects of Quercetin against Dimethoate–induced cytotoxicity and genotoxicity in Allium sativum test W Ahmad, S Shaikh, N Nazam, MI Lone 2014 Citations: 8
Recent advances in Alzheimer’s disease in relation to cholinesterase inhibitors and NMDA receptor antagonists N Nazam, A Farhana, S Shaikh Autism Spectrum Disorder and Alzheimer's Disease: Advances in Research, 135-151 , 2022 2022 Citations: 7
Integrative genome wide analysis of protein tyrosine phosphatases identifies CDC25C as prognostic and predictive marker for chemoresistance in breast cancer R Topno, N Nazam, P Kumari, M Kumar, P Agarwal Cancer Biomarkers 32 (4), 491-504 , 2021 2021 Citations: 7
Combined in silico and in vivo studies shed insights into the acute acetylcholinesterase response in rat and human brain N Nazam, S Shaikh, MI Lone, M Sharma, W Ahmad Biotechnology and applied biochemistry 62 (3), 407-415 , 2015 2015 Citations: 6
Novel PP2A-activating compounds in neuroblastoma N Nazam, LV Bownes, JR Julson, CH Quinn, MH Erwin, R Marayati, ... Cancers 16 (22), 3836 , 2024 2024 Citations: 5
Biochemical and cytoarchitechtural evaluation of dimethoate intoxication in rat liver and kidney: An in vivo study N Nazam, MI Lone, M Sharma, AA Khan, AM Kelany, W Ahmad Indo Am J Pharm Res 5 (3), 1127-1137 , 2015 2015 Citations: 4