Sarita G. Menon

ORCID: 0000-0001-9548-149X
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About
Contact & Profiles
Research Areas
  • Histone Deacetylase Inhibitors Research
  • Glutathione Transferases and Polymorphisms
  • Inflammatory mediators and NSAID effects
  • Cancer, Hypoxia, and Metabolism
  • Click Chemistry and Applications
  • Estrogen and related hormone effects
  • Genomics, phytochemicals, and oxidative stress
  • Chemical Synthesis and Analysis
  • Protein Kinase Regulation and GTPase Signaling
  • Cancer, Stress, Anesthesia, and Immune Response
  • Cancer-related Molecular Pathways
  • Vitamin C and Antioxidants Research
  • RNA modifications and cancer
  • Cellular Mechanics and Interactions
  • Wnt/β-catenin signaling in development and cancer
  • Trypanosoma species research and implications
  • Sulfur Compounds in Biology
  • Retinoids in leukemia and cellular processes
  • Microtubule and mitosis dynamics
  • Cancer-related gene regulation
  • Folate and B Vitamins Research
  • Cardiomyopathy and Myosin Studies
  • Redox biology and oxidative stress
  • Epigenetics and DNA Methylation
  • Aldose Reductase and Taurine

The University of Texas Health Science Center at Houston
2012-2013

University at Buffalo, State University of New York
2007-2012

Buffalo State University
2012

University of Iowa
2003-2007

University of Iowa Hospitals and Clinics
2007

Abstract Thiol antioxidants, including N-acetyl-l-cysteine (NAC), are widely used as modulators of the intracellular redox state. We investigated hypothesis that NAC-induced reactive oxygen species (ROS) signaling perturbs cellular proliferation by regulating cell cycle regulatory protein cyclin D1 and ROS scavenging enzyme Mn–superoxide dismutase (MnSOD). When cultured in media containing NAC, mouse fibroblasts showed G1 arrest with decreased levels. The absence a overexpressing (or...

10.1158/0008-5472.can-07-0225 article EN Cancer Research 2007-07-01

Abstract Celecoxib inhibits proliferation and induces apoptosis in human tumors, but the molecular mechanisms for these processes are poorly understood. In this study, we evaluated ability of celecoxib to induce toxicity head neck squamous cell carcinomas (HNSCC) explored relationships between celecoxib-induced cycle inhibition HNSCC. inhibited UM-SCC-1 UM-SCC-17B cells both vitro vivo, accompanied by G1 phase arrest apoptosis. induced p21waf1/cip1 at transcriptional level independent...

10.1158/0008-5472.can-06-3780 article EN Cancer Research 2007-04-15

RhoA is overexpressed in human cancer and contributes to aberrant cell motility metastatic progression; however, regulatory mechanisms controlling activity are poorly understood. Neuroepithelial transforming gene 1 (Net1) a guanine nucleotide exchange factor that cancer. It encodes two isoforms, Net1 Net1A, which cycle between the nucleus plasma membrane. proteins must leave activate RhoA, but extranuclear localization of isoforms have not been described. Here, we show Rac1 activation causes...

10.1128/mcb.00980-12 article EN Molecular and Cellular Biology 2012-11-27

Reactive oxygen species (ROS) and ROS signaling have been implicated in a variety of human pathophysiological conditions that involve aberrant cellular proliferation, particularly cancer. We hypothesize intracellular redox state differentially affects cell-cycle progression nonmalignant versus malignant cells. The thiol antioxidant, N-acetyl-L-cysteine (NAC), was used to alter breast epithelial (MCF-10A) cancer cells (MCF-7 MDA-MB-231). Treatment with NAC resulted significant augmentation...

10.1089/ars.2005.7.711 article EN Antioxidants and Redox Signaling 2005-05-01

Neuroepithelial transforming gene 1 (Net1) is a RhoA-subfamily-specific guanine nucleotide exchange factor that overexpressed in multiple human cancers and required for proliferation. Molecular mechanisms underlying its role cell proliferation are unknown. Here we show overexpression or knockdown of Net1 causes mitotic defects. chromosome congression during metaphase generation stable kinetochore microtubule attachments. Accordingly, inhibition expression results spindle assembly checkpoint...

10.1091/mbc.e13-01-0061 article EN cc-by-nc-sa Molecular Biology of the Cell 2013-07-17

Abstract This study was performed to compare the relative antineoplastic activity of 10 different non‐steroidal anti‐inflammatory drugs (NSAIDs) in clinical use, and investigate underlying mechanisms this a squamous cell carcinoma head neck model (SCCHN). A standard 5‐day MTT assay used calculate IC 50 values UM‐SCC‐1 cells for NSAIDs, including celecoxib, rofecoxib, sulindac sulfide, sulfone, indomethacin, ketoprofen, flurbiprofen, naproxen, piroxicam, aspirin. Celecoxib, COX‐2 specific...

10.1002/mc.20318 article EN Molecular Carcinogenesis 2007-04-05

Short, non-encoded oligo(A), oligo(U), or A/U tails can impact mRNA stability in kinetoplastid mitochondria. However, a comprehensive picture of the relative effects these modifications RNA is lacking. Furthermore, while U-preferring exoribonuclease TbRND acts on U-tailed gRNAs, its role decay uridylated mRNAs has only been cursorily investigated. Here, we analyzed roles 3′ tail composition and using cells harbouring single double knockdown KPAP1 poly(A) polymerase. Analysis abundance...

10.1371/journal.pone.0037639 article EN cc-by PLoS ONE 2012-05-21

AbstractSulindac sulfide and sulindac sulfone have demonstrated anti-neoplastic chemopreventive activity against various human tumors, but few studies examined the relative effectiveness of these drugs squamous cell carcinoma head neck (SCCHN). These compounds are metabolites non-steroidal anti-inflammatory drug sulindac, differ in their ability to inhibit cyclooxygenase-2 (COX-2) enzyme function. Sulindac (the metabolite with COX-2 inhibitory function) strong growth inhibition as measured...

10.4161/cbt.6.1.3470 article EN Cancer Biology & Therapy 2007-01-01

3186 Background: Standard treatment modalities for head and neck cancer remain surgery, radiation, chemotherapy. While surgical techniques, delivery of chemotherapy options have expanded, survival rates stagnant. Targeted therapy with novel anticancer molecules show future promise. However, in the interim, any agent added to improve conventional treatment, without significant side effects, is a needed addition. NSAIDs are demonstrating chemopreventative therapeutic benefits low side-effect...

10.1200/jco.2004.22.90140.3186 article EN Journal of Clinical Oncology 2004-07-15

Supplementary Figure 2 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367336.v1 preprint EN cc-by 2023-03-30

Supplementary Figure 2 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367336 preprint EN cc-by 2023-03-30

Supplementary Figure 3 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367333.v1 preprint EN cc-by 2023-03-30

Supplementary Figure 1 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367339.v1 preprint EN cc-by 2023-03-30

<div>Abstract<p>Thiol antioxidants, including <i>N</i>-acetyl-l-cysteine (NAC), are widely used as modulators of the intracellular redox state. We investigated hypothesis that NAC-induced reactive oxygen species (ROS) signaling perturbs cellular proliferation by regulating cell cycle regulatory protein cyclin D1 and ROS scavenging enzyme Mn–superoxide dismutase (MnSOD). When cultured in media containing NAC, mouse fibroblasts showed G<sub>1</sub> arrest...

10.1158/0008-5472.c.6495518 preprint EN 2023-03-30

Supplementary Figure 4 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367330.v1 preprint EN cc-by 2023-03-30

Supplementary Figure 1 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367339 preprint EN cc-by 2023-03-30

Supplementary Figure Legends 1-4 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367327.v1 preprint EN cc-by 2023-03-30

Supplementary Figure Legends 1-4 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367327 preprint EN cc-by 2023-03-30

Supplementary Figure 4 from Superoxide Signaling Mediates <i>N</i>-acetyl-l-cysteine–Induced G<sub>1</sub> Arrest: Regulatory Role of Cyclin D1 and Manganese Dismutase

10.1158/0008-5472.22367330 preprint EN cc-by 2023-03-30

<div>Abstract<p>Thiol antioxidants, including <i>N</i>-acetyl-l-cysteine (NAC), are widely used as modulators of the intracellular redox state. We investigated hypothesis that NAC-induced reactive oxygen species (ROS) signaling perturbs cellular proliferation by regulating cell cycle regulatory protein cyclin D1 and ROS scavenging enzyme Mn–superoxide dismutase (MnSOD). When cultured in media containing NAC, mouse fibroblasts showed G<sub>1</sub> arrest...

10.1158/0008-5472.c.6495518.v1 preprint EN 2023-03-30
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