A5101910681- Cancer, Lipids, and Metabolism
- Lipid metabolism and biosynthesis
- Cancer, Hypoxia, and Metabolism
- Endoplasmic Reticulum Stress and Disease
- Autophagy in Disease and Therapy
- RNA modifications and cancer
- Mechanisms of cancer metastasis
- Signaling Pathways in Disease
- Cancer Research and Treatments
- Metabolomics and Mass Spectrometry Studies
- Estrogen and related hormone effects
- Ovarian cancer diagnosis and treatment
- Cell Adhesion Molecules Research
- Surface and Thin Film Phenomena
- Genomics and Chromatin Dynamics
- Neuroendocrine regulation and behavior
- Advanced Electron Microscopy Techniques and Applications
- Retinoids in leukemia and cellular processes
- Ferroptosis and cancer prognosis
- Occupational and environmental lung diseases
- MicroRNA in disease regulation
- Cancer-related Molecular Pathways
- Galectins and Cancer Biology
- Peptidase Inhibition and Analysis
- Anesthesia and Neurotoxicity Research
Mayo Clinic
2013-2024
Alcorn State University
2020-2024
WinnMed
2017-2023
Mayo Clinic in Arizona
2015-2023
Massachusetts General Hospital
2023
Biological E (India)
2021
The University of Texas at El Paso
2018
Metabolic alterations are increasingly recognized as important novel anti‐cancer targets. Among several regulators of metabolic alterations, fructose 2,6 bisphosphate (F2,6BP) is a critical glycolytic regulator. Inhibition the active form PFKFB3 ser461 using inhibitor, PFK158 resulted in reduced glucose uptake, ATP production, lactate release well induction apoptosis gynecologic cancer cells. Moreover, we found that synergizes with carboplatin (CBPt) and paclitaxel (PTX) chemoresistant cell...
Dissemination of ovarian cancer cells can lead to inoperable metastatic lesions in the bowel and omentum that cause patient death. Here we show LRRC15, a type-I 15-leucine-rich repeat-containing membrane protein, highly overexpressed metastases compared with matched primary tumors acts as potent promoter omental metastasis. Complementary models demonstrated LRRC15 expression leads inhibition anoikis-induced cell death promotes adhesion invasion through matrices mimic omentum....
// Ashwani Khurana 1, * , Debarshi Roy Eleftheria Kalogera 2, Susmita Mondal 1 Xuyang Wen Xiaoping He Sean Dowdy 2 Viji Shridhar Department of Experimental Pathology, Mayo Clinic College Medicine, Rochester, MN, USA Obstetrics and Gynecology, These authors have contributed equally to this work Correspondence to: Shridhar, e-mail: shridhar.vijayalakshmi@mayo.edu Keywords: quinacrine, ovarian cancer, autophagy, apoptosis tumorigenesis Received: August 25, 2015 Accepted: October 05, Published:...
We have previously shown that the anti-malarial compound Quinacrine (QC) inhibits ovarian cancer (OC) growth by modulating autophagy. In present study we extended these studies to identify molecular pathways regulated QC promote apoptosis independent of p53 status in OC. exhibited strong anti-cancer properties OC cell lines contrast other autophagy inhibiting drugs. treatment selectively upregulated cycle inhibitor p21, and downregulated F box protein Skp2 p62/SQSTM1 expression status....
ObjectiveThis study is designed to identify genes and pathways that could promote metastasis the bowel in high-grade serous ovarian cancer (OC) evaluate their associations with clinical outcomes.MethodsWe performed RNA sequencing of OC primary tumors (PTs) corresponding metastases (n = 21 discovery set; n 18 replication set). Differentially expressed (DEGs) were those at least 2-fold higher (BMets) than PTs 30% patients (P < .05) no increased expression paired benign tissue validated...
The metabolic signatures of cancer cells are often associated with elevated glycolysis. Pharmacological (PFK158 treatment) and genetic inhibition 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a critical control point in the glycolytic pathway, decreases glucose uptake, ATP production, lactate dehydrogenase activity arrests malignant pleural mesothelioma (MPM) G0/G1 phase to induce cell death. To overcome this nutrient stress, PFKFB3 led an escalation endoplasmic reticulum...
Loss of the endosulfatase HSulf-1 is common in ovarian cancer, upregulates heparin binding growth factor signaling and potentiates tumorigenesis angiogenesis. However, metabolic differences between isogenic cells with without have not been characterized upon suppression vitro. Since closely tied to alterations, we determined extent which loss affects cancer cell metabolism.Ingenuity pathway analysis gene expression shRNA-silenced (Sh1 Sh2 cells) compared non-targeted control shRNA (NTC...
// Susmita Mondal 1 , Debarshi Roy Juliana Camacho-Pereira 2,7 Ashwani Khurana Eduardo Chini 2 Lifeng Yang 3 Joelle Baddour Katherine Stilles Seth Padmabandu Sam Leung 4 Steve Kalloger Blake Gilks Val Lowe 5 Thomas Dierks 6 Edward Hammond 8 Keith Dredge Deepak Nagrath and Viji Shridhar Department of Experimental Pathology, Mayo Clinic College Medicine, Rochester, MN, USA Anesthesiology, Chemical Biomolecular Engineering, Rice University, Houston, TX, Pathology Laboratory University British...
Abstract Background Aberrant lipogenicity and deregulated autophagy are common in most advanced human cancer therapeutic strategies to exploit these pathways currently under consideration. Group III Phospholipase A2 (sPLA2-III/PLA2G3), an atypical secretory PLA2, is recognized as a regulator of lipid metabolism associated with oncogenesis. Though recent studies reveal that high PLA2G3 expression significantly correlates poor prognosis several cancers, however, role ovarian (OC) pathogenesis...
Abstract Defective autophagy and deranged metabolic pathways are common in cancer; pharmacologic targeting of these two could provide a viable therapeutic option. However, how regulated by limited availability growth factors is still unknown. Our study shows that HSulf-1 (endosulfatase), known tumor suppressor which attenuates heparin sulfate binding factor signaling, also regulates interplay between lipogenesis. Silencing OV202 TOV2223 cells (ovarian cancer cell lines) resulted increased...
The expression of human Sulfatase1 (HSulf-1) is downregulated in the majority primary ovarian cancer tumors, but functional consequence this downregulation remains unclear. Using two different shRNAs (Sh1 and Sh2), HSulf-1 was stably OV202 cells. We found that HSulf-1-deficient Sh1 Sh2 cells formed colonies soft agar. In contrast, nontargeting control (NTC) shRNA-transduced did not form any colonies. Moreover, subcutaneous injection resulted tumor formation nude mice, whereas NTC not. Also,...
Understanding nanoscale structural changes can provide information about the physical state of cells/tissues. It has now been shown that increases in alterations are associated with progress carcinogenesis most cancer cases, including early carcinogenesis. Anti-cancerous therapies designed to inhibit growth cells; however, it is challenging detect efficacy such drugs stages treatment. A unique method assessing impact anti-cancerous on cancerous cells/tissues probe alterations. In this paper,...
Background: The migration of tumor cells is critical in spreading cancers through the lymphatic nodes and circulatory systems. Although arachidonic acid (AA) its soluble metabolites have been shown to induce breast colon cancer cells, mechanism by which it induces such has not fully understood. Objective: effect AA on migratory responses MDA-MB-231 cell line (a triple-negative cell) was examined compared with MCF-7 (estrogen-receptor positive) elucidate AA-induced migration. Methods:...
Protein disulfide isomerase (PDI), an important endoplasmic reticulum-resident oxidoreductase chaperone can bind to estrogens as well intact with its receptor proteins [i.e. estrogen receptors (ER) α and β]. It has been postulated that PDI also acts intracellular 17β-estradiol (E2)-binding protein transports accumulates E2 in live cells. Drop level promotes dissociation of from released cytosol; the augment receptor-mediated transcriptional activity mitogenic action cultured cells by...
Understanding the nanoscale structural changes can provide physical state of cells/tissues. It has been now shown that increases in alterations are associated with progress carcinogenesis most cancer cases, including early carcinogenesis. Anti-cancerous therapies intended for growth inhibition cells; however, it is challenging to detect efficacy such drugs stages treatment. A unique method assess impact anti-cancerous on cancerous cells/tissues probe alterations. In this paper, we study...
Abstract We have previously shown that loss of HSulf-1, an endosulfatase removes 6-O sulfation HSPGs augmented heparin binding growth factor (HB-GF) signaling resulting in enhanced tumorigenesis, angiogenesis and metastasis ovarian cancer. However, the role HSulf-1 energy metabolism how increased cells with altered cellular cancer yet to be investigated. Here, we show for first time batch clonal lines knockdown [OV202 (Sh1/2)] knock out (KO) MEFs showed a significantly higher glycolytic flux...
Abstract Metabolic alterations in cancer are increasingly being recognized as important novel targets. Among different regulators of altered metabolism, 6-PhosphoFructo-2-Kinase/Fructose-2,6-Bisphosphatases 3 (PFKFB3) a glycolytic enzyme required for tumorigenic growth, and produces fructose-2,6-bisphosphate (F2,6BP), is regulator glycolysis. We determined that the active form PFKFB3ser471 was overexpressed chemo-resistant ovarian (OVCA) cell lines resistant patient derived xenograft (PDX)...
MiRNAs are 20-22 nucleotide long single-stranded non-coding RNA sequences, which can regulate post transcriptional activity of mRNA by binding with it at 3&rsquo;UTR region (untranslated region). Thus deregulation miRNA expression is responsible for dysregulating function contributes in developing various diseases as well cancerous phenotypes. Alteration single sequence one the reasons behind expression. The most frequent carcinoma current day breast cancer causes a high mortality among...