LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Back to previous search Search history
Advanced search

Your last searches

  1. AU="Henry, Whitney S"
  2. AU="Pirnajmedin, Fatemeh"
  3. AU="Rebeyka, Ivan M"
  4. AU=Adgey A A J AU=Adgey A A J
  5. AU="Yagi, Yoshitaka"
  6. AU="Mirandola, Massimo"
  7. AU="Alkhatib, Sanaa G"
  8. AU="Ye, Guangming"
  9. AU="Yiyi, L"
  10. AU="Siles, Francisco"
  11. AU="Song, Sin-Mao"
  12. AU="Yaxuan He"
  13. AU="Wu, Jiaojie"
  14. AU="Tze Kwun Ng"
  15. AU="Leonard L Yeo"

Search results

Result 1 - 8 of total 8

Search options

  1. Article ; Online: Lipidomes define immune cell identity.

    Levental, Kandice R / Henry, Whitney S

    Nature cell biology

    2024  Volume 26, Issue 4, Page(s) 516–518

    MeSH term(s) Lipidomics
    Language English
    Publishing date 2024-04-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/s41556-024-01398-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5169: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 12: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: ATF3 characterizes aggressive drug-tolerant persister cells in HGSOC.

    Böpple, Kathrin / Oren, Yaara / Henry, Whitney S / Dong, Meng / Weller, Sandra / Thiel, Julia / Kleih, Markus / Gaißler, Andrea / Zipperer, Damaris / Kopp, Hans-Georg / Aylon, Yael / Oren, Moshe / Essmann, Frank / Liang, Chunguang / Aulitzky, Walter E

    Cell death & disease

    2024  Volume 15, Issue 4, Page(s) 290

    Abstract: High-grade serous ovarian cancer (HGSOC) represents the most common and lethal subtype of ovarian cancer. Despite initial response to platinum-based standard therapy, patients commonly suffer from relapse that likely originates from drug-tolerant ... ...

    Abstract High-grade serous ovarian cancer (HGSOC) represents the most common and lethal subtype of ovarian cancer. Despite initial response to platinum-based standard therapy, patients commonly suffer from relapse that likely originates from drug-tolerant persister (DTP) cells. We generated isogenic clones of treatment-naïve and cisplatin-tolerant persister HGSOC cells. In addition, single-cell RNA sequencing of barcoded cells was performed in a xenograft model with HGSOC cell lines after platinum-based therapy. Published single-cell RNA-sequencing data from neo-adjuvant and non-treated HGSOC patients and patient data from TCGA were analyzed. DTP-derived cells exhibited morphological alterations and upregulation of epithelial-mesenchymal transition (EMT) markers. An aggressive subpopulation of DTP-derived cells showed high expression of the stress marker ATF3. Knockdown of ATF3 enhanced the sensitivity of aggressive DTP-derived cells to cisplatin-induced cell death, implying a role for ATF3 stress response in promoting a drug tolerant persister cell state. Furthermore, single cell lineage tracing to detect transcriptional changes in a HGSOC cell line-derived xenograft relapse model showed that cells derived from relapsed solid tumors express increased levels of EMT and multiple endoplasmic reticulum (ER) stress markers, including ATF3. Single cell RNA sequencing of epithelial cells from four HGSOC patients also identified a small cell population resembling DTP cells in all samples. Moreover, analysis of TCGA data from 259 HGSOC patients revealed a significant progression-free survival advantage for patients with low expression of the ATF3-associated partial EMT genes. These findings suggest that increased ATF3 expression together with partial EMT promote the development of aggressive DTP, and thereby relapse in HGSOC patients.
    MeSH term(s) Humans ; Activating Transcription Factor 3/metabolism ; Activating Transcription Factor 3/genetics ; Female ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Drug Resistance, Neoplasm/drug effects ; Epithelial-Mesenchymal Transition/drug effects ; Epithelial-Mesenchymal Transition/genetics ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Ovarian Neoplasms/metabolism ; Animals ; Mice ; Xenograft Model Antitumor Assays ; Gene Expression Regulation, Neoplastic/drug effects
    Chemical Substances Activating Transcription Factor 3 ; Cisplatin (Q20Q21Q62J) ; ATF3 protein, human
    Language English
    Publishing date 2024-04-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-024-06674-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article: Ether lipids influence cancer cell fate by modulating iron uptake.

    Henry, Whitney S / Müller, Sebastian / Yang, Jia-Shu / Innes-Gold, Sarah / Das, Sunny / Reinhardt, Ferenc / Sigmund, Kim / Phadnis, Vaishnavi V / Wan, Zhengpeng / Eaton, Elinor / Sampaio, Julio L / Bell, George W / Viravalli, Amartya / Hammond, Paula T / Kamm, Roger D / Cohen, Adam E / Boehnke, Natalie / Hsu, Victor W / Levental, Kandice R /
    Rodriguez, Raphaël / Weinberg, Robert A

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Cancer cell fate has been widely ascribed to mutational changes within protein-coding genes associated with tumor suppressors and oncogenes. In contrast, the mechanisms through which the biophysical properties of membrane lipids influence cancer cell ... ...

    Abstract Cancer cell fate has been widely ascribed to mutational changes within protein-coding genes associated with tumor suppressors and oncogenes. In contrast, the mechanisms through which the biophysical properties of membrane lipids influence cancer cell survival, dedifferentiation and metastasis have received little scrutiny. Here, we report that cancer cells endowed with a high metastatic ability and cancer stem cell-like traits employ ether lipids to maintain low membrane tension and high membrane fluidity. Using genetic approaches and lipid reconstitution assays, we show that these ether lipid-regulated biophysical properties permit non-clathrin-mediated iron endocytosis via CD44, leading directly to significant increases in intracellular redox-active iron and enhanced ferroptosis susceptibility. Using a combination of in vitro three-dimensional microvascular network systems and in vivo animal models, we show that loss of ether lipids also strongly attenuates extravasation, metastatic burden and cancer stemness. These findings illuminate a mechanism whereby ether lipids in carcinoma cells serve as key regulators of malignant progression while conferring a unique vulnerability that can be exploited for therapeutic intervention.
    Language English
    Publishing date 2024-03-21
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.20.585922
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  4. Article ; Online: MMD collaborates with ACSL4 and MBOAT7 to promote polyunsaturated phosphatidylinositol remodeling and susceptibility to ferroptosis.

    Phadnis, Vaishnavi V / Snider, Jamie / Varadharajan, Venkateshwari / Ramachandiran, Iyappan / Deik, Amy A / Lai, Zon Weng / Kunchok, Tenzin / Eaton, Elinor Ng / Sebastiany, Carolin / Lyakisheva, Anna / Vaccaro, Kyle D / Allen, Juliet / Yao, Zhong / Wong, Victoria / Geng, Betty / Weiskopf, Kipp / Clish, Clary B / Brown, J Mark / Stagljar, Igor /
    Weinberg, Robert A / Henry, Whitney S

    Cell reports

    2023  Volume 42, Issue 9, Page(s) 113023

    Abstract: Ferroptosis is a form of regulated cell death with roles in degenerative diseases and cancer. Excessive iron-catalyzed peroxidation of membrane phospholipids, especially those containing the polyunsaturated fatty acid arachidonic acid (AA), is central in ...

    Abstract Ferroptosis is a form of regulated cell death with roles in degenerative diseases and cancer. Excessive iron-catalyzed peroxidation of membrane phospholipids, especially those containing the polyunsaturated fatty acid arachidonic acid (AA), is central in driving ferroptosis. Here, we reveal that an understudied Golgi-resident scaffold protein, MMD, promotes susceptibility to ferroptosis in ovarian and renal carcinoma cells in an ACSL4- and MBOAT7-dependent manner. Mechanistically, MMD physically interacts with both ACSL4 and MBOAT7, two enzymes that catalyze sequential steps to incorporate AA in phosphatidylinositol (PI) lipids. Thus, MMD increases the flux of AA into PI, resulting in heightened cellular levels of AA-PI and other AA-containing phospholipid species. This molecular mechanism points to a pro-ferroptotic role for MBOAT7 and AA-PI, with potential therapeutic implications, and reveals that MMD is an important regulator of cellular lipid metabolism.
    MeSH term(s) Cell Line ; Fatty Acids, Unsaturated ; Ferroptosis ; Phosphatidylinositols/metabolism ; Phospholipids/metabolism ; Humans
    Chemical Substances Fatty Acids, Unsaturated ; Phosphatidylinositols ; Phospholipids ; MMD protein, human ; long-chain-fatty-acid-CoA ligase (EC 6.2.1.3) ; MBOAT7 protein, human (EC 2.3.-)
    Language English
    Publishing date 2023-09-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.113023
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Aspirin Suppresses Growth in PI3K-Mutant Breast Cancer by Activating AMPK and Inhibiting mTORC1 Signaling.

    Henry, Whitney S / Laszewski, Tyler / Tsang, Tiffany / Beca, Francisco / Beck, Andrew H / McAllister, Sandra S / Toker, Alex

    Cancer research

    2017  Volume 77, Issue 3, Page(s) 790–801

    Abstract: Despite the high incidence of oncogenic mutations in PIK3CA, the gene encoding the catalytic subunit of PI3K, PI3K inhibitors have yielded little clinical benefit for breast cancer patients. Recent epidemiologic studies have suggested a therapeutic ... ...

    Abstract Despite the high incidence of oncogenic mutations in PIK3CA, the gene encoding the catalytic subunit of PI3K, PI3K inhibitors have yielded little clinical benefit for breast cancer patients. Recent epidemiologic studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts. Aspirin decreased viability and anchorage-independent growth of mutant PIK3CA breast cancer cells independently of its effects on COX-2 and NF-κB. We ascribed the effects of aspirin to AMP-activated protein kinase (AMPK) activation, mTORC1 inhibition, and autophagy induction. In vivo, oncogenic PIK3CA-driven mouse mammary tumors treated daily with aspirin resulted in decreased tumor growth kinetics, whereas combination therapy of aspirin and a PI3K inhibitor further attenuated tumor growth. Our study supports the evaluation of aspirin and PI3K pathway inhibitors as a combination therapy for targeting breast cancer. Cancer Res; 77(3); 790-801. ©2016 AACR.
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Aspirin/pharmacology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Class I Phosphatidylinositol 3-Kinases ; Female ; Gene Knockdown Techniques ; Humans ; Immunoblotting ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Multiprotein Complexes/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Polymerase Chain Reaction ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism ; Xenograft Model Antitumor Assays
    Chemical Substances Anti-Inflammatory Agents, Non-Steroidal ; Multiprotein Complexes ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CA protein, human (EC 2.7.1.137) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Aspirin (R16CO5Y76E)
    Language English
    Publishing date 2017-02-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-16-2400
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Plasticity of ether lipids promotes ferroptosis susceptibility and evasion.

    Zou, Yilong / Henry, Whitney S / Ricq, Emily L / Graham, Emily T / Phadnis, Vaishnavi V / Maretich, Pema / Paradkar, Sateja / Boehnke, Natalie / Deik, Amy A / Reinhardt, Ferenc / Eaton, John K / Ferguson, Bryan / Wang, Wenyu / Fairman, Joshua / Keys, Heather R / Dančík, Vlado / Clish, Clary B / Clemons, Paul A / Hammond, Paula T /
    Boyer, Laurie A / Weinberg, Robert A / Schreiber, Stuart L

    Nature

    2020  Volume 585, Issue 7826, Page(s) 603–608

    Abstract: Ferroptosis-an iron-dependent, non-apoptotic cell death process-is involved in various degenerative diseases and represents a targetable susceptibility in certain ... ...

    Abstract Ferroptosis-an iron-dependent, non-apoptotic cell death process-is involved in various degenerative diseases and represents a targetable susceptibility in certain cancers
    MeSH term(s) Animals ; CRISPR-Cas Systems/genetics ; Cell Differentiation ; Cell Line ; Ethers/chemistry ; Ethers/metabolism ; Female ; Ferroptosis ; Gene Editing ; Humans ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Lipid Peroxidation ; Male ; Mice ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Neurons/cytology ; Neurons/metabolism ; Ovarian Neoplasms/metabolism ; Ovarian Neoplasms/pathology ; Peroxisomes/genetics ; Peroxisomes/metabolism ; Phospholipids/chemistry ; Phospholipids/metabolism
    Chemical Substances Ethers ; Phospholipids
    Language English
    Publishing date 2020-09-16
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-020-2732-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article ; Online: NFAT1 promotes intratumoral neutrophil infiltration by regulating IL8 expression in breast cancer.

    Kaunisto, Aura / Henry, Whitney S / Montaser-Kouhsari, Laleh / Jaminet, Shou-Ching / Oh, Eun-Yeong / Zhao, Li / Luo, Hongbo R / Beck, Andrew H / Toker, Alex

    Molecular oncology

    2015  Volume 9, Issue 6, Page(s) 1140–1154

    Abstract: NFAT transcription factors are key regulators of gene expression in immune cells. In addition, NFAT1-induced genes play diverse roles in mediating the progression of various solid tumors. Here we show that NFAT1 induces the expression of the IL8 gene by ... ...

    Abstract NFAT transcription factors are key regulators of gene expression in immune cells. In addition, NFAT1-induced genes play diverse roles in mediating the progression of various solid tumors. Here we show that NFAT1 induces the expression of the IL8 gene by binding to its promoter and leading to IL8 secretion. Thapsigargin stimulation of breast cancer cells induces IL8 expression in an NFAT-dependent manner. Moreover, we show that NFAT1-mediated IL8 production promotes the migration of primary human neutrophils in vitro and also promotes neutrophil infiltration in tumor xenografts. Furthermore, expression of active NFAT1 effectively suppresses the growth of nascent and established tumors by a non cell-autonomous mechanism. Evaluation of breast tumor tissue reveals that while the levels of NFAT1 are similar in tumor cells and normal breast epithelium, cells in the tumor stroma express higher levels of NFAT1 compared to normal stroma. Elevated levels of NFAT1 also correlate with increased neutrophil infiltrate in breast tumors. These data point to a mechanism by which NFAT1 orchestrates the communication between breast cancer cells and host neutrophils during breast cancer progression.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Interleukin-8/genetics ; Interleukin-8/metabolism ; Mice ; Mice, Nude ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/metabolism ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neutrophil Infiltration ; Neutrophils/metabolism ; Neutrophils/pathology
    Chemical Substances CXCL8 protein, human ; Interleukin-8 ; NFATC Transcription Factors ; NFATC2 protein, human ; Neoplasm Proteins
    Language English
    Publishing date 2015-02-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1016/j.molonc.2015.02.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6637: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  8. Article ; Online: LINC00520 is induced by Src, STAT3, and PI3K and plays a functional role in breast cancer.

    Henry, Whitney S / Hendrickson, David G / Beca, Francisco / Glass, Benjamin / Lindahl-Allen, Marianne / He, Lizhi / Ji, Zhe / Struhl, Kevin / Beck, Andrew H / Rinn, John L / Toker, Alex

    Oncotarget

    2016  Volume 7, Issue 50, Page(s) 81981–81994

    Abstract: Long non-coding RNAs (lncRNAs) have been implicated in normal cellular homeostasis as well as pathophysiological conditions, including cancer. Here we performed global gene expression profiling of mammary epithelial cells transformed by oncogenic v-Src, ... ...

    Abstract Long non-coding RNAs (lncRNAs) have been implicated in normal cellular homeostasis as well as pathophysiological conditions, including cancer. Here we performed global gene expression profiling of mammary epithelial cells transformed by oncogenic v-Src, and identified a large subset of uncharacterized lncRNAs potentially involved in breast cancer development. Specifically, our analysis revealed a novel lncRNA, LINC00520 that is upregulated upon ectopic expression of oncogenic v-Src, in a manner that is dependent on the transcription factor STAT3. Similarly, LINC00520 is also increased in mammary epithelial cells transformed by oncogenic PI3K and its expression is decreased upon knockdown of mutant PIK3CA. Additional expression profiling highlight that LINC00520 is elevated in a subset of human breast carcinomas, with preferential enrichment in the basal-like molecular subtype. ShRNA-mediated depletion of LINC00520 results in decreased cell migration and loss of invasive structures in 3D. RNA sequencing analysis uncovers several genes that are differentially expressed upon ectopic expression of LINC00520, a significant subset of which are also induced in v-Src-transformed MCF10A cells. Together, these findings characterize LINC00520 as a lncRNA that is regulated by oncogenic Src, PIK3CA and STAT3, and which may contribute to the molecular etiology of breast cancer.
    Language English
    Publishing date 2016-12-13
    Publishing country United States
    Document type Journal Article
    ISSN 1949-2553
    ISSN (online) 1949-2553
    DOI 10.18632/oncotarget.11962
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top