Axel H. Schönthal

ORCID: 0000-0003-0662-5653
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About
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Research Areas
  • Glioma Diagnosis and Treatment
  • Cancer-related Molecular Pathways
  • Inflammatory mediators and NSAID effects
  • Autophagy in Disease and Therapy
  • Endoplasmic Reticulum Stress and Disease
  • Brain Metastases and Treatment
  • Cancer, Hypoxia, and Metabolism
  • Ubiquitin and proteasome pathways
  • Nanoplatforms for cancer theranostics
  • Adenosine and Purinergic Signaling
  • PARP inhibition in cancer therapy
  • Cancer, Stress, Anesthesia, and Immune Response
  • RNA Interference and Gene Delivery
  • Microtubule and mitosis dynamics
  • Heat shock proteins research
  • ATP Synthase and ATPases Research
  • Protein Kinase Regulation and GTPase Signaling
  • Estrogen and related hormone effects
  • Nanoparticle-Based Drug Delivery
  • Receptor Mechanisms and Signaling
  • Organic Chemistry Cycloaddition Reactions
  • Epigenetics and DNA Methylation
  • PI3K/AKT/mTOR signaling in cancer
  • Click Chemistry and Applications
  • Cancer therapeutics and mechanisms

University of Southern California
2016-2025

Keck Hospital of USC
2009-2025

LAC+USC Medical Center
2023

Neurological Surgery
2023

Center of Molecular Immunology (Cuba)
2022

Keck Graduate Institute
2014-2015

Southern California University for Professional Studies
2002-2014

USC Norris Comprehensive Cancer Center
1996-2011

Weatherford College
2008

University of California, Riverside
2006

Abstract Poor chemosensitivity and the development of chemoresistance remain major obstacles to successful chemotherapy malignant gliomas. GRP78 is a key regulator unfolded protein response (UPR). As Ca2+-binding molecular chaperone in endoplasmic reticulum (ER), maintains ER homeostasis, suppresses stress-induced apoptosis, controls UPR signaling. We report here that expressed at low levels normal adult brain, but significantly elevated glioma specimens human cell lines, correlating with...

10.1158/0008-5472.can-07-0625 article EN Cancer Research 2007-10-15

The transient induction of c-fos mRNA and protein suggests that regulation occurs not only by transcriptional activation but also at the level turnover gene product. Here we present evidence for rapid some requirements its specific degradation. half life induced mature cytoplasmic is 9 min in both serum-starved growing primary human fibroblasts NIH 3T3 cells. A structure 3' end molecule involved low stability since substitution or removal untranslated portion prolongues RNA time. fos...

10.1093/nar/15.4.1643 article EN Nucleic Acids Research 1987-01-01

Overexpression of p53 causes G2 arrest, attributable in part to the loss CDC2 activity. Transcription cdc2 andcyclin B1, determined using reporter constructs driven by two promoters, was suppressed response induction p53. Suppression requires regions −287 −123 thecyclin B1 promoter and −104 −74 thecdc2 promoter. did not affect inhibitory phosphorylations at threonine 14 or tyrosine 15 activity cyclin-dependent kinase that activates phosphorylating it 161. may also interfere with accumulation...

10.1091/mbc.10.11.3607 article EN Molecular Biology of the Cell 1999-11-01

OBJECT Chloroquine (CQ) is a quinoline-based drug widely used for the prevention and treatment of malaria. More recent studies have provided evidence that this may also harbor antitumor properties, whereby CQ possesses ability to accumulate in lysosomes blocks cellular process autophagy. Therefore, authors study set out investigate whether analogs, particular clinically established antimalaria drugs, would be able exert with specific focus on glioma cells. METHODS Toward goal, treated...

10.3171/2014.12.focus14748 article EN Neurosurgical FOCUS 2015-03-01

In a recent clinical trial, patients with newly diagnosed glioblastoma multiforme benefited from chloroquine (CQ) in combination conventional therapy (resection, temozolomide [TMZ], and radiation therapy). the present study, authors report mechanism by which CQ enhances therapeutic efficacy of TMZ to aid future studies aimed at improving this regimen.Using vitro vivo experiments, determined cytotoxicity. They focused on inhibition-of-autophagy knockdown autophagy-associated proteins or...

10.3171/2014.9.focus14504 article EN Neurosurgical FOCUS 2014-12-01

Abstract The tumor vasculature is essential for growth and survival a key target anticancer therapy. Glioblastoma multiforme, the most malignant form of brain tumor, highly vascular contains abnormal vessels, unlike blood vessels in normal brain. Previously, we showed that primary cultures human endothelial cells, derived from glioma tissues (TuBEC), are physiologically functionally different cells nonmalignant (BEC) substantially more resistant to apoptosis. Resistance TuBEC wide range...

10.1158/1541-7786.mcr-08-0060 article EN Molecular Cancer Research 2008-08-01

10.1074/jbc.273.30.19019 article EN cc-by Journal of Biological Chemistry 1998-07-01

Abstract HIV type 1 (HIV-1) protease inhibitors (PI) have been shown to anticancer activity in non–HIV-associated human cancer cells. The underlying mechanism of this effect is unclear. Here, we show that the PIs nelfinavir and atazanavir cause cell death various malignant glioma lines vitro. antitumor involves potent stimulation endoplasmic reticulum (ER) stress response (ESR), as indicated by increased expression two ESR markers, GRP78 CHOP, activation ESR-associated caspase-4. Induction...

10.1158/0008-5472.can-07-0796 article EN Cancer Research 2007-11-15

Androgen plays a critical role in regulating the growth and differentiation of normal prostate epithelia, as well initial cancer cells. Nevertheless, carcinomas eventually become androgen-unresponsive, is refractory to hormonal therapy. To gain insight into mechanism involved this hormone-refractory phenomenon, we have examined potential androgen receptor (AR) that process. We investigated expression AR two prostate-specific androgen-responsive antigens, prostatic acid phosphatase (PAcP)...

10.1074/jbc.273.10.5939 article EN cc-by Journal of Biological Chemistry 1998-03-01

Abstract The proteasome inhibitor bortezomib (Velcade) is known to trigger endoplasmic reticulum (ER) stress via the accumulation of obsolete and damaged proteins. selective cyclooxygenase-2 (COX-2) celecoxib (Celebrex) causes ER through a different mechanism (i.e., by causing leakage calcium from into cytosol). Each these two mechanisms has been implicated in anticancer effects respective drug. We therefore investigated whether combination drugs would lead further increased enhance their...

10.1158/0008-5472.can-07-5555 article EN Cancer Research 2008-02-01

Abstract A drawback of extensive coxib use for antitumor purposes is the risk life-threatening side effects that are thought to be a class effect and probably due resulting imbalance eicosanoid levels. 2,5-Dimethyl-celecoxib (DMC) close structural analogue selective cyclooxygenase-2 inhibitor celecoxib lacks cyclooxygenase-2–inhibitory function but nonetheless able potently mimic in vitro vivo. To further establish potential usefulness DMC as an anticancer agent, we compared various coxibs...

10.1158/1535-7163.mct-06-0629 article EN Molecular Cancer Therapeutics 2007-04-01

Perillyl alcohol (POH) is a monoterpene that has been used orally for the treatment of systemic cancer. However, when significant gastrointestinal side effects and lack overall efficacy were documented. Recently, in phase II trial Brazil temozolomide (TMZ)-resistant malignant gliomas, POH was well tolerated administered intranasally. The present study explores mechanisms on TMZ-sensitive TMZ-resistant glioma cells. In vitro studies showed cytotoxic to as cells, this effect independent...

10.1158/1535-7163.mct-12-0321 article EN Molecular Cancer Therapeutics 2012-08-29
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