Shi‐Yong Sun

ORCID: 0000-0002-0117-8826
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About
Contact & Profiles
Research Areas
  • Cell death mechanisms and regulation
  • PI3K/AKT/mTOR signaling in cancer
  • Lung Cancer Treatments and Mutations
  • Ubiquitin and proteasome pathways
  • Cancer-related Molecular Pathways
  • Protein Degradation and Inhibitors
  • Retinoids in leukemia and cellular processes
  • Melanoma and MAPK Pathways
  • interferon and immune responses
  • Peptidase Inhibition and Analysis
  • Protein Kinase Regulation and GTPase Signaling
  • Cancer Mechanisms and Therapy
  • Cancer therapeutics and mechanisms
  • HER2/EGFR in Cancer Research
  • Lung Cancer Research Studies
  • RNA modifications and cancer
  • Cancer, Lipids, and Metabolism
  • Synthesis and biological activity
  • Magnolia and Illicium research
  • Inflammatory mediators and NSAID effects
  • Polyamine Metabolism and Applications
  • Endoplasmic Reticulum Stress and Disease
  • Histone Deacetylase Inhibitors Research
  • Autophagy in Disease and Therapy
  • Colorectal Cancer Treatments and Studies

Emory University
2016-2025

Winship Cancer Institute
2015-2025

Beijing Chest Hospital
2024

Capital Medical University
2024

Nanjing Institute of Technology
2024

Henan University of Technology
2023

University School
2020

Piedmont Cancer Institute
2007-2014

Cancer Institute (WIA)
2005-2013

AID Atlanta
2011-2013

Background: Celecoxib, a cyclooxygenase 2 inhibitor, has chemopreventive and therapeutic activities toward lung cancer other epithelial malignancies. Celecoxib can induce apoptosis in various cell lines through mechanism that is independent of its inhibitory activity but otherwise largely uncharacterized. We investigated the celecoxib-induced further. Methods: All experiments were conducted human non-small-cell carcinoma (NSCLC) lines; results celecoxib-treated untreated cells compared. Cell...

10.1093/jnci/djh322 article EN JNCI Journal of the National Cancer Institute 2004-11-30

Because lung cancer is the leading cause of cancer-related death, new approaches for preventing and controlling disease are needed. Chemoprevention both feasible effective. We evaluated potential deguelin, a natural plant product, as chemopreventive agent investigated its mechanism action.The effects deguelin on proliferation apoptosis normal, premalignant, malignant human bronchial epithelial (HBE) cells were assessed by using MTT assay, flow cytometry-based TUNEL western blot analyses. The...

10.1093/jnci/95.4.291 article EN JNCI Journal of the National Cancer Institute 2003-02-18

Abstract Death receptor 4 (DR4) is one of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors and triggers apoptosis on ligation with TRAIL or overexpression. Our previous study demonstrated that DR4 expression could be regulated in a p53-dependent fashion. In present study, we have p53 target gene by through functional intronic binding site (p53BS) based following lines evidence: (a) p53BS almost identical to found first intron DR5 terms their locations sequences;...

10.1158/0008-5472.can-04-1195 article EN Cancer Research 2004-08-01

Abstract The proteasome inhibitor PS-341 (bortezomib or Velcade), an approved drug for treatment of patients with multiple myeloma, is currently being tested in clinical trials against various malignancies, including lung cancer. Preclinical studies have shown that induces apoptosis and enhances tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)–induced human cancer cells undefined mechanisms. In the present study, we show induced caspase-8–dependent apoptosis, cooperated TRAIL...

10.1158/0008-5472.can-06-4274 article EN Cancer Research 2007-05-15

It has been shown that mammalian target of rapamycin (mTOR) inhibitors activate Akt while inhibiting mTOR signaling. However, the underlying mechanisms and effect activation on mTOR-targeted cancer therapy are unclear. The present work focused addressing role mTOR/rictor in inhibitor-induced sustained therapy. Thus, we have increase phosphorylation through a mechanism independent because assembly was inhibited by silencing rictor did not abrogate activation. Moreover, during inhibition is...

10.1158/0008-5472.can-08-1522 article EN Cancer Research 2008-09-14

The nuclear factor-κB (NF-κB) signaling pathway has been targeted for therapeutic applications in a variety of human diseases, includuing cancer. Many naturally occurring substances, including curcumin, have investigated their actions on the NF-κB because significant potential and safety profile. A synthetic monoketone compound termed 3,5-bis(2-flurobenzylidene)piperidin-4-one (EF24) was developed from curcumin exhibited potent anticancer activity. Here, we report mechanism by which EF24...

10.1124/mol.108.046201 article EN Molecular Pharmacology 2008-06-24

Head and neck squamous cell carcinoma (HNSCC) is one of the most common types human cancer frequently metastasizes to LNs. Identifying metastasis-promoting factors immense clinical interest, as prognosis for patients with even a single unilateral LN metastasis extremely poor. Here, we report that p90 ribosomal S6 kinase 2 (RSK2) promotes HNSCC invasion metastasis. We determined RSK2 was overexpressed activated in highly invasive lines compared poorly lines. Expression also correlated...

10.1172/jci40582 article EN Journal of Clinical Investigation 2010-03-16

The emergence of resistance to EGF receptor (EGFR) inhibitor therapy is a major clinical problem for patients with non-small cell lung cancer (NSCLC). mechanisms underlying tumor inhibitors the kinase activity EGFR are not fully understood. Here, we found that inhibition by erlotinib induces STAT3 phosphorylation at Tyr705 in association increased Bcl2/Bcl-XL both mRNA and protein levels various human cells. PTPMeg2 physiologic phosphatase can directly dephosphorylate site. Intriguingly,...

10.1158/1535-7163.mct-13-0095 article EN Molecular Cancer Therapeutics 2013-07-27

Perifosine is an alkylphospholipid exhibiting antitumor activity as shown in both preclinical studies and clinical trials. This partly associated with its ability to inhibit Akt activity. It has been that the mammalian target of rapamycin (mTOR) axis plays a critical role regulation cell proliferation survival primarily through functioning downstream upstream Akt. The current study reveals novel mechanism by which perifosine inhibits mTOR axis. In addition inhibition Akt, inhibited assembly...

10.1158/0008-5472.can-09-2190 article EN Cancer Research 2009-11-18

IntroductionThe clinical and biological significance of the newly described SCLC subtypes, SCLC-A, SCLC-N, SCLC-Y, SCLC-P, defined by dominant expression transcription factors ASCL1, NeuroD1, YAP1, POU2F3, respectively, remain to be established.MethodsWe generated new RNA sequencing data from a discovery set 59 archival tumor samples neuroendocrine tumors protein immunohistochemistry in 99 cases. We validated findings this two independent validation sets consisting 51 cell lines 81 primary...

10.1016/j.jtho.2020.11.006 article EN cc-by Journal of Thoracic Oncology 2020-11-25

Abstract Purpose: The mechanisms accounting for anticancer activity of AZD9291 (osimertinib or TAGRISSO), an approved third-generation EGFR inhibitor, in EGFR-mutant non–small cell lung cancer (NSCLC) cells and particularly the subsequent development acquired resistance are unclear thus focus this study. Experimental Design: AZD9219-resistant lines were established by exposing sensitive to AZD9291. Protein alterations detected with Western blotting. Apoptosis was measured annexin V/flow...

10.1158/1078-0432.ccr-17-1574 article EN Clinical Cancer Research 2017-08-02

Abstract Death receptor (DR) 4 or 5, on binding to its ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), triggers apoptosis via activating the caspase-8–mediated caspase cascade. Certain anticancer drugs up-regulate expression of these receptors and thereby induce enhance TRAIL-induced apoptosis. In this study, we explored ability methyl-2-cyano-3,12-dioxooleana-1,9-dien-28-oate (CDDO-Me) activate extrinsic DR-mediated apoptotic pathway in human lung cancer cells. We...

10.1158/0008-5472.can-04-1238 article EN Cancer Research 2004-10-15

The family of 14-3-3 proteins has emerged as critical regulators diverse cellular responses under both physiological and pathological conditions. Here, we report an important role 14-3-3ζ in tumorigenesis through a mechanism that involves anoikis resistance. is up-regulated number cancer types, including lung cancer. Through RNAi approach using human adenocarcinoma-derived A549 cells model system, have found knockdown single ζ isoform sufficient to restore the sensitivity impair their...

10.1073/pnas.0710905105 article EN Proceedings of the National Academy of Sciences 2007-12-28

Abstract DR4 (TRAIL‐R1), a member of the tumor necrosis factor receptor superfamily, is cell surface that triggers apoptotic machinery upon binding to its ligand factor‐related apoptosis‐inducing (TRAIL). Although three other TRAIL receptors DR5, DcR1, and DcR2 are induced by DNA damage regulated wild‐type p53 suppressor, it was not known whether these factors also affect expression. In this study, we found expression enhanced ionizing radiation or chemotherapeutic agents. The induction...

10.1002/jcp.1101 article EN Journal of Cellular Physiology 2001-05-25

Abstract Purpose: Our previous study revealed that simultaneously targeting epidermal growth factor receptor (EGFR) tyrosine kinase and cyclooxygenase-2 (COX-2) additively or synergistically inhibited of squamous cell carcinoma the head neck (SCCHN) in vitro. However, an vivo efficacy this combined treatment SCCHN has not been studied. Experimental Design: Nude mice were pretreated with control (1% Tween 80), ZD1839 (50 mg/kg) alone, celecoxib a combination at same dosages for 7 days before...

10.1158/1078-0432.ccr-04-2102 article EN Clinical Cancer Research 2005-09-01

The synthetic triterpenoid methyl-2-cyano-3,12-dioxoolean-1,9-dien-28-oate (CDDO-Me) is in phase I clinical trials as a novel cancer therapeutic agent. We previously showed that CDDO-Me induces c-Jun NH(2)-terminal kinase (JNK)-dependent death receptor 5 (DR5) expression and augments receptor-induced apoptosis. current study focused on addressing how JNK-dependent DR5 expression. Analysis of promoter regions defines the CCAAT/enhancer binding protein homologous (CHOP) site responsible for...

10.1158/0008-5472.can-08-1318 article EN Cancer Research 2008-09-14
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