New possible silver lining for pancreatic cancer therapy: Hydrogen sulfide and its donors
| Autor: | Jianan Sun, Bo Wu, Dahong Li, Hui-Ming Hua, Bao Ji, Shanshan Luo, Fanxing Xu, Yan Xiao, Peng Wang, Chao Zheng, Keguang Cheng, Xu Hu |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
BCL-2
B-cell lymphoma-2 HDAC histone deacetylase Disease Review CBS cystathionine-β-synthase RASAL2 RAS protein activator like 2 OCT-4 octamer-binding transcription factor 4 SHH sonic hedgehog 0302 clinical medicine ERU erucin General Pharmacology Toxicology and Pharmaceutics ITCs isothiocyanates Cell proliferation DATS diallyl trisulfide NF-κB nuclear factor kappa B SMAD4 mothers against decapentaplegic homolog 4 SFN sulforaphane XIAP X-linked inhibitor of apoptosis protein 0303 health sciences CDK1 cyclin-dependent kinase 1 Antitumor effect Signaling pathway CAT cysteine aminotransferase PI3K/AKT phosphoinositide 3-kinase/v-AKT murine thymoma viral oncogene TRAIL The human tumor necrosis factor-related apoptosis-inducing ligand Cell cycle VEGF vascular endothelial growth factor 030220 oncology & carcinogenesis JNK c-Jun N-terminal kinase iNOS inducible nitric oxide synthase HEATR1 human HEAT repeat-containing protein 1 HIF-1α hypoxia inducible factor PEITC phenethyl isothiocyanate Signal transduction EMT epithelial–mesenchymal transition KEAP1‒NRF2‒ARE the recombinant protein 1-nuclear factor erythroid-2 related factor 2-antioxidant response element GLUTs glucose transporters BRCA2 breast cancer 2 3-MST 3-mercaptopyruvate sulfurtransferase PDGFRα platelet-derived growth factor receptor AMPK adenosine 5′-monophosphate-activated protein kinase Hydrogen sulfide donor RM1-950 DR4 death receptor BITC benzyl isothiocyanate H2S hydrogen sulfide STAT-3 signal transducer and activator of transcription 3 03 medical and health sciences PARP poly(ADP-ribose)-polymerase Mediator ROS reactive oxygen species ZEB1 zinc finger E box-binding protein-1 Pancreatic cancer medicine ERK1/2 extracellular signal-regulated kinase Sulfur-containing compound 030304 developmental biology NO nitric oxide Cell growth business.industry KRAS kirsten rat sarcoma viral oncogene Cancer medicine.disease equipment and supplies CHK2 checkpoint kinase 2 FOXM1 forkhead box protein M1 CSE cystathionine-γ-lyase RPL10 human ribosomal protein L10 CDC25B cell division cycle 25B Apoptosis P16 multiple tumor suppressor 1 Cancer research Therapeutics. Pharmacology business |
| Zdroj: | Acta Pharmaceutica Sinica. B Acta Pharmaceutica Sinica B, Vol 11, Iss 5, Pp 1148-1157 (2021) |
| ISSN: | 2211-3835 |
| Popis: | As one of the most lethal diseases, pancreatic cancer shows a dismal overall prognosis and high resistance to most treatment modalities. Furthermore, pancreatic cancer escapes early detection during the curable period because early symptoms rarely emerge and specific markers for this disease have not been found. Although combinations of new drugs, multimodal therapies, and adjuvants prolong survival, most patients still relapse after surgery and eventually die. Consequently, the search for more effective treatments for pancreatic cancer is highly relevant and justified. As a newly re-discovered mediator of gasotransmission, hydrogen sulfide (H2S) undertakes essential functions, encompassing various signaling complexes that occupy key processes in human biology. Accumulating evidence indicates that H2S exhibits bimodal modulation of cancer development. Thus, endogenous or low levels of exogenous H2S are thought to promote cancer, whereas high doses of exogenous H2S suppress tumor proliferation. Similarly, inhibition of endogenous H2S production also suppresses tumor proliferation. Accordingly, H2S biosynthesis inhibitors and H2S supplementation (H2S donors) are two distinct strategies for the treatment of cancer. Unfortunately, modulation of endogenous H2S on pancreatic cancer has not been studied so far. However, H2S donors and their derivatives have been extensively studied as potential therapeutic agents for pancreatic cancer therapy by inhibiting cell proliferation, inducing apoptosis, arresting cell cycle, and suppressing invasion and migration through exploiting multiple signaling pathways. As far as we know, there is no review of the effects of H2S donors on pancreatic cancer. Based on these concerns, the therapeutic effects of some H2S donors and NO–H2S dual donors on pancreatic cancer were summarized in this paper. Exogenous H2S donors may be promising compounds for pancreatic cancer treatment. Graphical abstract The review summarizes the antitumor mechanisms of H2S donating derivatives against pancreatic cancer by modulating signaling pathways, including PI3K/AKT/mTOR, SHH, NF-κB, MAPK, NOTCH, STAT3, DR4, etc. Perspectives on future directions and challenges are also discussed.Image 1 |
| Databáze: | OpenAIRE |
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