Hydrogen sulfide in cancer: Friend or foe?

Wu, Dongdong; Si, Weirong; Wang, Mingjie; Lv, Shuangyu; Ji, Ailing

doi:10.1016/j.niox.2015.08.004

Cited by 193 publications

(163 citation statements)

References 91 publications

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“…As an endogenous enzyme, CSE is crucial to the generation of H 2 S. Previous studies have shown that CSE is involved in a variety of physiological and tumor processes (32)(33)(34), and the knockdown of CSE by shRNA can decrease cell proliferation, migration and tumor xenograft growth in nude mice (35). Consistent with this, the present data showed that the upregulation of the CSE protein in HepG2 cells overexpressing CXCL5 is positively associated with the proliferation and migration of HepG2 cells.…”

Section: Discussionsupporting

confidence: 89%

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

et al. 2017

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Abstract. C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma. IntroductionHepatoblastoma (HB) is a prevalent malignancy among children, which histologically derives from pluripotent stem cells that may differentiate into liver cells and biliary epithelial cells, and accounts for almost two-thirds of pediatric malignant liver tumors (1,2). Although the survival rate of HB has increased from 35 to 75% during the last 30 years with the application of surgical excision, adjuvant chemotherapy and liver transplantation (3), additional investigation of the underlying molecular mechanism will be beneficial for the improving diagnosis and treatment of patients with HB.Previous studies have supported the hypothesis that the development of malignancies is closely associated with various cytokines, in which chemokines appear to have crucial roles. Chemokines are members of the cytokine super family and are secreted by various cell types, including immune, mesothelial, endometrial glandular and stromal cells, and trophoblasts (4). According to the order of conserved cysteine residues, chemokines are classified as C, CC, CXC and C (X) 3 C. Additionally, CXC chemokines are further grouped into ELR + CXC and ELR -CXC on the b...

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Section: Discussionsupporting

confidence: 89%

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

et al. 2017

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“…Apoptosis is an intrinsic cell-suicide program that is critical for the normal development and maintenance of tissue homeostasis in multicellular organisms 46 . There are two main apoptotic signaling pathways: the death receptor-mediated extrinsic pathway and the mitochondria-mediated intrinsic pathway 47 .…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Luo

Wang

et al. 2017

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Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H2S significantly improved the kidney structure and function of CRF rats. We found that H2S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H2S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H2S significantly abolished the phosphorylation of extracellular signal-regulated protein kinase 1/2, c-Jun N-terminal kinase, and p38 in the kidney of CRF rats. Furthermore, H2S decreased the expression levels of tumor necrosis factor-α, interleukin (IL)-6, IL-10, and monocyte chemoattractant protein-1, as well as the protein levels of p50, p65, and p-p65 in the kidney of CRF rats. In conclusion, H2S could ameliorate adenine-induced CRF in rats by inhibiting apoptosis and inflammation through ROS/mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways.

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“…[76][77][78] It is argued that dithiocarbonate formation has a slightly higher barrier of activation owing to a decreased electrophilicity of CS 2 . (10) The presence of CS 2 hydrolases in some microorganisms and clear divergence in evolution imply an evolutionary need for a CS 2 -specific enzyme. Thiobacillus thioparus and Thiobacillus denitrificans are microbes that use reduced sulfur species (dimethyl sulfide, methyl mercaptan, and H 2 S) for energy production.…”

Section: Hydrolysis (Or Not)mentioning

confidence: 99%

Carbon disulfide. Just toxic or also bioregulatory and/or therapeutic?

et al. 2017

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The overview presented here has the goal of examining whether carbon disulfide (CS 2 ) may play a role as an endogenously generated bioregulator and/or has therapeutic value. The neuro-and reproductive system toxicity of CS 2 has been documented from its long-term use in the viscose rayon industry. CS 2 is also used in the production of dithiocarbamates (DTCs), which are potent fungicides and pesticides, thus raising concern that CS 2 may be an environmental toxin. However, DTCs also have recognized medicinal use in the treatment of heavy metal poisonings as well as having potency for reducing inflammation. Three known small molecule bioregulators (SMBs) nitric oxide, carbon monoxide, and hydrogen sulfide were initially viewed as environmental toxins. Yet each is now recognized as having intricate, though not fully elucidated, biological functions at concentration regimes far lower than the toxic doses. The literature also implies that the mammalian chemical biology of CS 2 has broader implications from inflammatory states to the gut microbiome. On these bases, we suggest that the very nature of CS 2 poisoning may be related to interrupting or overwhelming relevant regulatory or signaling process(es), much like other SMBs. TOC Image 1 CONTENTS

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Hydrogen sulfide in cancer: Friend or foe?

Cited by 193 publications

References 91 publications

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Carbon disulfide. Just toxic or also bioregulatory and/or therapeutic?

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