Wnt/β-catenin signaling induces the transcription of cystathionine-γ-lyase, a stimulator of tumor in colon cancer

Fan, Kun; Li, Na; Qi, Jingjing; Peng, Yin; Zhao, Chao; Wang, Liying; Li, Zengxia; Zha, Xiliang

doi:10.1016/j.cellsig.2014.08.023

Cited by 69 publications

(51 citation statements)

References 46 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: 79%

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: 79%

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

et al. 2017

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“…miR-21 is an important negative regulator of Sp1 expression and thus can indirectly affect CSE transcription (63). In colon carcinoma cells, ␤-catenin binds to the promoter of CSE to enhance its expression, which in turn augments cell proliferation (64). In the current study, CSE-specific inhibition showed that nearly all the increment in H 2 S generation by tadalafil in the podocyte could be accounted for by the increase in CSE.…”

Section: Discussionmentioning

confidence: 68%

Tadalafil Integrates Nitric Oxide-Hydrogen Sulfide Signaling to Inhibit High Glucose-induced Matrix Protein Synthesis in Podocytes

Lee

Féliers

Mariappan³

et al. 2015

Journal of Biological Chemistry

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“…It was reported that colon cancer cells selectively over-express CBS to maintain the cell bioenergetics and to support tumor growth (42 ). Moreover, the WNT pathway regulates the expression of CTH, which plays important roles in colon cancer (43 ). Additional studies on the physiological function of these enzymes in CTC-MCC-41 cells will help better understand their role in colon cancer.…”

Section: Discussionmentioning

confidence: 99%

Molecular Portrait of Metastasis-Competent Circulating Tumor Cells in Colon Cancer Reveals the Crucial Role of Genes Regulating Energy Metabolism and DNA Repair

et al. 2017

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Wnt/β-catenin signaling induces the transcription of cystathionine-γ-lyase, a stimulator of tumor in colon cancer

Cited by 69 publications

References 46 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

Tadalafil Integrates Nitric Oxide-Hydrogen Sulfide Signaling to Inhibit High Glucose-induced Matrix Protein Synthesis in Podocytes

Molecular Portrait of Metastasis-Competent Circulating Tumor Cells in Colon Cancer Reveals the Crucial Role of Genes Regulating Energy Metabolism and DNA Repair

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