FGF-2 inhibits TNF-α mediated apoptosis through up-regulation of Bcl2-A1 and Bcl-xL in ATDC5 cells

Kim, Hey-Ryun; Heo, Youn-Moo; Jeong, Kyoung-Il; Kim, Yongmin; Jang, Hae Lan; Lee, Kwang-Yeol; Yeo, Chang Yeol; Kim, Sung Hoon; Lee, Hak-Kyo; Kim, Seung‐Ryul; Kim, Eung‐Gook; Choi, Joong-Kook

doi:10.5483/bmbrep.2012.45.5.287

Cited by 38 publications

(25 citation statements)

References 22 publications

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“…Bcl2 downregulation has been shown to increase caspase-3 in breast cancer cells (25). Furthermore, Bcl2A mediates anti-apoptotic effects of fibroblast growth factor in chrondogenic progenitor-like cell line (26). Therefore, these pathways may be involved in reducing/counteracting caspase-3 activity in hemSCs but not mature endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Propranolol inhibits growth of hemangioma-initiating cells but does not induce apoptosis

Kum

Khan

2013

Pediatr Res

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BackgroundInfantile hemangioma (IH) is the most common tumor of infancy. The first-line therapy for IH is propranolol, a non-selective β-adrenergic receptor antagonist. However, mechanisms for the therapeutic effect of propranolol and regrowth of IH following cessation of treatment in some cases are not clear. We have recently shown that IH arises from multipotent stem cells. Whether IH stem cells are responsive to propranolol and are selectively targeted is unknown, and is the focus of this study.MethodsIH stem cells were exposed to propranolol and assayed for cellular and molecular alterations. We used endothelial cells (ECs) as controls and bone marrow-mesenchymal progenitor cells (bm-MPCs) as normal stem/progenitor counterparts to determine selectivity.ResultsOur results show that propranolol significantly reduced IH stem cell growth but failed to induce caspase-3 activation. Normal bm-MPCs and mature ECs showed maintained or increased caspase-3 activation and significantly reduced cyclin-D1 levels. We further show that IH stem cells may escape apoptosis by inducing anti-apoptotic pathways.ConclusionsThis study reveals that propranolol does not induce apoptosis in IH stem cells, which is in contrast to ECs. Escape from apoptosis in IH stem cells may involve induction of anti-apoptotic pathways.

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Section: Discussionmentioning

confidence: 99%

Propranolol inhibits growth of hemangioma-initiating cells but does not induce apoptosis

Kum

Khan

2013

Pediatr Res

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“…To evaluate the effect of the antibody on the growth of cells, an MTT assay was performed as described previously [48, 49]. Cells were treated with PBS, normal IgG, or anti-TM4SF5 monoclonal antibody (10 μg/ml) for up to 5 days.…”

Section: Methodsmentioning

confidence: 99%

Therapeutic effect of a TM4SF5-specific monoclonal antibody against colon cancer in a mouse model

Kim

Kwon

et al. 2014

Oncotarget

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Transmembrane 4 superfamily member 5 protein (TM4SF5) is presumed to serve as a molecular target to prevent or treat hepatocellular carcinoma (HCC) and colon cancer in a mouse model. Previously, we reported the efficacy of anti-cancer peptide vaccine targeting TM4SF5. In addition, we reported an anti-proliferative effect of anti-TM4SF5 monoclonal antibody in HCC. Here, we investigated expression of TM4SF5 in 45 primary colon cancer tissues. Almost all of the colon cancer tissues expressed TM4SF5 based on immunohistochemistry using anti-TM4SF5 monoclonal antibody. The treatment of human colon cancer cells with anti-TM4SF5 antibody reduced growth of TM4SF5 expressing cells and enhanced expression of E-cadherin and β-catenin. Using mouse colon cancer models, we then evaluated the in vivo anti-cancer effect of anti-TM4SF5 antibody. Injection of the antibody significantly reduced growth of tumors priorly established by subcutaneous injection of human colon cancer cells HT-29 in a xenograft setting. We obtained similar results with mouse colon cancer cell line CT-26 in an allograft setting. Therefore, we suggest that the TM4SF5-specific monoclonal antibody has a therapeutic effect against colon cancer.

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“…Low doses of endogenous TNF-α produced by normal epithelial cells or epithelial-derived cancer cells can also act as a tumor promoter, in NSCLC cells, the TNF-α expression may affect the normal lung adjacent to the tumor [27], in human breast cancer cell, TNF-α enhanced invasiveness of the malignant cells dependent on matrix metalloprotease [28], in ovarian cancer cells the CXCR4 expression also in a TNF-α–dependent manner [29]. Many studies have demonstrated the role of TNF-α in cell proliferation, and some reports have shown that TNF-α acts as an apoptotic mediator in some cell lines, such as hematopoietic cells [30] and cartilage progenitor cells [31]. This proapoptotic effect can be weakened by other substances in the body, such as miRNAs.…”

Section: Introductionmentioning

confidence: 99%

NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells

Zhang

et al. 2014

J Transl Med

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BackgroundNuclear factor-κB (NF-κB) induces a variety of biological processes through transcriptional gene control whose products are components in various signaling pathways. MicroRNAs are a small endogenous non-coding RNAs that regulate gene expression and are involved in tumorigenesis. Using human cervical cancer cell lines, this study aimed to investigate whether NF-κB could regulate miR-130a expression and the functions and targets of miR-130a.MethodsWe used the HeLa and C33A cervical cancer cell lines that were transfected with NF-κB or miR-130a overexpression plasmids to evaluate their effects on cell growth. We utilized bioinformatics, a fluorescent reporter assay, qRT-PCR and Western blotting to identify downstream target genes.ResultsIn HeLa and C33A cells, NF-κB and miR-130a overexpression promoted cell growth, but genetic knockdowns suppressed growth. TNF-α was identified as a target of miR-130a by binding in a 3’-untranslated region (3’UTR) EGFP reporter assay and by Western blot analysis. Furthermore, low TNF-α concentrations stimulated NF-κB activity and then induced miR-130a expression, and TNF-α overexpression rescued the effects of miR-130a on cervical cancer cells.ConclusionsOur findings indicate that TNF-α can activate NF-κB activity, which can reduce miR-130a expression, and that miR-130a targets and downregulates TNF-α expression. Hence, we shed light on the negative feedback regulation of NF-κB/miR-130a/TNF-α/NF-κB in cervical cancer and may provide insight into the carcinogenesis of cervical cancer.

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FGF-2 inhibits TNF-α mediated apoptosis through up-regulation of Bcl2-A1 and Bcl-xL in ATDC5 cells

Abstract: FGF-2 is involved in cell survival

Cited by 38 publications

References 22 publications

Propranolol inhibits growth of hemangioma-initiating cells but does not induce apoptosis

Propranolol inhibits growth of hemangioma-initiating cells but does not induce apoptosis

Therapeutic effect of a TM4SF5-specific monoclonal antibody against colon cancer in a mouse model

NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells

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