Gene expression profile of multiple myeloma cell line treated by arsenic trioxide

Wang, Mengchang; Liu, Shaanxi; Liu, Pengbo

doi:10.1007/s11596-007-0606-z

Cited by 17 publications

(19 citation statements)

References 19 publications

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“…The last exon is common, whereas usage of other exons differs across variants (Supplementary Figure S1). Several reports have shown that TNFAIP8 is overexpressed in human cancers, [3][4][5]8,[19][20][21][22] yet none of these publications have used methods with adequate specificity to discriminate among TNFAIP8 variants. In order to determine the expression patterns of the variants in human tumors compared with normal tissue, we analyzed cataloged RNA-sequencing (RNA-seq) data from primary human tumor and normal tissue for 11 cancer types in The Cancer Genome Atlas (TCGA) (Figure 1a and Supplementary Figure S2A).…”

Section: Resultsmentioning

confidence: 99%

“…The last exon is common, whereas usage of other exons differs across variants (Supplementary Figure S1). Several reports have shown that TNFAIP8 is overexpressed in human cancers, [3][4][5]8,[19][20][21][22] yet none of these publications have used methods with adequate specificity to discriminate among Abbreviations: BrdU, 5-bromo-2'-deoxyuridine; ChIP-seq, chromatin immunoprecipitation sequencing; DOX, doxorubicin; Gadd45A, growth arrest and DNA damageinducible 45a; H3K4me1, histone H3 mono-methylation on lysine 4; H3K4me3, histone H3 tri-methylation on lysine 4; H3K27ac, histone H3 acetylation on lysine 27; p53RE, p53 response element; PCNA, proliferating cell nuclear antigen; Scri, cells expressing scrambled shRNA; shRNA, short hairpin RNA; TCGA, The Cancer Genome Atlas; TNFAIP8, tumor necrosis factor-α-induced protein 8; TP8i, cells expressing TNFAIP8 shRNA …”

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confidence: 99%

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The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression

et al. 2016

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Tumor necrosis factor-α-induced protein 8 (TNFAIP8) is a stress-response gene that has been associated with cancer, but no studies have differentiated among or defined the regulation or function of any of its several recently described expression variants. We found that TNFAIP8 variant 2 (v2) is overexpressed in multiple human cancers, whereas other variants are commonly downregulated in cancer (v1) or minimally expressed in cancer or normal tissue (v3-v6). Silencing v2 in cancer cells induces p53-independent inhibition of DNA synthesis, widespread binding of p53, and induction of target genes and p53-dependent cell cycle arrest and DNA damage sensitization. Cell cycle arrest induced by v2 silencing requires p53-dependent induction of p21. In response to the chemotherapeutic agent doxorubicin, p53 regulates v2 through binding to an intragenic enhancer, together indicating that p53 and v2 engage in complex reciprocal regulation. We propose that TNFAIP8 v2 promotes human cancer by broadly repressing p53 function, in essence offsetting p53-dependent tumor suppression. Cell Death and Differentiation (2017) 24, 181-191; doi:10.1038/cdd.2016 published online 11 November 2016 Tumor necrosis factor-α-induced protein 8 (TNFAIP8) is the founding member of a recently described family of environmental stress response genes that are induced by TNFα. TNFAIP8 has been shown to promote or inhibit apoptosis, depending on cell type and context. 1,2 Although little is known about TNFAIP8, it has recently been found to be overexpressed in a wide range of human cancers. Some studies have suggested protumor functions for TNFAIP8, including enhancement of cell survival, proliferation, and metastasis [3][4][5][6][7][8][9] and resistance to cancer chemotherapeutics in mice. 4,10Nonetheless, nothing is known about how TNFAIP8 influences responses to DNA damage in cancer cells. Moreover, several transcript variants from the TNFAIP8 gene were recently registered in the NCBI reference sequence database, but no study to date has differentiated among them or defined the factors that govern their expression.The tumor suppressor p53 is a transcription factor that regulates many biological processes through its target gene network. Some of the well-characterized p53 target genes including p21/CDKN1A, growth arrest and DNA damageinducible 45a (GADD45A) and Bcl-2-like protein 4 (BAX) together promote senescence, cell cycle arrest, and apoptosis, all of which may contribute to the tumor suppressing functions of p53. 11,12Additional noncanonical tumorsuppressive pathways from p53 have recently been identified. [13][14][15] Improved characterization of the p53 DNAbinding sequence with modern sequencing techniques has led to the identification of a rapidly expanding list of p53 target genes. [16][17][18] Continued identification of these genes and characterization of their mechanisms of regulation and function will be critical to a full understanding of p53 and for full realization of opportunities to intervene upon p53 in cancer.Here, we identify ...

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Section: Resultsmentioning

confidence: 99%

“…The last exon is common, whereas usage of other exons differs across variants (Supplementary Figure S1). Several reports have shown that TNFAIP8 is overexpressed in human cancers, [3][4][5]8,[19][20][21][22] yet none of these publications have used methods with adequate specificity to discriminate among Abbreviations: BrdU, 5-bromo-2'-deoxyuridine; ChIP-seq, chromatin immunoprecipitation sequencing; DOX, doxorubicin; Gadd45A, growth arrest and DNA damageinducible 45a; H3K4me1, histone H3 mono-methylation on lysine 4; H3K4me3, histone H3 tri-methylation on lysine 4; H3K27ac, histone H3 acetylation on lysine 27; p53RE, p53 response element; PCNA, proliferating cell nuclear antigen; Scri, cells expressing scrambled shRNA; shRNA, short hairpin RNA; TCGA, The Cancer Genome Atlas; TNFAIP8, tumor necrosis factor-α-induced protein 8; TP8i, cells expressing TNFAIP8 shRNA …”

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confidence: 99%

The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression

et al. 2016

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“…The effect of NREA on cell signalling pathways may differ, because it induces less oxidative DNA damage and is less genotoxic in comparison to ATO. REA treatment increases some genes, including CCL2 , CCL3 , BTG1 , TNFAIP3 , TNFAIP8 , SLC38A2 and IGFBP4 , associated with cell growth, cell‐cell signalling, regulation of apoptosis and cell homeostasis (Wang et al , ). Especially in MM, rearrangement or translocation of MYC is one of the most common events, resulting in activation of Myc pathway in patient MM cells.…”

Section: Discussionmentioning

confidence: 99%

Realgar nanoparticles versus ATO arsenic compounds induce in vitro and in vivo activity against multiple myeloma

et al. 2017

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Summary Multiple myeloma (MM), a B cell malignancy characterized by clonal proliferation of plasma cells in the bone marrow, remains incurable despite the use of novel and conventional therapies. In this study, we demonstrated MM cell cytotoxicity triggered by realgar (REA; As4S4) nanoparticles (NREA) versus Arsenic trioxide (ATO) against MM cell lines and patient cells. Both NREA and ATO showed in vivo anti-MM activity, resulting in significantly decreased tumour burden. The anti-MM activity of NREA and ATO is associated with apoptosis, evidenced by DNA fragmentation, depletion of mitochondrial membrane potential, cleavage of caspases and anti-apoptotic proteins. NREA induced G2/M cell cycle arrest and modulation of cyclin B1, p53 (TP53), p21 (CDNK1A), Puma (BBC3) and Wee-1 (WEE1). Moreover, NREA induced modulation of key regulatory molecules in MM pathogenesis including JNK activation, c-Myc (MYC), BRD4, and histones. Importantly, NREA, but not ATO, significantly depleted the proportion and clonogenicity of the MM stem-like side population, even in the context of the bone marrow stromal cells. Finally, our study showed that both NREA and ATO triggered synergistic anti-MM activity when combined with lenalidomide or melphalan. Taken together, the anti-MM activity of NREA was more potent compared to ATO, providing the preclinical framework for clinical trials to improve patient outcome in MM.

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“…3 (Du and Ho 2001;Lu and Wang 2002;Luo et al, 2006;Wang et al, 2006, 2008b, Zhong et al, 2003 2. Monocytic Differentiation; 3.…”

Section: Appropriate Dosagementioning

confidence: 99%

Anticancer Drugs from Traditional Toxic Chinese Medicines

Man

Gao

Wei

et al. 2012

Phytotherapy Research

109

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Many anticancer drugs are obtained from natural sources. Nature produces a variety of toxic compounds, which are often used as anticancer drugs. Up to now, there are at least 120 species of poisonous botanicals, animals and minerals, of which more than half have been found to possess significant anticancer properties. In spite of their clinical toxicity, they exhibit pharmacological effects and have been used as important traditional Chinese medicines for the different stages of cancer. The article reviews many structures such as alkaloids of Camptotheca acuminata, Catharanthus roseus and Cephalotaxus fortunei, lignans of Dysosma versipellis and Podophyllum emodi, ketones of Garcinia hanburyi, terpenoids of Mylabris and Ginkgo biloba, diterpenoids of Tripterygium wilfordii, Euphorbia fischeriana, Euphorbia lathyris, Euphorbia kansui, Daphne genkwa, Pseudolarix kaempferi and Brucea javanica, triterpenoids of Melia toosendan, steroids of Periploca sepium, Paris polyphylla and Venenum Bufonis, and arsenic compounds including Arsenicum and Realgar. By comparing their related phytochemistry, toxic effects and the recent advances in understanding the mechanisms of action, this review puts forward some ideals and examples about how to increase antitumour activity and/or reduce the side effects experienced with Chinese medicine.

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Gene expression profile of multiple myeloma cell line treated by arsenic trioxide

Cited by 17 publications

References 19 publications

The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression

The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression

Realgar nanoparticles versus ATO arsenic compounds induce in vitro and in vivo activity against multiple myeloma

Anticancer Drugs from Traditional Toxic Chinese Medicines

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