Oct transcription factors mediate t(14;18) lymphoma cell survival by directly regulating bcl-2 expression

Heckman, Caroline A.; Duan, Hong; Garcia, Patty B.; Boxer, Linda M.

doi:10.1038/sj.onc.1209127

Cited by 38 publications

(33 citation statements)

References 54 publications

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“…Recently, Largo et al (2006) reported that POU2AF1 locates within frequently Amplification of POU2AF1 in multiple myeloma C Zhao et al gained region and is overexpressed regardless of copynumber status in MM cells compared with universal human RNA. Heckman et al (2006) reported that Oct factors and POU2AF1 mediate cell survival in t(14;18) lymphoma cells by directly activating the antiapoptotic gene Bcl-2, and they may therefore play a role in malignant transformation. However, they evaluated only the number of apoptotic cells, not total cell growth or the numbers of proliferative cells, after knockdown of those factors.…”

Section: Discussionmentioning

confidence: 99%

“…Amplification of POU2AF1 in multiple myeloma C Zhao et al considered to participate in aspects of neoplastic development or progression such as proliferation, survival, cell cycling, adhesion or migration (Ladanyi et al, 1992;Claudio et al, 2002;Hideshima et al, 2004;Novak et al, 2004;Standal et al, 2004;Heckman et al, 2006). To investigate whether, as a transcriptional coactivator, POU2AF1 regulates expression of those genes in MM cells, we examined the mRNA level of each of them in MM cells treated with POU2AF1-siRNA or in a MM cell line stably expressing POU2AF1, by real-time quantitative RT-PCR.…”

Section: Regulation Of Tnfrsf17 Expression By Pou2af1mentioning

confidence: 99%

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POU2AF1, an amplification target at 11q23, promotes growth of multiple myeloma cells by directly regulating expression of a B-cell maturation factor, TNFRSF17

Zhao¹,

Inoue

Imoto

et al. 2007

Oncogene

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Multiple myeloma (MM), a progressive hematological neoplasm, is thought to result from multiple genetic events affecting the terminal plasma cell. However, genetic aberrations related to MM are seldom reported. Using our in-house array-based comparative genomic hybridization system to locate candidate target genes with following their expression analysis, we identified POU2AF1 at 11q23.1 as a probable amplification target in MM cell lines. POU2AF1 is a B-cell-specific transcriptional coactivator, which interacts with octamer-binding transcription factors Oct-1 and Oct-2, and augments their function. Downregulation of POU2AF1 expression by specific smallinterfering RNA (siRNA) inhibited MM cell growth, whereas ectopic expression of POU2AF1 promoted growth of MM cells. Among putative transcriptional targets for POU2AF1, B-cell maturation factor, TNFRSF17, enhanced its transcription by POU2AF1, and POU2AF1 directly bound to an octamer site within the 5 0 region of TNFRSF17. Expression level of TNFRSF17 was closely correlated with that of POU2AF1 in cell lines and primary samples of MM, and decreasing TNFRSF17 expression by means of TNFRSF17 siRNA inhibited MM cell growth. Taken together, our results suggest that POU2AF1, when activated by amplification or other mechanisms, may contribute to progression of MM by accelerating growth of MM cells through direct transactivation of one of its target genes, TNFRSF17.

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Section: Discussionmentioning

confidence: 99%

Section: Regulation Of Tnfrsf17 Expression By Pou2af1mentioning

confidence: 99%

POU2AF1, an amplification target at 11q23, promotes growth of multiple myeloma cells by directly regulating expression of a B-cell maturation factor, TNFRSF17

Zhao¹,

Inoue

Imoto

et al. 2007

Oncogene

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“…Abcb5 is associated with drug resistance in certain melanomas (29). Pou2f2 (Oct2) promotes resistance to apoptosis via Bcl2 induction (30). Olig1, a basic helix-loop-helix transcription factor, is associated with the development of certain forms of brain tumors (31).…”

Section: Loss Of Grim-19 Promotes the Expression Of Several Genes Invmentioning

confidence: 99%

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice

Kalakonda¹,

Nallar²,

Jaber

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Significance Gene-associated with retinoid-interferon induced mortality-19 (GRIM-19) is an interferon-retinoid–regulated growth suppressor that inhibits cell growth by targeting the transcription factor STAT3 for inhibition. In primary human tumors GRIM-19 is suppressed or mutated, leading to constitutive STAT3 activity and indicating the tumor-suppressive function of GRIM-19. To understand the in vivo role of Grim-19 in tumor development, we generated a Grim-19 conditional knockout mouse. We found that deletion of even a single Grim-19 allele is sufficient to augment skin tumorigenesis in mice, thus establishing a critical role for Grim-19 as a tumor suppressor. Tumors that developed in the absence of Grim-19 exhibited mitochondrial respiratory chain dysfunction, elevated glycolysis, and Stat3-responsive gene expression.

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“…Several of these genes contain octamer motifs in their regulatory regions. In addition, a recent study has suggested that Oct-1 may be involved in the survival of lymphoma cells through the regulation of bcl-2 expression (Heckman et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage

et al. 2007

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Oct transcription factors mediate t(14;18) lymphoma cell survival by directly regulating bcl-2 expression

Cited by 38 publications

References 54 publications

POU2AF1, an amplification target at 11q23, promotes growth of multiple myeloma cells by directly regulating expression of a B-cell maturation factor, TNFRSF17

POU2AF1, an amplification target at 11q23, promotes growth of multiple myeloma cells by directly regulating expression of a B-cell maturation factor, TNFRSF17

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice

DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage

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