Synergistic tumoricidal effect between celecoxib and adenoviral-mediated delivery of mda-7 in human breast cancer cells

Suh, Young Jin; Chada, Sunil; McKenzie, Tamra; Liu, Yanna; Swisher, Stephen G.; Lucci, Anthony; Hunt, Kelly K.

doi:10.1016/j.surg.2005.06.032

Cited by 23 publications

(13 citation statements)

References 44 publications

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“…In these studies, independently from the origin of the cancer cells, the exact same anti-proliferative pathways were activated once mda-7/IL-24 reached a certain transcriptional threshold in these cells. Surprisingly, this induction of high-level mda-7/IL-24 expression could be achieved by treatment of cancer cells with several, structurally not related non-steroidal anti-inflammatory drugs (NSAIDs) in vitro and in vivo [11][12][13]. The purpose of this study was to evaluate, if these pathways can also be activated in AML cells and thereby render a potentially novel therapeutic strategy for the treatment of all subtypes of AML.…”

Section: Introductionmentioning

confidence: 99%

The non-steroidal anti-inflammatory drugs Sulindac sulfide and Diclofenac induce apoptosis and differentiation in human acute myeloid leukemia cells through an AP-1 dependent pathway

et al. 2011

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Acute myeloid leukemia is a heterogeneous disease with varying genetic and molecular pathologies. Non-steroidal anti-inflammatory drugs (NSAIDs) have been proven to possess significant anti-proliferative potential in various cancer cells in vitro and in vivo. Hence, treatment with these agents can be utilized to study disease specific anti-proliferative pathways. In this study, a total number of 42 bone marrow derived CD34(+) selected de novo AML patient samples and the AML cell lines THP-1 and HL-60 were treated with the NSAIDs Sulindac sulfide and Diclofenac. We analyzed viability, apoptosis, differentiation and addressed the molecular mechanisms involved. We found a consistent induction of apoptosis and to some extent an increased myeloid differentiation capacity in NSAID treated AML cells. Comprehensive protein and gene expression profiling of Diclofenac treated AML cells revealed transcriptional activation of GADD45α and its downstream MAPK/JNK pathway as well as increased protein levels of the caspase-3 precursor. This pointed towards a role of the c-Jun NH(2)-terminal kinase (JNK) in NSAID mediated apoptosis that we found indeed to be dependent on JNK activity as addition of a specific JNK-inhibitor abrogated apoptosis. Furthermore, the AP-1 transcription factor family members' c-Jun, JunB and Fra-2 were transcriptionally activated in NSAID treated AML cells and re-expression of these transcription factors led to activation of GADD45α with induction of apoptosis. Mechanistically, we demonstrate that NSAIDs induce apoptosis in AML through a novel pathway involving increased expression of AP-1 heterodimers, which by itself is sufficient to induce GADD45α expression with consecutive activation of JNK and induction of apoptosis.

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Section: Introductionmentioning

confidence: 99%

The non-steroidal anti-inflammatory drugs Sulindac sulfide and Diclofenac induce apoptosis and differentiation in human acute myeloid leukemia cells through an AP-1 dependent pathway

et al. 2011

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“…In a more recent study, we showed that Ad-mda7 treatment in combination with administration of sulindac, a nonsteroidal anti-inflammatory drug, enhanced lung tumor cell killing (22). Similarly, the treatment of human breast cancer cells with Ad-mda7 and celecoxib, a cyclooxygenase-2 inhibitor, resulted in synergistic cell killing (23). Although enhanced tumor cell killing after treatment with Ad-mda7 and sulindac or celecoxib was shown in these studies, the underlying molecular mechanism was not described.…”

Section: Introductionmentioning

confidence: 80%

Inhibition of nuclear factor-κB augments antitumor activity of adenovirus-mediated melanoma differentiation-associated gene-7 against lung cancer cells via mitogen-activated protein kinase kinase kinase 1 activation

Oida¹,

Gopalan²,

Miyahara³

et al. 2007

Molecular Cancer Therapeutics

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Nuclear factor-KB (NF-KB) activation promotes cell survival and growth. Reports show that chemotherapeutic agents and cytokines that are used for cancer therapy activate NF-KB expression in tumor cells and its suppression enhanced the antitumor activity. We hypothesized that adenovirus-mediated overexpression of melanoma differentiation-associated gene-7/interleukin-24 (Admda7/IL-24) induces NF-KB expression and that inhibition of this expression results in enhanced tumor cell killing.

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“…27,37,38,[81][82][83][84][85][86] McKenzie et al 81 investigated the combinatorial effects of Ad.mda-7 and Herceptin (Trastuzumab), an anti-p185ErbB2 murine monoclonal antibody (4D5) on Her-2/ neu-overexpressing breast cancer cells. This combination treatment resulted in decreased levels of β-catenin, Akt and phosphorylated Akt as compared with a single treatment with Ad.mda-7 or Herceptin.…”

Section: Combinatorial Effects Of Mda-7/il-24: Overcoming Chemo-resismentioning

confidence: 99%

Historical perspective and recent insights into our understanding of the molecular and biochemical basis of the antitumor properties of mda-7/IL-24

Emdad

Lebedeva

et al. 2009

Cancer Biology & Therapy

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A subtraction hybridization approach combined with a differentiation therapy model of human melanoma identified melanoma differentiation associated gene-7 (mda-7) as a gene upregulated during induction of terminal differentiation. Based on conserved structure, chromosomal location and cytokine-like properties, mda-7, has now been classified as a member of the expanding interleukin (IL)-10 gene family and designated as mda-7/IL-24. Extensive in vitro and in vivo human tumor xenograft studies confirm that mda-7/IL-24 induces apoptosis specifically in tumor cells without harming normal cells. Unique properties of mda-7/IL-24 action also include potent "bystander antitumor" activity, an ability to exert anti-angiogenic effects, immune modulating ability and a capacity to enhance the sensitivity of tumor cells to radiotherapy, chemotherapy and monoclonal antibody therapy. Very recent studies from our groups further reveal autocrine regulation and chemoprevention facilitating properties of mda-7/IL-24. Based on these remarkable antitumor attributes, mda-7/IL-24 was evaluated by intratumoral injection with a replication incompetent adenovirus expressing this gene (Ad.mda-7; INGN 241) in a phase I clinical trial in patients with metastatic melanomas and other advanced solid cancers. mda-7/IL-24 was well tolerated with significant clinical activity. This review highlights our current understanding of the molecular and biochemical basis of mda-7/IL-24 antitumor properties and highlights its potential as a viable gene-based therapy for a wide spectrum of primary and advanced cancers.

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Synergistic tumoricidal effect between celecoxib and adenoviral-mediated delivery of mda-7 in human breast cancer cells

Cited by 23 publications

References 44 publications

The non-steroidal anti-inflammatory drugs Sulindac sulfide and Diclofenac induce apoptosis and differentiation in human acute myeloid leukemia cells through an AP-1 dependent pathway

The non-steroidal anti-inflammatory drugs Sulindac sulfide and Diclofenac induce apoptosis and differentiation in human acute myeloid leukemia cells through an AP-1 dependent pathway

Inhibition of nuclear factor-κB augments antitumor activity of adenovirus-mediated melanoma differentiation-associated gene-7 against lung cancer cells via mitogen-activated protein kinase kinase kinase 1 activation

Historical perspective and recent insights into our understanding of the molecular and biochemical basis of the antitumor properties of mda-7/IL-24

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