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Downregulation of p53-inducible microRNAs 192, 194, and 215 impairs the p53/MDM2 autoregulatory loop in multiple myeloma development.
Evidence is provided that miR-192, 194, and 215, which are downregulated in a subset of newly diagnosed MMs, can be transcriptionally activated by p53 and then modulate MDM2 expression, and that their downregulation plays a key role in MM development. Expand
Inhibition of constitutively active Stat3 suppresses growth of human ovarian and breast cancer cells
It is shown that inhibition of the Stat3 signaling pathway using the Janus Kinase-selective inhibitor, AG490, and a dominant negative Stat3 (Stat3β) significantly suppresses the growth of ovarian and breast cancer cell lines harboring constitutively active Stat3. Expand
Promoter hypermethylation of FBXO32, a novel TGF-β/SMAD4 target gene and tumor suppressor, is associated with poor prognosis in human ovarian cancer
The novel tumor suppressor FBXO32 is epigenetically silenced in ovarian cancer cell lines with disrupted TGF-β/SMAD4 signaling, and FBX O32 methylation status predicts survival in patients with ovarian cancer. Expand
Epigenetic Repression of RARRES1 Is Mediated by Methylation of a Proximal Promoter and a Loss of CTCF Binding
Background The cis-acting promoter element responsible for epigenetic silencing of retinoic acid receptor responder 1 (RARRES1) by methylation is unclear. Likewise, how aberrant methylationExpand
STAT3 is necessary for proliferation and survival in colon cancer-initiating cells.
It is established that STAT3 is constitutively activated in colon cancer-initiating cells and that these cells are sensitive to STAT3 inhibition, a powerful rationale to develop STAT3 inhibitory strategies for treating advanced colorectal cancers. Expand
Epigenetic silencing mediated through activated PI3K/AKT signaling in breast cancer.
It is shown that activation of PI3K/AKT signaling can be a trigger of this epigenetic processing at many downstream target genes and DNA methylation can be acquired at the same loci in cancer cells, thereby reinforcing permanent repression in those losing the H3K27me3 mark. Expand
An integrative ChIP-chip and gene expression profiling to model SMAD regulatory modules
Together, the computational results further the understanding of the interactions between SMAD and other transcription factors at specific target promoters, and provide the basis for more targeted experimental verification of the co-regulatory modules. Expand
Aberrant TGFβ/SMAD4 signaling contributes to epigenetic silencing of a putative tumor suppressor, RunX1T1 in ovarian cancer
Dysregulated TGFβ/SMAD4 signaling may lead to epigenetic silencing of a putative tumor suppressor, RunX1T1, during ovarian carcinogenesis. Expand
Breast cancer-associated fibroblasts confer AKT1-mediated epigenetic silencing of Cystatin M in epithelial cells.
The findings suggest that microenvironmental stimuli are triggers in this epigenetic cascade, leading to the long-term silencing of CST6 in breast tumors, and the described coculture system can be used to determine the effect of epithelial factors on fibroblasts in future studies. Expand
Evaluation of STAT3 Signaling in ALDH+ and ALDH+/CD44+/CD24− Subpopulations of Breast Cancer Cells
An important role is demonstrated for STAT3 signaling in ALDH+ and ALDH/CD44+/CD24− subpopulations of breast cancer cells which may have cancer stem cell properties and pharmacologic inhibition of STAT3 represents an effective strategy to selectively target the cancer stem-like subpopulation. Expand