Publications by authors named "Frank H C Cheng"
Article Synopsis
- MicroRNAs (miRNAs) regulate gene expression by either degrading or inhibiting the translation of specific mRNAs, and their interactions can explain indirect relationships among different mRNAs in the body.
- Current research suggests that the involvement of the proteins produced from these targeted mRNAs has not been adequately examined in the competition dynamics of competing endogenous RNA (ceRNA) networks.
- A new deterministic model indicates that significant changes in the levels of mRNAs targeted by miRNAs also depend on the transcriptional inhibition of miRNAs by those target proteins, especially observed in ovarian cancer scenarios where miR-193a's epigenetic silencing by E2F6 is crucial for altering the levels of c-KIT and PBX1 associated with
Tumor immune infiltration plays a key role in the progression of solid tumors, including ovarian cancer, and immunotherapies are rapidly emerging as effective treatment modalities. However, the role of cancer-associated fibroblasts (CAFs), a predominant stromal constituent, in determining the tumor-immune microenvironment and modulating efficacy of immunotherapies remains poorly understood. We have conducted an extensive bioinformatic analysis of our and other publicly available ovarian cancer datasets (GSE137237, GSE132289 and GSE71340), to determine the correlation of fibroblast subtypes within the tumor microenvironment (TME) with the characteristics of tumor-immune infiltration.
View Article and Find Full Text PDFOvarian cancer is the most lethal cancer of the female reproductive system. In that regard, several epidemiological studies suggest that long-term exposure to estrogen could increase ovarian cancer risk, although its precise role remains controversial. To decipher a mechanism for this, we previously generated a mathematical model of how estrogen-mediated upregulation of the transcription factor, E2F6, upregulates the ovarian cancer stem/initiating cell marker, c-Kit, by epigenetic silencing the tumor suppressor miR-193a, and a competing endogenous (ceRNA) mechanism.
View Article and Find Full Text PDFAccumulating data indicate that cancer stem cells contribute to tumor chemoresistance and their persistence alters clinical outcome. Our previous study has shown that ovarian cancer may be initiated by ovarian cancer initiating cells (OCIC) characterized by surface antigen CD44 and c-KIT (CD117). It has been experimentally demonstrated that a microRNA, namely miR-193a, targets c-KIT mRNA for degradation and could play a crucial role in ovarian cancer development.
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