New Gene Promoting Incidence of Leukemia Indentified

Scientists from National University of Singapore have found the overexpression of Leo1 gene will significantly influence other genes which have directly relations with Acute Myelogenous leukemia(AML), then enhance the incidence of cancer. Through inhibiting Leo1 and its downstream signaling pathway, this study, published in Cancer Research, potentially provides a new regimen for AML patients.

PRL-3 is a small dual specificity phosphatase and has been shown to promote cellular processes, such as cell motility, invasion and survival. PRL-3 was first linked to cancer when it was consistently found at elevated levels in colorectal cancer metastases, but at much lower levels in matched early-staged tumor and normal colorectal epithelium. Stable expression of PRL-3 confers cytokine independence and growth advantage of AML. However, how PRL-3 mediates these functions in AML is still unknown.

In this study, researchers have indicated that Leo1, a component of RNA polymerase -associated factor(PAE) complex, is a novel and important mediator of PRL-3 oncogenic activities in AML. They have described a novel mechanism where elevated PRL-3 protein increases JMJD2C histone demethylase occupancy on Leo1 promoter, thereby reducing the H3K9me3 repressive signals and promoting Leo1 gene expression. Inhibition of Leo1 reverses PRL-3 oncogenic phenotypes in AML. Loss of Leo1 leads to destabilization of PAF complex and downregulation of SOX2 and SOX4, potent oncogenes in myeloid transformation.

This finding has implicated a pro-oncogenic role of PRL-3 in AML, and reveals Leo1 as a novel downstream molecule required for PRL-3 oncogenic function in leukemia.

Researchers from Ottawa and Taiwan have demonstrated a new insight into the common existence of chemoresistance in women ovarian cancer and provided a new possibility in its diagnosis and treatment. Their study was published in PNAS.

According to related data, about 2700 Canadian women were diagnosed ovarian cancer in 2014 and 1750 of them died. The ovarian cancer was always diagnosed in the terminal stage, and chemoresistance has already shown up at the time. Chemoresistance is a major hurdle in cancer treatment. Down-regulation of apoptosis pathways in one of the key determinants for chemoresistance.

In this study, researchers have tested the hypothesis that gelsolin (Gsn) plays an important role in gynecological chemoressistance. They have provided strong evidence in support of GSN as an important etiologic factor in chemoresistance in vitro and determined the mechanism by which GSN exerts its prosurvival action. The findings also suggest that the application for C-terminal GSN may represent a new therapeutic strategy for chemoresistance gynecologic cancer. The in vitro findings have been validated with a clinical investigation that determines the relationship between GSN expression and cis-Diammine dichloroplatinium (?) sensitivity in human ovarian tumor.

These findings agree with the notion that GSN plays a key role in the regulation of gynecological cell fate as reflected in chemoresistance.