Let-7d increases ovarian cancer cell sensitivity to a genistein analog by targeting c-Myc.

c-Myc is a key oncogenic transcription factor that participates in tumor pathogenesis. In this study, we found that levels of c-Myc mRNA and protein were higher in early ovarian cancer tissues than normal ovary samples. Increased c-Myc levels correlated positively with clinical stage I (Ia+b/Ic) in ovarian cancer patients. Patients with higher nuclear c-Myc expression had shorter overall survival times than patients with low c-Myc expression. Knocking down c-Myc sensitized ovarian cancer cells to 7-difluoromethoxyl-5,4'-di-n-octylgenistein (DFOG), a novel synthetic genistein analogue that suppressed PI3K/AKT signaling in vitro and in vivo. Finally, c-Myc was confirmed to be a direct target of let-7d, and let-7d-induced suppression of c-Myc increased the DFOG-sensitivity of ovarian cancer cells. These results indicate that nuclear c-Myc expression is an unfavorable factor in early ovarian cancer, and that let-7d increases ovarian cancer cell sensitivity to DFOG by suppressing c-Myc and PI3K/AKT signaling.

7-difluoromethoxyl-5,4'-di-n-octyl genistein inhibits ovarian cancer stem cell characteristics through the downregulation of FOXM1.

7-Difluoromethoxyl-5,4'-di-n-octylgenistein (DFOG) is a novel synthetic genistein analogue that possesses anti-cancer activity in a variety of cancers, including ovarian cancer. The objective of the present study was to investigate whether DFOG inhibits the self-renewal capacity of ovarian cancer stem-like cells (OCSLCs) and to identify its potential mechanism of action. It was found that the sphere-forming cells (SFCs) of the SKOV3 cell line exhibited a self-renewal capacity and high tumorigenicity, indicating that they possessed the properties of ovarian cancer stem cells (OCSCs). It was also shown for the first time that DFOG preferentially inhibited proliferation, self-renewal capacity and expression of stem cell markers [cluster of differentiation (CD)133, CD44 and aldehyde dehydrogenase 1 (ALDH1)] in the SFCs derived from the SKOV3 cells. These effects were accompanied by the downregulation of forkhead box M1 (FOXM1) expression. Overexpression of FOXM1 rescued the DFOG-induced downregulation of FOXM1, CD133, CD44 and ALDH1 protein expression. It also inhibited the self-renewal capacity of the SFCs derived from the SKOV3 cells. Thus, DFOG appears to inhibit the characteristics of OCSLCs by downregulating FOXM1 expression.

Septicemic melioidosis: a case report and literature review.

This report was about a 22-year-old male patient who died from acute and severe septicemic melioidosis. He was initially misdiagnosed as having pneumonia in a local hospital in Hainan but transferred to Guangzhou Red Cross Hospital after ineffective treatment and detection of Burkholderia pseudomallei in his blood sample. Unfortunately, right diagnosis and antibiotic treatment of melioidosis had been delayed so that his condition deteriorated rapidly out of control. The victim's death highlights the importance of early diagnosis and effective antibiotic treatment of septicemic melioidosis in areas where this disease is prevalent.