HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway.

Cervical cancer (CC) is one of the most common malignancy and is the second leading cause of death in gynecologic malignancies worldwide. The homeobox transcription factor homeobox C13 (HOXC13) has been demonstrated to play crucial roles in various cancers. However, its function in CC remains to be addressed.

miR-544a Stimulates endometrial carcinoma growth via targeted inhibition of reversion-inducing cysteine-rich protein with Kazal motifs.

Endometrial carcinoma (EC) is a female-specific malignant tumor. Although current treatments can achieve good outcomes and improve patient survival, there remains a high incidence of treatment-induced infertility, a serious side effect that is unacceptable to those of childbearing age. Studies have demonstrated that micro ribonucleic acids (microRNAs or miRNAs) such as miR-544a regulate tumor-related gene expression.

L-Tetrahydropalmatine enhances the sensitivity of human ovarian cancer cells to cisplatin via microRNA-93/PTEN/Akt cascade.

Purpose: Το evaluate the effect of L-Tetrahydropalmatine (L-THP) on the sensitivity of a cisplatin resistant ovarian cancer (OC) cell line. As miR-93 is reported to be overexpressed in OC and cisplatin resistance, we also evaluated its pathway in OC.

Methods: The levels of miR-93 were evaluated using RT-PCR and Luciferase assay was performed to confirm the target of miR-93.

The role of Dby mRNA in early development of male mouse zygotes.

Ejaculated mammalian spermatozoa contain a complex yet specific population of mRNA. However, the possible roles that mRNA has in early zygotic and embryonic development remain unclear. We found that Dby mRNA is selectively retained in capacitated mouse spermatozoa, and is transferred into the oocyte during fertilization by reverse transcription-polymerase chain reaction even though no DBY protein expression is detected.

Nicotine induces cyclooxygenase-2 and prostaglandin E(2) expression in human umbilical vein endothelial cells.

Nicotine is a major component of cigarette smoking which may be involved in the progress of atherogenesis. In order to explain the mechanism of nicotine-induced endothelium dysfunction, we investigated the effects of nicotine on cyclooxygenase-2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1) expression in human umbilical vein endothelial cells (HUVECs). Nicotine treatment increased the expressions of COX-2 at mRNA and protein level in a dose-dependent manner, following prostaglandin E(2) (PGE(2)) release enhancement.