F10, a novel hydatidiform mole-associated gene, inhibits the paclitaxel sensitivity of A549 lung cancer cells by downregulating BAX and caspase-3

Abstract

F10 is a novel hydatidiform mole (HM)-associated gene that was initially identified during a study into the pathogenesis of HMs. However, the role of the F10 gene requires further investigation. Our, previous studies have indicated that F10 may be involved in the malignant transformation of HMs and the development of certain types of adenocarcinoma, and that the overexpression of F10 may lead to excessive proliferation and decreased apoptosis of A549 cells. The present study aimed to investigate whether F10 may suppress the sensitivity of A549 lung cancer cells to paclitaxel therapy. A previously established F10-overexpressing A549 cell line (A549-F10) was treated with paclitaxel, using untransfected A549 cells and A549-mock cells (non-carrier A549) as the controls. These three groups of cells were subsequently examined by an MTT cell proliferation assay and a TUNEL-fluorescein isothiocyanate/Hoechst 33258 apoptosis assay. A western blot analysis was used to determine the expression levels of the pro-apoptotic genes B-cell lymphoma-2-associated X protein (BAX) and caspase-3. The effects of paclitaxel treatment on the proliferation and apoptosis of A549 cells were compared between the aforementioned cell lines. It was revealed that F10 inhibited the chemosensitivity of A549 cells to paclitaxel, as demonstrated by the decreased rates of growth inhibition and apoptosis in the A549-F10 group compared with the two control groups. Furthermore, the A549-F10 cells treated with paclitaxel exhibited significantly lower expression levels of the pro-apoptotic genes. The results of the current study demonstrate that F10 may inhibit the chemosensitivity of A549 cells to paclitaxel and that this inhibitory effect may be mediated by the downregulation of BAX and caspase-3 expression, which subsequently inhibits cell apoptosis.

Matrine Treatment Triggers Apoptosis in Colon Cancer Cells

“…5). Previous studies [30,31] have demonstrated that Bcl-2 and its potent inhibitor Bax served a critical role in regulating the cellular expansion and apoptosis. Upregulated Bcl-2 increases cell survival by interfering with apoptosis, whereas elevated expression of Bax accelerates cell death.…”

Microwave-Assisted Synthesis of Imidazo[4,5-f][1,10]phenanthroline Derivatives as Apoptosis Inducers in Chemotherapy by Stabilizing Bcl-2 G-quadruplex DNA

“…At concentration of 20 µM for 1 , the ratio of G1-phase reached about 67.37%, which was about 12% higher than that of the control (55.75%) [ 17 , 18 ]. These data indicating that 1 may inhibit the growth of A549 cells through inducing apoptosis of tumor cells since G1 phase arrest was more related to cell apoptosis, and pro-apoptotic proteins like Bcl-2 usually plays key roles in accelerating the apoptosis of tumor cells [ 19 , 20 , 21 , 22 , 23 ].…”

Expression Profiles of Long Noncoding RNAs and Messenger RNAs in a Rat Model of Spinal Cord Injury

“…lncRNA XR_001838273.1 acts as a sponge for rno-miR-6318 to regulate Iqgap3 or F10. Numerous study literatures have reported that Cdca3, Mcm10, Mki67, Iqgap3, and F10 are all related to tumor cell proliferation [51][52][53][54][55][56]. Knocking down the expression of these genes could reduce tumor cell proliferation and invasion.…”