Open Access

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

  • Authors:
    • Yali Song
    • Wei Cao
    • Xi Zhu
    • Zhuolin Qiu
    • Xiaoping Yang
    • Jing Liu
    • Ruoting Xu
    • Weizhuang Yuan
    • Song Quan
  • View Affiliations

  • Published online on: February 20, 2017     https://doi.org/10.3892/ol.2017.5749
  • Pages: 2563-2568
  • Copyright: © Song et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.

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April-2017
Volume 13 Issue 4

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Song Y, Cao W, Zhu X, Qiu Z, Yang X, Liu J, Xu R, Yuan W and Quan S: F10, a novel hydatidiform mole-associated gene, inhibits the paclitaxel sensitivity of A549 lung cancer cells by downregulating BAX and caspase-3. Oncol Lett 13: 2563-2568, 2017.
APA
Song, Y., Cao, W., Zhu, X., Qiu, Z., Yang, X., Liu, J. ... Quan, S. (2017). F10, a novel hydatidiform mole-associated gene, inhibits the paclitaxel sensitivity of A549 lung cancer cells by downregulating BAX and caspase-3. Oncology Letters, 13, 2563-2568. https://doi.org/10.3892/ol.2017.5749
MLA
Song, Y., Cao, W., Zhu, X., Qiu, Z., Yang, X., Liu, J., Xu, R., Yuan, W., Quan, S."F10, a novel hydatidiform mole-associated gene, inhibits the paclitaxel sensitivity of A549 lung cancer cells by downregulating BAX and caspase-3". Oncology Letters 13.4 (2017): 2563-2568.
Chicago
Song, Y., Cao, W., Zhu, X., Qiu, Z., Yang, X., Liu, J., Xu, R., Yuan, W., Quan, S."F10, a novel hydatidiform mole-associated gene, inhibits the paclitaxel sensitivity of A549 lung cancer cells by downregulating BAX and caspase-3". Oncology Letters 13, no. 4 (2017): 2563-2568. https://doi.org/10.3892/ol.2017.5749