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ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells

  • Authors:
    • Lin Wang
    • Zhihui Tan
    • Ying Zhang
    • Nankoria Kady Keita
    • Huining Liu
    • Yu Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Cardiovascular Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China, Department of Gynecology, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1162-1174
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    Published online on: March 5, 2020
       https://doi.org/10.3892/ijo.2020.5007
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Abstract

ADAM metallopeptidase domain 12 (ADAM12) has been demonstrated to mediate cell proliferation and apoptosis resistance in several types of cancer cells. However, the effect of ADAM12 silencing on the proliferation and apoptosis of choriocarcinoma cells remains unknown. The present study revealed that ADAM12 silencing significantly inhibited cellular activity and proliferation in the human choriocarcinoma JEG3 cell line and increased the rate of apoptosis. In addition, ADAM12 silencing significantly increased the expression levels of the autophagy proteins microtubule‑associated protein‑light‑chain 3 (LC3B) and autophagy related 5 (ATG5) and the fluorescence density of LC3B in JEG‑3 cells. However, the suppression of autophagy by 3‑methyladenine could block ADAM12 silencing‑induced cellular apoptosis. ADAM12 silencing reduced the levels of the inflammatory factors interleukin‑1β, interferon‑γ and TNF‑α, and inactivated nuclear p65‑NF‑κB and p‑mTOR in JEG‑3 cells. The downregulation of p‑mTOR expression by ADAM12 silencing was rescued in 3‑methyladenine‑treated JEG‑3 cells, indicating that mTOR might participate in the autophagy‑mediated pro‑apoptotic effect of ADAM12 silencing. In conclusion, ADAM12 silencing promoted cellular apoptosis in human choriocarcinoma JEG3 cells, which might be associated with autophagy and the mTOR response. These findings indicate that ADAM12 silencing might be a potential novel therapeutic target for choriocarcinoma.
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Copy and paste a formatted citation
Spandidos Publications style
Wang L, Tan Z, Zhang Y, Kady Keita N, Liu H and Zhang Y: ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells. Int J Oncol 56: 1162-1174, 2020.
APA
Wang, L., Tan, Z., Zhang, Y., Kady Keita, N., Liu, H., & Zhang, Y. (2020). ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells. International Journal of Oncology, 56, 1162-1174. https://doi.org/10.3892/ijo.2020.5007
MLA
Wang, L., Tan, Z., Zhang, Y., Kady Keita, N., Liu, H., Zhang, Y."ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells". International Journal of Oncology 56.5 (2020): 1162-1174.
Chicago
Wang, L., Tan, Z., Zhang, Y., Kady Keita, N., Liu, H., Zhang, Y."ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells". International Journal of Oncology 56, no. 5 (2020): 1162-1174. https://doi.org/10.3892/ijo.2020.5007
Copy and paste a formatted citation
x
Spandidos Publications style
Wang L, Tan Z, Zhang Y, Kady Keita N, Liu H and Zhang Y: ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells. Int J Oncol 56: 1162-1174, 2020.
APA
Wang, L., Tan, Z., Zhang, Y., Kady Keita, N., Liu, H., & Zhang, Y. (2020). ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells. International Journal of Oncology, 56, 1162-1174. https://doi.org/10.3892/ijo.2020.5007
MLA
Wang, L., Tan, Z., Zhang, Y., Kady Keita, N., Liu, H., Zhang, Y."ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells". International Journal of Oncology 56.5 (2020): 1162-1174.
Chicago
Wang, L., Tan, Z., Zhang, Y., Kady Keita, N., Liu, H., Zhang, Y."ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells". International Journal of Oncology 56, no. 5 (2020): 1162-1174. https://doi.org/10.3892/ijo.2020.5007
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