4.4 Article

miR-489-3p inhibits proliferation and migration of bladder cancer cells through downregulation of histone deacetylase 2

Journal

ONCOLOGY LETTERS
Volume 20, Issue 4, Pages -

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2020.11869

Keywords

microRNA-489-3p; HDAC2; BC; progression

Categories

Funding

  1. National Natural Science Foundation of China [81672523, 81472404, 81472403, 81572831]
  2. 2018 Support Plan for innovative talents in Colleges and Universities of Liaoning Province
  3. 2018 'Million Talents Project' - Project of Liaoning Province
  4. 2019 Key R&D projects of Shenyang [19-112-4-102]
  5. Science and Technology Research Project of Education Department of Liaoning Province [LK201616]

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Since human bladder cancer (BC) is a common malignancy of the urinary system with poor prognosis, it is crucial to clarify the molecular mechanisms of BC development and progression. To the best of our knowledge, the current study demonstrated for the first time that miR-489-3p suppressed BC cell-derived tumor growthin vivovia the downregulation of histone deacetylase 2 (HDAC2). According to the results, expression levels of miR-489-3p were lower in BC tissues compared with corresponding normal tissues. Expression of miR-489-3p mimics in BC-derived T24 and 5637 cells resulted in a significant reduction in proliferation and migration rates. Furthermore, bioinformatics analyses indicated that HDAC2 may be a potential downstream target of miR-489-3p. In contrast to miR-489-3p, HDAC2 was expressed at higher levels in BC tissues compared with corresponding normal tissues. Additionally, small interfering RNA-mediated knockdown of HDAC2 caused a marked decrease in the proliferation and migration rates of T24 and 5637 cells. Consistent with these observations, expression of miR-489-3p mimics attenuated the growth of xenograft tumors arising from T24 cells and resulted in HDAC2 downregulation. In conclusion, the results of the current study indicated that the miR-489-3p/HDAC2 axis serves a role in the development and/or the progression of BC and may be a potential molecular target for the development of a novel strategy to treat patients with BC.

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