Journal Article DKFZ-2017-05720

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MicroRNA-210 induces apoptosis in colorectal cancer via induction of reactive oxygen.

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2016
BioMed Central London

Cancer cell international 16(1), 42 () [10.1186/s12935-016-0321-6]
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Abstract: Deregulation of miRNA-210 is a common event in several types of cancer. However, increased expression levels in the cancer tissue have been associated with both poor and good prognosis of patients. Similarly, the function of miR-210 with regard to cell growth and apoptosis is still controversial.Overexpression of miR-210 was performed in HCT116, SW480 and SW707 colorectal cancer (CRC) cell lines. Functional effects of a modulated miR-210 expression were analyzed with regard to proliferation, clonogenicity, cell cycle distribution, reactive oxygen species (ROS) generation, and apoptosis. Furthermore, quantitative real time (RT)-PCR and immunoblot analyses were performed to investigate signaling pathways affected by miR-210.We show that in CRC cells miR-210 inhibits clonogenicity and proliferation which was accompanied by an accumulation of cells in the G2/M phase of the cell cycle. Additionally, overexpression of miR-210 results in an increase of ROS generation. Moreover, miR-210 mediated the induction of apoptosis which was associated with an upregulation of pro-apoptotic Bim expression and enhanced processing of Caspase 2. Importantly, inhibition of ROS generation rescued cells from miR-210-induced apoptosis.Taken together, miR-210 induces apoptosis in CRC cells via a ROS-dependent mechanism.

Classification:

Contributing Institute(s):
  1. Molekulare Tumorpathologie (G150)
Research Program(s):
  1. 317 - Translational cancer research (POF3-317) (POF3-317)

Appears in the scientific report 2016
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Medline ; Creative Commons Attribution CC BY (No Version) ; DOAJ ; BIOSIS Previews ; DOAJ Seal ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection
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 Record created 2017-11-23, last modified 2024-02-28


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