Evidence map›Paper›PMID 27293381›Full record

ArticleCancer cell international2016

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

Katrin E Tagscherer, Anne Fassl, Tabea Sinkovic, Jutta Richter, Sabrina Schecher, Stephan Macher-Goeppinger, Wilfried Roth

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 52 citations in OpenAlex.

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  15. MicroRNAs and Apoptosis in Colorectal Cancer.International journal of molecular sciences · 2020
    Review
  16. Article
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  18. Review
  19. Deregulation of miRNA inJournal of clinical medicine · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Katrin E TagschererMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany ; Institute of Pathology, University Medical Center Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Anne FasslMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany ; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215 USA ; Department of Genetics, Harvard Medical School, Boston, MA 02215 USA.
Tabea SinkovicMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany.
Jutta RichterMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany ; Institute of Pathology, University Medical Center Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Sabrina SchecherMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany ; Institute of Pathology, University Medical Center Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Stephan Macher-GoeppingerMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany ; Institute of Pathology, University Medical Center Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Wilfried RothMolecular Tumor-Pathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany ; Institute of Pathology, University of Heidelberg, 69120 Heidelberg, Germany ; Institute of Pathology, University Medical Center Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Heidelberg University · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDeregulation 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.

methodsOverexpression 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.

resultsWe 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.

conclusionsTaken together, miR-210 induces apoptosis in CRC cells via a ROS-dependent mechanism.

Indexed as

ApoptosisBimColorectal carcinomamiR-210ROS

Identifiers

PMID27293381
PMCPMC4901463
OpenAlexW2409811039

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.