Evidence map›Paper›PMID 27478778›Full record

ArticleAdvanced pharmaceutical bulletin2016

Silencing of High Mobility Group Isoform I-C (HMGI-C) Enhances Paclitaxel Chemosensitivity in Breast Adenocarcinoma Cells (MDA-MB-468).

Behzad Mansoori, Ali Mohammadi, Samira Goldar, Dariush Shanehbandi, Leila Mohammadnejad, Elham Baghbani, Tohid Kazemi, Saeed Kachalaki, Behzad Baradaran

Open access · diamondAbstract read
In one paragraph

Article in Advanced pharmaceutical bulletin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. MicroRNA-421-targeted PDCD4 regulates breast cancer cell proliferation.International journal of molecular medicine · 2019
    Article
  5. Article
  6. Article
  7. Review
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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

9 authors at 1 institution in 1 country.

Behzad MansooriImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Ali MohammadiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Samira GoldarImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Dariush ShanehbandiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Leila MohammadnejadImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Elham BaghbaniImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Tohid KazemiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Saeed KachalakiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Behzad BaradaranImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Tabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHMGI-C (High Mobility Group protein Isoform I-C) protein is a member of the high-mobility group AT-hook (HMGA) family of small non-histone chromosomal protein that can modulate transcription of an ample number of genes. Genome-wide studies revealed up regulation of the HMGI-C gene in many human cancers. We suggested that HMGI-C might play a critical role in the progression and migration of various tumors. However, the exact role of HMGI-C in breast adenocarcinoma has not been cleared.

methodsThe cells were transfected with siRNAs using transfection reagent. Relative HMGI-C mRNA and protein levels were measured by quantitative real-time PCR and Western blotting, respectively. The cytotoxic effects of HMGI-C siRNA, Paclitaxel alone and combination on breast adenocarcinoma cells were determined using MTT assay. The migration after treatment by HMGI-C siRNA, Paclitaxel alone and combination were detected by wound-healing respectively.

resultsHMGI-C siRNA significantly reduced both mRNA and protein expression levels in a 48 hours after transfection and dose dependent manner. We observed that the knockdown of HMGI-C led to the significant reduced cell viability and inhibited cells migration in MDA-MB-468 cells in vitro.

conclusionThese results propose that HMGI-C silencing and Paclitaxel treatment alone can inhibit the proliferation and migration significantly, furthermore, synergic effect of HMGI-C siRNA and Paclitaxel showed higher inhibition compared to mono treatment. Taken together, HMGI-C could be used as a promising therapeutic agent in the treatment of human breast adenocarcinoma. Therefore HMGI-C siRNA may be an effective adjuvant in human breast adenocarcinoma.

Indexed as

Breast adenocarcinomaHMGI-C (High mobility group protein isoform I-C)PaclitaxelSmall interference RNA (siRNA)

Identifiers

PMID27478778
PMCPMC4961974
OpenAlexW2460638600

What OpenQuestion holds

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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.