Evidence map›Paper›PMID 27959385›Full record

ArticleInternational journal of oncology2017

Microtubule actin cross-linking factor 1, a novel target in glioblastoma.

Najlaa Afghani, Toral Mehta, Jialiang Wang, Nan Tang, Omar Skalli, Quincy A Quick

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. A Multifaceted Giant Protein Microtubule-Actin Cross-Linking Factor 1.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Susceptibility of cytoskeletal-associated proteins for tumor progression.Cellular and molecular life sciences : CMLS · 2021
    Review
  9. Article
  10. Article
  11. Strength Through Unity: The Power of the Mega-Scaffold MACF1.Frontiers in cell and developmental biology · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Biomedical potential of mammalian spectraplakin proteins: Progress and prospect.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review
  17. Review
  18. Article
  19. Review
  20. Review
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

6 authors at 4 institutions in 2 countries.

Najlaa AfghaniDepartment of Biological Sciences, Tennessee State University, Nashville, TN, USA.
Toral MehtaDepartment of Biological Sciences, Tennessee State University, Nashville, TN, USA.
Jialiang WangDepartment of Neurological Surgery, Vanderbilt Medical Center, Nashville, TN, USA.
Nan TangUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, P.R. China.
Omar SkalliDepartment of Biological Sciences, University of Memphis, Memphis, TN, USA.
Quincy A QuickDepartment of Biological Sciences, Tennessee State University, Nashville, TN, USA.
Tennessee State University · USNeurological Surgery · USUniversity of Memphis · USWuhan Union Hospital · CN

Funding

Targeting MACF1 in GlioblastomaSC3GM121178 · NIGMS · TENNESSEE STATE UNIVERSITY · PI QUICK, QUINCY ANTOINE · 2017 to 2020
$426k
NIGMS NIH HHS SC3 GM121178
6 · The paper itself

Abstract

Genetic heterogeneity is recognized as a major contributing factor of glioblastoma resistance to clinical treatment modalities and consequently low overall survival rates. This genetic diversity results in variations in protein expression, both intratumorally and between individual glioblastoma patients. In this regard, the spectraplakin protein, microtubule actin cross-linking factor 1 (MACF1), was examined in glioblastoma. An expression analysis of MACF1 in various types of brain tumor tissue revealed that MACF1 was predominately present in grade III-IV astroctyomas and grade IV glioblastoma, but not in normal brain tissue, normal human astrocytes and lower grade brain tumors. Subsequent genetic inhibition experiments showed that suppression of MACF1 selectively inhibited glioblastoma cell proliferation and migration in cell lines established from patient derived xenograft mouse models and immortalized glioblastoma cell lines that were associated with downregulation of the Wnt-signaling mediators, Axin1 and β-catenin. Additionally, concomitant MACF1 silencing with the chemotherapeutic agent temozolomide (TMZ) used for the clinical treatment of glioblastomas cooperatively reduced the proliferative capacity of glioblastoma cells. In conclusion, the present study represents the first investigation on the functional role of MACF1 in tumor cell biology, as well as demonstrates its potential as a unique biomarker that can be targeted synergistically with TMZ as part of a combinatorial therapeutic approach for the treatment of genetically multifarious glioblastomas.

Indexed as

AnimalsAxin Proteinbeta CateninDacarbazineDrug Resistance, NeoplasmGenetic HeterogeneityGlioblastomaHumansMiceMicrofilament ProteinsTemozolomideWnt Signaling PathwayXenograft Model Antitumor AssaysAXIN1 protein, humanAxin Proteinbeta CateninDacarbazineMACF1 protein, humanMicrofilament ProteinsTemozolomide

Identifiers

PMID27959385
PMCPMC6903898
OpenAlexW2560648869

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.