Evidence map›Paper›PMID 39847238›Full record

ReviewJournal of molecular neuroscience : MN2025

Decoding the Role of Kinesin Superfamily Proteins in Glioma Progression.

Mohamed J Saadh, Zahraa Sabah Ghnim, Morug Salih Mahdi, Muktesh Chandra, Suhas Ballal, Lakshay Bareja, Kamlesh Chaudhary, R S K Sharma, Sofia Gupta, Waam Mohammed Taher and 3 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

13 authors.

Mohamed J SaadhFaculty of Pharmacy, Middle East University, Amman, 11831, Jordan. mohamedjsaadh@gmail.com.
Zahraa Sabah GhnimCollege of Pharmacy, Alnoor University, Nineveh, Iraq.
Morug Salih MahdiCollege of MLT, Ahl Al Bayt University, Karbala, Iraq.
Muktesh ChandraDepartment of Microbiology, Faculty of Science, Marwadi University Research Center, Marwadi University, Rajkot, 360003, Gujarat, India.
Suhas BallalDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to Be University), Bangalore, Karnataka, India.
Lakshay BarejaCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
Kamlesh ChaudharyDepartment of Neurology, National Institute of Medical Sciences, NIMS University Rajasthan, Jaipur, India.
R S K SharmaDepartment of Chemistry, Raghu Engineering College, Visakhapatnam, Andhra Pradesh, 531162, India.
Sofia GuptaDepartment of Applied Sciences, Chandigarh Engineering College, Chandigarh Group of Colleges-Jhanjeri, Mohali, 140307, Punjab, India.
Waam Mohammed TaherCollege of Nursing, National University of Science and Technology, Dhi Qar, Iraq.
Mariem AlwanPharmacy College, Al-Farahidi University, Baghdad, Iraq.
Mahmood Jasem JawadDepartment of Pharmacy, Al-Zahrawi University College, Karbala, Iraq.
Atheer Khdyair HamadGilgamesh Ahliya University, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is a highly aggressive and invasive brain tumor with limited treatment options, highlighting the need for novel therapeutic approaches. Kinesin superfamily proteins (KIFs) are a diverse group of motor proteins that play essential roles in cellular processes such as mitosis, intracellular transport, and signal transduction, all of which are crucial for tumorigenesis. This review focuses on the multifaceted role of KIFs in glioma, examining their clinical relevance, contribution to tumor progression, and potential as therapeutic targets. We discuss how KIFs influence key aspects of glioma biology, including cell proliferation, invasion, migration, and metastasis. Furthermore, we explore the regulation of the cell cycle and critical signaling pathways associated with glioma, such as PI3K-Akt, Wnt/β-catenin, and Hedgehog signaling by KIFs. The review also addresses the emerging interplay between KIFs and non-coding RNAs, including circular RNAs (circRNAs) and microRNAs (miRNAs), in glioma progression. Finally, we examine current therapeutic strategies targeting KIFs, including immunotherapy, chemotherapy, and small-molecule inhibitors, and their potential to improve treatment outcomes for glioma patients. By synthesizing these insights, this review underscores the significance of KIFs in glioma pathogenesis and their promise as novel therapeutic targets in the fight against glioma.

Indexed as

Brain NeoplasmsGliomaKinesinsAnimalsHumansMicroRNAsKinesinsMicroRNAsGlioblastomaGliomaKinesin superfamilyMotor proteinsSignaling pathway

Identifiers

PMID39847238

What OpenQuestion holds

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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.