ArticleOncology reports2022
Kinesin family member 2A acts as a potential prognostic marker and treatment target via interaction with PI3K/AKT and RhoA/ROCK pathways in acute myeloid leukemia.
Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
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.
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.
Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Ubiquitin E3 ligase MYCBP2 targets KIF14 and contributes to acute myeloid leukemia progression.The Journal of biological chemistry · 2026Article
- Article
- KIF2A Upregulates PI3K/AKT Signaling through Polo-like Kinase 1 (PLK1) to Affect the Proliferation and Apoptosis Levels ofBiology · 2024Article
- Transcriptomic alterations in hypertrophy of the ligamentum flavum: interactions of Rho GTPases, RTK, PIK3, and FGF.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2023Article
- Aberrant kinesin family member 2A signifies tumor size and invasion, and may help predict prognosis of patients with papillary thyroid carcinoma.Oncology letters · 2022Article
- Synergic effect of anticancer peptide CIGB-552 and Cisplatin in lung cancer models.Molecular biology reports · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KIF2A has been shown to be involved in the regulation of AML pathology, however, the mechanistic role of KIF2A in AML has not been fully identified. The present study aimed to identify the underlying mechanism of KIF2A regulation of AML cell function and chemosensitivity. A total of 58 patients with AML and 30 healthy subjects were enrolled for clinical analysis. AML cells (KG‑1 and Kasumi‑1) were transfected with KIF2A or control small interfering (si)RNA. PI3K/AKT pathway activator (740 Y‑P) and RhoA overexpression plasmid were added to rescue the effect of KIF2A siRNA. Cell proliferation, apoptosis, chemosensitivity to ADR and AraC, expression levels of mRNA/proteins associated with PI3K/AKT and RhoA/ROCK pathways were measured by Cell Counting Kit‑8, flow cytometry, reverse transcription‑quantitative PCR and western blotting. KIF2A was overexpressed, and correlated with higher levels of bone marrow blast, poor risk classification, lower treatment response and unfavorable survival profile in patients with AML. KIF2A siRNA inhibited proliferation but enhanced apoptosis and chemosensitivity to ADR and AraC in KG‑1 and Kasumi‑1 cells, which also inactivated PI3K/AKT and RhoA/ROCK pathways. Subsequent rescue experiments showed that 740 Y‑P and RhoA overexpression plasmid promoted cell survival and decreased chemosensitivity, which reversed the effect of KIF2A siRNA in KG‑1 and Kasumi‑1 cells. KIF2A was correlated with worse clinical features and survival in patients with AML; its knockdown promoted apoptosis and chemosensitivity by inactivating PI3K/AKT and RhoA/ROCK signaling pathways in AML cells. These data suggested KIF2A may be a potential prognostic marker and treatment target for AML management.
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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 Socratic graph.