Functional analysis of AKT1 knockout in fibrosarcoma cells using CRISPR/Cas9 technology.

So-Hee Kim, Moon-Moo Kim

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Article in Journal of human genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

2 authors.

So-Hee KimDepartment of Cosmetics Engineering, and Graduate School of Applied Chemistry·Food Engineering, Dong-Eui University, Busan, Republic of Korea.

Moon-Moo KimDepartment of Cosmetics Engineering, and Graduate School of Applied Chemistry·Food Engineering, Dong-Eui University, Busan, Republic of Korea. mmkim@deu.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AKT1 (Protein Kinase B alpha) is a serine/threonine kinase that plays a pivotal role in regulating various cellular processes. To elucidate the role of the AKT1 gene in signaling pathways, this study generated AKT1 knockout (KO) HT-1080 cells using the CRISPR/Cas9 system. Gene-editing efficiency was validated through Sanger DNA sequencing and insertion/deletion (InDel) analysis. Quantitative real-time PCR and Western blot analyses were performed to evaluate the expression levels of AKT1 mRNA and protein, as well as to examine the expression of AKT1 downstream effectors: mTOR, BCL-2, and FOXO1. The AKT1 single-guide RNA sequence was successfully cloned into the CRISPR/Cas9 vector, leading to the establishment of AKT1 KO cells. InDel analysis identified eight editing types, with two dominant populations. The expression levels of AKT1 mRNA and protein were significantly reduced in the KO cells. The expression levels of mTOR, BCL-2, and FOXO1 were significantly altered in the KO cells compared to normal cells. These findings highlight the impact of AKT1 disruption on signaling pathways and provide fundamental insights into the regulatory role of the AKT1 gene.

Indexed as

CRISPR-Cas SystemsGene Knockout TechniquesProto-Oncogene Proteins c-aktCell Line, TumorForkhead Box Protein O1Gene EditingGene Expression Regulation, NeoplasticHumansINDEL MutationProto-Oncogene Proteins c-bcl-2Signal TransductionTOR Serine-Threonine KinasesAKT1 protein, humanBCL2 protein, humanForkhead Box Protein O1FOXO1 protein, humanMTOR protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2TOR Serine-Threonine Kinases

Identifiers

PMID41298833

DOI10.1038/s10038-025-01436-9

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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.