ArticleMolecular genetics and genomics : MGG2025
CKMT1B regulates the proliferation, migration, invasion, and apoptosis of colorectal cancer cells through the AKT/mTOR/STAT3 pathway.
Article in Molecular genetics and genomics : MGG, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Integrated genome-wide high-throughput screening and functional validation identifies Sm proteins as essential splicing regulators for gastric cancer progression.Functional & integrative genomics · 2026Article
- Scutellarin triggers ferroptosis in ovarian cancer cells via inhibiting AKT/mTOR and JAK2/STAT3 pathways.Medical oncology (Northwood, London, England) · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the role of CKMT1B in the growth, migration, invasion, and apoptosis of colorectal cancer (CRC) cells, focusing on its regulation of the AKT/mTOR/STAT3 signaling pathway. Bioinformatics analysis indicated that the CK family expression exhibited heterogeneity and correlation across various cancers, with CKMT1B significantly underexpressed in CRC, suggesting its potential role as a tumor suppressor gene. Additionally, reverse transcription quantitative real-time PCR (RT-qPCR) and Western blot were employed to evaluate CKMT1B expression in CRC cell lines. To assess the effects of CKMT1B knockdown and overexpression in LOVO cells, CCK-8, plate cloning, scratch, Transwell chamber, and Muse assays were used to measure cell proliferation, migration, invasion, and apoptosis. The regulatory mechanism of CKMT1B in CRC was further explored through the AKT/mTOR/STAT3 pathway and related proteins. Downregulation of CKMT1B enhanced the proliferation, migration, and invasion of LOVO cells while inhibiting apoptosis, while CKMT1B overexpression had the opposite effect. Moreover, CKMT1B overexpression led to a decrease in the anti-apoptotic protein BCL2 and an increase in the tumor suppressor protein p53, suggesting its role in modulating apoptotic pathways. The expression levels of the pathway-related proteins P-AKT, P-mTOR, and P-STAT3 were significantly reduced, suggesting that CKMT1B regulates the AKT/mTOR/STAT3 signaling pathway, thereby modulating CRC progression. Taken together, these findings suggest that CKMT1B could serve as a promising molecular target for CRC treatment.
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Registered trials
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.