Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway

Lactoferrin (LTF) has gained attention as a potential anti-cancer biomarker, but its role in left-sided colon cancer (LCC) remains poorly understood. This study explores the function of LTF in LCC and its underlying mechanisms. LTF expression was significantly elevated in tumor tissues compared to normal tissues (59.67-fold increase, <i>p</i> < .001). LTF overexpression significantly enhanced LCC cell proliferation, migration, and invasion (<i>p</i> < .01), while suppressing apoptosis (<i>p</i> < .05). In contrast, LTF knockdown markedly inhibited these oncogenic behaviors. Western blot analysis demonstrated that LTF overexpression led to increased phosphorylation of PI3K and Akt proteins (<i>p</i> < .01), suggesting activation of the PI3K/AKT signaling pathway, while LTF knockdown resulted in decreased phosphorylation levels (<i>p</i> < .01). This study identifies LTF as a promoter of LCC development via activation of the PI3K/AKT pathway, suggesting LTF as a promising therapeutic target. Further research is warranted to evaluate its clinical potential in LCC treatment.

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Publication Details

Journal
Cell Adhesion & Migration
Published
2026-01-09
DOI
https://doi.org/10.1080/19336918.2026.2613628
Primary Topic
Infant Nutrition and Health
Type
article
Field-Weighted Citation Impact
0.00
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article

Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway

Peng Chen, Xuefeng Bai, Mingrui Zhang
Cell Adhesion & Migration
Infant Nutrition and Health
article

Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway

Peng Chen, Xuefeng Bai, Mingrui Zhang
article en

Abstract

Lactoferrin (LTF) has gained attention as a potential anti-cancer biomarker, but its role in left-sided colon cancer (LCC) remains poorly understood. This study explores the function of LTF in LCC and its underlying mechanisms. LTF expression was significantly elevated in tumor tissues compared to normal tissues (59.67-fold increase, <i>p</i> < .001). LTF overexpression significantly enhanced LCC cell proliferation, migration, and invasion (<i>p</i> < .01), while suppressing apoptosis (<i>p</i> < .05). In contrast, LTF knockdown markedly inhibited these oncogenic behaviors. Western blot analysis demonstrated that LTF overexpression led to increased phosphorylation of PI3K and Akt proteins (<i>p</i> < .01), suggesting activation of the PI3K/AKT signaling pathway, while LTF knockdown resulted in decreased phosphorylation levels (<i>p</i> < .01). This study identifies LTF as a promoter of LCC development via activation of the PI3K/AKT pathway, suggesting LTF as a promising therapeutic target. Further research is warranted to evaluate its clinical potential in LCC treatment.

Cell Adhesion & MigrationVol. 20(1)
Harbin Medical University (CN), Chifeng University (CN), Third Affiliated Hospital of Harbin Medical University (CN), Inner Mongolia Medical University (CN)
Good health and well-being
Openalex Percentile: Top 92%
Infant Nutrition and Health
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