Evidence map›Paper›PMID 41658425›Full record

ArticleInternational journal of clinical and experimental pathology2026

Lactoferrin inhibits anoikis-resistance and metastasis of nasopharyngeal carcinoma cells via the AKT signaling pathway.

Yingying Wang, Yin Fu, Xin Deng, Xiaorui Xu, Ying Wu, Junyu He, Qi Guo, Guoying Zou

Abstract read
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Article in International journal of clinical and experimental pathology, 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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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yingying WangCollege of Clinical Medicine, Hunan University of Chinese Medicine Changsha, Hunan, China.
Yin FuDepartment of Medical Laboratory, Hunan Chest Hospital Changsha, Hunan, China.
Xin DengDepartment of Laboratory Medicine, The First Hospital of Changsha Changsha, Hunan, China.
Xiaorui XuChangsha Medical University Changsha, Hunan, China.
Ying WuDepartment of Clinical Laboratory, Rugao People's Hospital Nantong, Jiangsu, China.
Junyu HeDepartment of Clinical Laboratory, The Second People's Hospital of Hunan Province Changsha, Hunan, China.
Qi GuoDepartment of Clinical Laboratory, The Second People's Hospital of Hunan Province Changsha, Hunan, China.
Guoying ZouCollege of Clinical Medicine, Hunan University of Chinese Medicine Changsha, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the influence of lactoferrin (LTF) on the anoikis-resistance of nasopharyngeal carcinoma (NPC) cells and explore its relationship with the protein kinase B (AKT) signaling pathway.

methodsAnoikis-resistant HNE-1 and HONE-1 NPC cell lines were established. The proliferation and survival of cells were detected by Cell Counting Kit-8 (CCK8), while cell cycle and apoptosis were measured by flow cytometry. The transwell assay was used to evaluate invasion and metastasis abilities. The expression of matrix metallopeptidase-9 (MMP-9), vascular endothelial growth factor-A (VEGF-A), E-cadherin and Vimentin were assessed by Western blot. LTF plasmids and LTF shRNA plasmids were transfected into HNE-1 and HONE-1 cells, respectively, and the expression of E-cadherin, Vimentin, AKT and tropomyosin receptor kinase B (TrkB) proteins was detected by Western blot to clarify the role of LTF in anoikis-resistant NPC cells.

resultsAnoikis-resistant HNE-1 and HONE-1 NPC cell lines were successfully established. Compared to parental cells, these anoikis-resistant cells exhibited enhanced survival, reduced apoptosis, and significantly increased invasive ability. They also demonstrated elevated expression of VEGF-A, MMP-9, and Vimentin, alongside decreased E-cadherin, indicating epithelial-mesenchymal transition (EMT). Furthermore, the expression of AKT and TrkB was significantly upregulated in anoikis-resistant cells. Critically, LTF overexpression reversed this aggressive phenotype: it suppressed cell survival and invasion, induced G0/G1 cell cycle arrest, promoted apoptosis, and downregulated the expression of AKT and TrkB. Conversely, LTF knockdown produced opposing effects.

conclusionOur study revealed that LTF inhibits anoikis-resistance and metastasis of NPC cells via the AKT signaling pathway.

Indexed as

anoikis-resistantLactoferrinnasopharyngeal carcinomatropomyosin receptor kinase B/protein kinase B (TrkB/AKT)

Identifiers

PMID41658425
PMCPMC12877335

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