ArticleCell death & disease2022
Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
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- New horizons in B-cell lymphoma immunotherapy: From immune checkpoints to precision medicine.Neoplasia (New York, N.Y.) · 2025Review
- Emerging role of circular RNAs in gastric cancer: From basic biology to clinical applications (Review).Molecular medicine reports · 2025Review
- Unveiling urinary extracellular vesicle mRNA signature for early diagnosis and prognosis of bladder cancer.Theranostics · 2025Article
- Interplay between JAK/STAT pathway and non-coding RNAs in different cancers.Non-coding RNA research · 2024Review
- PFKFB3 facilitates cell proliferation and migration in anaplastic thyroid carcinoma via the WNT/β-catenin signaling pathway.Endocrine · 2024Article
- GC‑MSC‑derived circ_0024107 promotes gastric cancer cell lymphatic metastasis via fatty acid oxidation metabolic reprogramming mediated by the miR‑5572/6855‑5p/CPT1A axis.Oncology reports · 2023Article
- Investigation of Diagnostic and Prognostic Value of CLEC4M of Non-Small Cell Lung Carcinoma Associated with Immune Microenvironment.International journal of general medicine · 2023Article
- Killer instincts: natural killer cells as multifactorial cancer immunotherapy.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver and lymph node sinusoidal endothelial cell C-type lectin (LSECtin) plays an important regulatory role in a variety of diseases, including tumors. However, the underlying mechanism of LSECtin in gastric cancer (GC) remains largely unknown. In our research, LSECtin promoted the adhesion and invasion of GC cells, and was involved in lymphatic metastasis of GC cells. Mechanistically, LSECtin promoted the adhesion, proliferation and migration of GC cells by downregulating STAT1 expression. The circular RNA circFBXL4, which is regulated by LSECtin, sponges the microRNA miR-146a-5p to regulate STAT1 expression. The promotion of GC cell proliferation, migration and invasion mediated by LSECtin was largely inhibited by circFBXL4 overexpression or miR-146a-5p silencing. Moreover, in its role as a transcription factor, STAT1 modulated the expression of FN1 and CHD4. In conclusion, LSECtin might be involved in the lymphatic metastasis of GC by upregulating the expression of FN1 and CHD4 via the circFBXL4/miR-146a-5p/STAT1 axis, possibly indicating a newly discovered pathogenic mechanism.
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