2. Academic Validation
  3. Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis

Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis

  • Cell Death Dis. 2022 Jul 11;13(7):593. doi: 10.1038/s41419-022-05026-x.
Yinan Zhang 1 2,  Zhen Feng 1,  Yue Xu 2,  Sufen Jiang 2,  Qianshi Zhang 1,  Zhenyu Zhang 2,  Keyong Wang 2,  Xiaomeng Li 2,  Lijie Xu 2,  Menglang Yuan 1,  Zihao Chen 1,  Jingyi Cui 2,  Han Wu 2,  Yina Gao 2,  Wei Wei 3,  Bo Wang 4,  Yunfei Zuo  # 5,  Shuangyi Ren  # 6
Affiliations

Affiliations

  • 1 Department of General Surgery, The Second Hospital of Dalian Medical University, 116023, Dalian, China.
  • 2 Department of Clinical Biochemistry, College of Laboratory Medicine, Dalian Medical University, 116044, Dalian, China.
  • 3 Department of Functional Laboratory, College of Laboratory Medicine, Dalian Medical University, 116044, Dalian, China.
  • 4 Department of Pathology and Forensics, Dalian Medical University, Dalian, 116044, China.
  • 5 Department of Clinical Biochemistry, College of Laboratory Medicine, Dalian Medical University, 116044, Dalian, China. [email protected].
  • 6 Department of General Surgery, The Second Hospital of Dalian Medical University, 116023, Dalian, China. [email protected].
  • # Contributed equally.
PMID: 35821222 DOI: 10.1038/s41419-022-05026-x
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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