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


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.

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC9276708 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature

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

Zhang Yinan Y   Feng Zhen Z   Xu Yue Y   Jiang Sufen S   Zhang Qianshi Q   Zhang Zhenyu Z   Wang Keyong K   Li Xiaomeng X   Xu Lijie L   Yuan Menglang M   Chen Zihao Z   Cui Jingyi J   Wu Han H   Gao Yina Y   Wei Wei W   Wang Bo B   Zuo Yunfei Y   Ren Shuangyi S  

Cell death & disease 20220711 7


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  ...[more]

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