BST2 promotes gastric cancer metastasis under the regulation of HOXD9 and PABPC1

Gastric cancer (GC) constitutes substantial cancer mortality worldwide. Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcrip...

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Published in:Molecular carcinogenesis 2024-04, Vol.63 (4), p.663-676
Main Authors: Li, Jiaying, Yang, Ping, Hong, Linjie, Xiao, Wushuang, Zhang, Luyu, Yu, Zhen, Zhang, Jieming, Pei, Miaomiao, Peng, Ying, Wei, Xiangyang, Wu, Xiaosheng, Tang, Weimei, Zhao, Yingying, Yang, Juanying, Lin, Zhizhao, Jiang, Ping, Xiang, Li, Zhang, Hui, Lin, Jianjiao, Wang, Jide
Format: Article
Language:English
Subjects:
3' Untranslated regions
Bone cancer
BST2
Cell migration
Gastric cancer
Homeobox
HOXD9
Metastases
Metastasis
Mortality
mRNA stability
PABPC1
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Summary:Gastric cancer (GC) constitutes substantial cancer mortality worldwide. Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcriptionally activated by homeobox D9 (HOXD9). BST2 was significantly upregulated in GC tissues and promoted epithelial–mesenchymal transition and metastasis of GC. BST2 knockdown reversed HOXD9's oncogenic effect on GC metastasis. Moreover, BST2 messenger RNA stability could be enhanced by poly(A) binding protein cytoplasmic 1 (PABPC1) through the interaction between BST2 3′‐UTR and PABPC1 in GC cells. PABPC1 promoted GC metastasis, which BST2 silencing attenuated in vitro and in vivo. In addition, positive correlations among HOXD9, BST2, and PABPC1 were established in clinical samples. Taken together, increased expression of BST2 induced by HOXD9 synergizing with PABPC1 promoted GC cell migration and invasion capacity.
ISSN:0899-1987
1098-2744
DOI:10.1002/mc.23679