Your browser doesn't support javascript.
loading
An alternative spliced UPF2 transcript in pancreatic inflammatory myofibroblastic tumors.
Jiang, Hui; Zhang, Yunshuo; Hu, Jiayang; Wang, Zhen; Li, Gang; Lu, Yanjun.
Afiliación
  • Jiang H; Department of Pathology, First Affiliated Hospital, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
  • Zhang Y; Department of Pathology, First Affiliated Hospital, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
  • Hu J; Department of Hepatopancreatobiliary Surgery, First Affiliated Hospital, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
  • Wang Z; Department of Hepatopancreatobiliary Surgery, First Affiliated Hospital, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
  • Li G; Department of Hepatopancreatobiliary Surgery, First Affiliated Hospital, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China. Electronic address: ligangsurgeon@smmu.edu.cn.
  • Lu Y; Department of Hepatopancreatobiliary Surgery, First Affiliated Hospital, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China. Electronic address: yanjunlu@hotmail.com.
Biochem Biophys Res Commun ; 691: 149306, 2024 Jan 08.
Article en En | MEDLINE | ID: mdl-38056247
BACKGROUND: Inflammatory myofibroblastic tumors (IMTs) are characterized by myofibroblast proliferation and an inflammatory cell infiltrate. Our previous study on IMTs reveals that disrupt NMD pathway causes to lower the threshold for triggering the immune cell infiltration, thereby resulting in inappropriate immune activation. However, myofibroblast differentiation and proliferation is not yet known. METHODS: RT-PCR, RT-qPCR, DNA sequence, western bolt, 5'race analysis and site-specific mutagenesis were used in this study. RESULTS: Here, an alternative spliced (ALS) UPF2 mRNA skipping exon 2 and 3 and corresponding to the truncated UPF2 protein were found in 2 pancreatic IMTs. We showed that the uORF present in the 5'UTR of UPF2 mRNA is responsible for the translation inhibition, whiles ALS UPF2 is more facilitated to be translated into the truncated UPF2 protein. Several mRNA targets of the NMD were upregulated in IMT samples, indicating that the truncated UPF2 function is strongly perturbed, resulted in disrupted NMD pathway in IMTs. These upregulated NMD targets included cdkn1a expression and the generation of high levels of p21 (waf1/cip1), which may contribute to triggering IMTs. CONCLUSION: The disrupt UPFs/NMD pathway may link to molecular alteration associated with differentiation and proliferation for IMTs.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neoplasias Límite: Humans Idioma: En Revista: Biochem Biophys Res Commun Año: 2024 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neoplasias Límite: Humans Idioma: En Revista: Biochem Biophys Res Commun Año: 2024 Tipo del documento: Article País de afiliación: China