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Succinylation of 14-3-3 theta by CPT1A promotes survival and paclitaxel resistance in nasal type extranodal natural killer/T-cell lymphoma.
Cui, Xiao; Cao, Chengcheng; Li, Xinyang; Lin, Biyan; Yan, Aihui; Yang, Ying.
Afiliación
  • Cui X; Department of Otorhinolaryngology, The First Hospital of China Medical University, Shenyang 110003, China.
  • Cao C; Department of Pathology, Shengjing Hospital of China Medical University, Shenyang 110004, China.
  • Li X; Department of Hematology, Shengjing Hospital of China Medical University, Shenyang 110022, China.
  • Lin B; Department of Otorhinolaryngology, The First Hospital of China Medical University, Shenyang 110003, China.
  • Yan A; Department of Otorhinolaryngology, The First Hospital of China Medical University, Shenyang 110003, China. Electronic address: yanmenxueshu@163.com.
  • Yang Y; Department of Hematology, Shengjing Hospital of China Medical University, Shenyang 110022, China. Electronic address: yangy5@sj-hospital.org.
Transl Oncol ; 46: 102006, 2024 Aug.
Article en En | MEDLINE | ID: mdl-38823259
ABSTRACT

BACKGROUND:

The aggressive and refractory extranodal natural killer/T-cell lymphoma, nasal type (ENKTL-NT) is a subtype of non-Hodgkin's lymphoma. Succinylation promotes progression in a variety of tumors, but its mechanism in ENKTL-NT is unclear.

METHODS:

Bioinformatic analysis was performed to screen differentially expressed genes in the ENKTL dataset. Cell transfection techniques were used for knockdown and overexpression of genes. The mRNA and protein expression were detected using RT-qPCR and western blot, respectively. Immunohistochemical staining was used to assess protein expression in situ. For the detection of cell proliferation activity, CCK-8, clonal formation, and EDU staining assays were used. Flow cytometry was employed to detect apoptosis. Co-immunoprecipitation was utilized for the identification of protein interactions and succinylation modifications.

RESULTS:

Succinyltransferase CPT1A was highly elevated in ENKTL-NT and was associated with a dismal prognosis. CPT1A knockdown suppressed SNK-6 cells' proliferation and induced apoptosis, while these effects were reversed by the overexpression of 14-3-3theta. Co-immunoprecipitation results showed that CPT1A caused succinylation of 14-3-3theta at site of K85, thereby enhancing the protein stability. Suppression of CPT1A-induced succinylation of 14-3-3theta by ST1326 resulted in the inhibition of SNK-6 cell proliferation and increased apoptosis. Paclitaxel combined with knockdown of CPT1A significantly inhibited the proliferation of ENKTL-NT compared to paclitaxel alone.

CONCLUSION:

CPT1A induces succinylation of 14-3-3theta at the K85 site, promoting ENKTL-NT proliferation. The anti-ENKTL activity of paclitaxel was improved when combined with CPT1A knockdown.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Transl Oncol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Transl Oncol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos