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Long non-coding RNA small nucleolar RNA host gene 29 drives chronic myeloid leukemia progression via microRNA-483-3p/Casitas B-lineage Lymphoma axis-mediated activation of the phosphoinositide 3-kinase/Akt pathway.
Feng, XueFeng; Yang, Lin; Liu, Xiaojun; Liu, Menghan; Liu, Lu; Liu, Jing; Luo, JianMin.
Afiliación
  • Feng X; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China.
  • Yang L; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China.
  • Liu X; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China.
  • Liu M; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China.
  • Liu L; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China.
  • Liu J; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China.
  • Luo J; Department of Second Ward of Hematology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang City, 050000, Hebei, China. luojianmin1960@hotmail.com.
Med Oncol ; 41(2): 60, 2024 Jan 22.
Article en En | MEDLINE | ID: mdl-38252204
ABSTRACT
The aberrant expression of the long non-coding RNA (lncRNA) Small Nucleolar RNA Host Gene 29 (SNHG29) has been associated with various human cancers. However, the role of SNHG29 in chronic myeloid leukemia (CML) remains elusive. Therefore, this study aimed to investigate the function of SNHG29 in CML and unveil its potential underlying mechanisms. Herein, peripheral blood samples from 44 CML patients and 17 healthy subjects were collected. The expressions of SNHG29, microRNA-483-3p (miR-483-3p), and Casitas B-lineage Lymphoma (CBL) were measured using quantitative polymerase chain reaction (qPCR) or Western Blot. Cell viability, apoptosis, and cell cycle progression were evaluated using the Cell Counting Kit-8 assay, 5-ethynyl-2'-deoxyuridine incorporation, and flow cytometry, respectively. Western Blot analysis was employed to assess protein expressions related to cellular proliferation, apoptosis, and oncogenesis. RNA immunoprecipitation and dual-luciferase reporter assays were utilized to verify the interactions among SNHG29, miR-483-3p, and CBL. SNHG29 was significantly overexpressed in both blood samples of CML patients and CML cell lines. In CML, increased expression of SNHG29 was positively correlated with clinical staging, and patients with high SNHG29 expression had poorer survival outcomes. Functionally, knocking down SNHG29 effectively inhibited CML cell proliferation and promoted apoptosis. Mechanistically, SNHG29 acted as a competing endogenous RNA for miR-483-3p to modulate CBL expression, thereby activating the Phosphoinositide 3-Kinase/Akt signaling pathway and mediating CML progression. In summary, these findings reveal that SNHG29 promotes tumorigenesis in CML, offering a potential therapeutic strategy for CML treatment.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Leucemia Mielógena Crónica BCR-ABL Positiva / MicroARNs / ARN Largo no Codificante / Linfoma Límite: Humans Idioma: En Revista: Med Oncol Asunto de la revista: NEOPLASIAS Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Leucemia Mielógena Crónica BCR-ABL Positiva / MicroARNs / ARN Largo no Codificante / Linfoma Límite: Humans Idioma: En Revista: Med Oncol Asunto de la revista: NEOPLASIAS Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos