[Potential Oncogenic Role of Genes in PLC Family on T-ALL Cell Lines by Suppression of Apoptosis].

Zhongguo Shi Yan Xue Ye Xue Za Zhi

Department of Clinical Molecular Medicine of Children's Hospital in Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing 400014, China,Clinical Research Unit of Children's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine; Institute of Pediatric Infection, Immunity and Critical Care Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai 200062, China,E-mail:

Published: August 2023

AI Article Synopsis

  • The study investigates how the phospholipase C (PLC) family contributes to the development and progression of acute T lymphoblastic leukemia (T-ALL).
  • Methods included analyzing cell death in T-ALL cells after using PLC inhibitors and assessing the influence of PLC expressions on patient survival using various statistical analyses.
  • Results indicated that certain T-ALL cell lines were sensitive to PLC inhibitors, while others were resistant, and high expression of specific PLC genes was linked to poor patient prognosis, suggesting these genes could be potential targets for therapy.

Article Abstract

Objective: To explore the role of phospholipase C(PLC) family in the progression of acute T lymphoblastic leukemia (T-ALL).

Methods: The apoptosis of T-ALL cells was determined by Annexin V-PE/7-AAD staining after treatment of PLC inhibitor U73122 and Edelfosine. Cox regression and Kaplan-Meier were used to analyze the impact of PLC expressions on the event-free survival (EFS) of T-ALL patients. PLC expression in each subtype of T-ALL were analyzed by One-way ANOVA. The siRNA expression plasmids targeting the , , gene were constructed, and T-ALL cells were infected with retrovirus packaging in HEK-293T cells. The mRNA and protein level were tested by RT-PCR and Western blot.

Results: P12-ICH and CCRF-CEM cell line were sensitive to U73122 and Edelfosine treatment, while Jurkat and MOLT4 were resistant to them. In the TARGET-ALL database, the prognosis of T-ALL patients with high expression of , and was poor, and , , were unevenly distributed in T-ALL subtypes. , and maintained the survival of P12-ICH and CCRF-CEM cell lines, respectively, while they had no effect on the survival of MOLT4.

Conclusion: , and can maintain the growth of T-ALL cell lines in vitro and promote the malignant progression of T-ALL, which are potential therapeutic targets.

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Source
http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2023.04.001DOI Listing

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