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BP‑1‑102 exerts antitumor effects on T‑cell acute lymphoblastic leukemia cells by suppressing the JAK2/STAT3/c‑Myc

Can Ye1,2,3, Xueqin Ruan1,2,3, Yan Zhao1,2,3

  • 1Department of Hematology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410000, P.R. China.

Experimental and Therapeutic Medicine
|April 6, 2023
PubMed

Insights

BP-1-102 effectively targets STAT3 phosphorylation in T-cell acute lymphoblastic leukemia (T-ALL). This small-molecule inhibitor demonstrated significant antitumor effects by inhibiting proliferation, inducing apoptosis, and suppressing the JAK2/STAT3/c-Myc pathway in T-ALL cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Drug resistance and relapse in T-cell acute lymphoblastic leukemia (T-ALL) necessitate novel therapeutic strategies.
  • Signal transducer and activator of transcription 3 (STAT3) is a recognized therapeutic target for T-ALL.
  • Targeted drug development for T-ALL is crucial for improving patient outcomes.

Purpose of the Study:

  • To evaluate the efficacy of BP-1-102, a STAT3 phosphorylation inhibitor, against T-ALL.
  • To investigate the molecular mechanisms underlying BP-1-102's antitumor activity in T-ALL cell lines.
  • To assess BP-1-102's potential as a targeted therapeutic agent for T-ALL.

Main Methods:

  • T-ALL cell lines (MOLT-4 and CUTLL1) were treated with BP-1-102.
  • Cell proliferation and colony formation were assessed using Cell Counting Kit-8 and colony formation assays.
  • Apoptosis, cell cycle arrest, and signaling pathway activity (JAK2/STAT3/c-Myc) were analyzed via flow cytometry, morphological examination, and Western blotting.

Main Results:

  • BP-1-102 significantly inhibited T-ALL cell proliferation and colony formation.
  • BP-1-102 induced substantial apoptosis and G0/G1 cell cycle arrest in T-ALL cell lines.
  • BP-1-102 suppressed the JAK2/STAT3/c-Myc signaling pathway in T-ALL cells.

Conclusions:

  • BP-1-102 demonstrates potent antitumor effects against T-ALL cells.
  • BP-1-102 functions by inhibiting the JAK2/STAT3/c-Myc signaling pathway.
  • BP-1-102 represents a promising targeted inhibitor for T-ALL therapy.
Keywords:
STAT3T-cell acute lymphoblastic leukemiaapoptosiscell cyclecolony formationproliferationsmall-molecule inhibitor

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