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Updated: Dec 25, 2025
Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
eIF3b regulates the cell proliferation and apoptosis processes in chronic myelogenous leukemia cell lines via
Laiquan Huang1, Zhongling Wei1, Xiangxiang Chang2
1Department of Hematology, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu City, 241001, Anhui Province, China.
Objective:
To investigate the functions of eIF3b in chronic myelogenous leukemia (CML).
Methods:
The expression of eIF3b was inhibited by transfecting aspecifically designed shRNA into the CML cell lines of TK-6 and K562. The CCK8 assay was conducted to determine cell viability, and flow cytometry was used to examine the change in the cell cycle and cell apoptosis. RNAsequencing was applied to screen the candidate targets of eIF3b to identify the underlying mechanisms of eIF3b.An in vivo tumour xenograft mouse model was established by injecting shRNA transfected cells into the NCG mice. The tumour size and body weight of mice were monitored every other day. The mice were sacrificed 2 weeks after the tumour cell injection. The expression of eIF3b and target genes in the tumour tissues were determined by immunohistochemical staining and Western blotting.
Results:
The group with inhibited expression of eIF3b led to about 50% lower cell viability compared with that of the control group (P < 0.05). Flow cytometry suggested that the percentage of increase in apoptotic cells was eight times higher than those in control group for TK-6 and K562 cells (P < 0.05). However, the difference between the cell amounts in the S phase for the experiment and control groups was not significant. After RNAsequencing and further validation via qPCR, C3G was screened as the potential target of eIF3b involved in the cell proliferation and apoptosis of CML cell lines. Subsequent in vivo analysis proved that the inhibition of eIF3b suppressed tumour formation and decreased C3G expression, thereby indicating that C3G was the potential target of eIF3b.
Conclusion:
eIF3b is correlated with the cell proliferation and cell apoptosis of CML. Moreover, eIF3b regulation most probably occurs via regulating the expression of C3G.
Insights
Inhibiting eukaryotic initiation factor 3 subunit b (eIF3b) significantly reduced chronic myelogenous leukemia (CML) cell viability and increased apoptosis. eIF3b likely regulates CML progression by controlling C3G expression.
Area of Science:
- Hematology
- Molecular Biology
- Oncology
Background:
- Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasm.
- Understanding the molecular mechanisms driving CML progression is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role and functional significance of eukaryotic initiation factor 3 subunit b (eIF3b) in chronic myelogenous leukemia (CML).
- To identify potential molecular targets of eIF3b involved in CML pathogenesis.
Main Methods:
- eIF3b expression was inhibited in CML cell lines (TK-6, K562) using shRNA.
- Cell viability, cell cycle, and apoptosis were assessed using CCK8 assay and flow cytometry.
- RNA sequencing identified potential eIF3b targets.
- An in vivo tumor xenograft mouse model was used to evaluate eIF3b inhibition's effect on tumor growth and C3G expression.
Main Results:
- Inhibition of eIF3b reduced CML cell viability by approximately 50% and increased apoptosis eightfold.
- RNA sequencing and validation identified C3G as a potential target of eIF3b.
- In vivo studies confirmed that eIF3b inhibition suppressed tumor formation and decreased C3G expression.
Conclusions:
- eIF3b plays a significant role in regulating cell proliferation and apoptosis in CML.
- eIF3b's oncogenic function in CML is likely mediated through the regulation of C3G expression.
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