Golgi signalling proteins GOLPH3, MYO18A, PITPNC1 and RAB1B: implications in prognosis and survival outcomes of AML patients

Abstract

Background

The role of different Golgi signalling proteins remains unexplored in the progression and spread of acute myeloid leukaemia (AML), whom all interact together in a way that facilitates proliferation and differentiation of myeloid lineage cells.

Objective

Since Golgi apparatus acts as master brain in membrane trafficking and signalling events that affect cell polarity necessary for migration, division, or differentiation; this study aims to explore the association between signalling proteins and the diagnosis, prognosis, and survival of AML patients.

Material and methods

This study comprised 70 newly diagnosed AML patients and 20 healthy controls to investigate the serum levels of signalling proteins; Golgi Phosphoprotein 3 (GOLPH3), Myosin 18A (MYO18A), Cytoplasmic Phosphatidylinositol Transfer Protein 1 (PITPNC1) and Ras-Associated Binding Protein 1B (RAB1B).

Results

AML patients showed higher serum levels of GOLPH3, MYO18A, PITPNC1 and RAB1B when compared to control (p < 0.001). A significant negative correlation was found between the patients’ overall survival and GOLPH3 (p = 0.001), MYO18A (p = 0.011), PITPNC1 (p = 0.001) and RAB1B (p = 0.042). Results were confirmed by Kaplen–Meier survival analysis showing lower survival estimates in patients with higher GOLPH3 (p = 0.014), MYO18A (p = 0.047), PITPNC1 (p = 0.008) and RAB1B (p = 0.033) serum levels.

Conclusion

GOLPH3, MYO18A, PITPNC1 and RAB1B maybe promising diagnostic and prognostic biomarkers in AML patients.

Keywords:

• AML
• Golgi
• GOLPH3
• MYO18A
• PITPNC1
• RAB

Acknowledgments

We would like to acknowledge the contribution of the study patients in this study.

Consent to participate

Informed consent was obtained from all individual participants included in this study.

Data availability

The authors confirm that the data supporting the findings of this study are available within the article.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.