Choline kinase and miR-32-5p: A crucial interaction promoting apoptosis and delaying wound repair in cervical cancer cells

Sweta Raikundalia; Ling Ling Few; Siti Asma' Hassan; Get Bee Yvonne-Τee; Wei Cun See Too; Sweta Raikundalia; Ling Ling Few; Siti Asma' Hassan; Get Bee Yvonne-Τee; Wei Cun See Too

doi:10.3934/biophy.2024016

AIMS Biophysics

2024, Volume 11, Issue 3: 281-295. doi: 10.3934/biophy.2024016

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Research article

Choline kinase and miR-32-5p: A crucial interaction promoting apoptosis and delaying wound repair in cervical cancer cells

1.
School of Health Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia
2.
School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kubang Kerian, Kelantan 16150, Malaysia

Received: 12 May 2024 Revised: 08 August 2024 Accepted: 19 August 2024 Published: 21 August 2024

Cervical cancer remains a significant global health challenge, especially in low- and middle-income countries. The elucidation of the molecular pathways underlying the carcinogenesis of cervical cancer is vital to develop targeted therapies. Our study investigates the regulatory effects of miR-32-5p on the choline kinase alpha (chka) gene in HeLa cells, a well-established cervical cancer cell line. Choline kinase alpha is recognized for its role in phosphatidylcholine biosynthesis, which is crucial for cell membrane formation, and is implicated in the oncogenic transformation of cells. Utilizing a combination of in silico prediction, luciferase assays, RT-qPCR, and Western blot analyses, we demonstrated that miR-32-5p directly targets the 3′ untranslated region (3′UTR) of chka mRNA, leading to a significant downregulation of chka expression. Our results demonstrate that miR-32-5p significantly downregulates chka at both the mRNA and protein levels, thus leading to decreased cellular proliferation and increased apoptosis. This was further confirmed by a cell cycle analysis, which showed a notable arrest in the G0/G1 phase. Additionally, scratch assays indicated a reduced migratory capacity in miR-32-5p-transfected cells, suggesting the potential anti-metastatic properties of miR-32-5p. These findings highlight the therapeutic potential of miR-32-5p as a biomarker and a target in cervical cancer treatment strategies. By modulating chka expression, miR-32-5p could serve as a novel approach to curb the progression and spread of cervical cancer, thus offering a promising avenue for future research and clinical applications. This study contributes to the growing understanding of miRNA-mediated gene regulation in cancer biology and underscores the importance of targeted genetic research in the development of cancer therapeutics.
- cervical cancer,
- choline kinase alpha (chka),
- gene regulation,
- microRNAs,
- miR-32-5p
Citation: Sweta Raikundalia, Ling Ling Few, Siti Asma' Hassan, Get Bee Yvonne-Τee, Wei Cun See Too. Choline kinase and miR-32-5p: A crucial interaction promoting apoptosis and delaying wound repair in cervical cancer cells[J]. AIMS Biophysics, 2024, 11(3): 281-295. doi: 10.3934/biophy.2024016

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Abstract

Cervical cancer remains a significant global health challenge, especially in low- and middle-income countries. The elucidation of the molecular pathways underlying the carcinogenesis of cervical cancer is vital to develop targeted therapies. Our study investigates the regulatory effects of miR-32-5p on the choline kinase alpha (chka) gene in HeLa cells, a well-established cervical cancer cell line. Choline kinase alpha is recognized for its role in phosphatidylcholine biosynthesis, which is crucial for cell membrane formation, and is implicated in the oncogenic transformation of cells. Utilizing a combination of in silico prediction, luciferase assays, RT-qPCR, and Western blot analyses, we demonstrated that miR-32-5p directly targets the 3′ untranslated region (3′UTR) of chka mRNA, leading to a significant downregulation of chka expression. Our results demonstrate that miR-32-5p significantly downregulates chka at both the mRNA and protein levels, thus leading to decreased cellular proliferation and increased apoptosis. This was further confirmed by a cell cycle analysis, which showed a notable arrest in the G0/G1 phase. Additionally, scratch assays indicated a reduced migratory capacity in miR-32-5p-transfected cells, suggesting the potential anti-metastatic properties of miR-32-5p. These findings highlight the therapeutic potential of miR-32-5p as a biomarker and a target in cervical cancer treatment strategies. By modulating chka expression, miR-32-5p could serve as a novel approach to curb the progression and spread of cervical cancer, thus offering a promising avenue for future research and clinical applications. This study contributes to the growing understanding of miRNA-mediated gene regulation in cancer biology and underscores the importance of targeted genetic research in the development of cancer therapeutics.

Conflict of interest

The authors declare no conflict of interest.

Author contributions

Wei Cun See Too, Ling Ling Few, Siti Asma' Hassan and Get Bee Yvonne-Τee contributed to the study conception and design. Material preparation, data collection and analysis were performed by Sweta Raikundalia. The first draft of the manuscript was written by Ling Ling Few and Sweta Raikundalia. The funding was procured by Wei Cun See Too, Siti Asma' Hassan, Get Bee Yvonne-Τee and Ling Ling Few. All authors read and approved the final manuscript.

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