1Department of Biochemistry, Faculty of Medicine, Universitas Andalas, 25163, Padang, Indonesia
2Biomedical Science Study Program, Faculty of Medicine, Universitas Andalas, 25163, Padang, Indonesia
3Faculty of Pharmacy, Universiti Teknologi MARA, 40450, Selangor, Malaysia
4 Faculty of Pharmacy, Universitas Andalas, 25163, Padang, Indonesia
5 Department of Biology, Faculty of Mathematics and Sciences, Universitas Negeri Padang, 25171, Padang, Indonesia
6 Biomedical Science Program Study, Faculty of Medicine, Universitas Andalas, 25163, Padang, Indonesia
BibTex Citation Data :
@article{JKSA73358, author = {Dessy Arisanty and Zolkapli Eshak and Fatma Sri Wahyuni and Afifatul Achyar and Salsabila Putri Khairani}, title = {The Effect of miR-10b Mimic Transfection on Invasion and Proliferation Gene Expression as the Direct Target of the miR-10b Pathway in T47D Breast Cancer Cell Lines}, journal = {Jurnal Kimia Sains dan Aplikasi}, volume = {29}, number = {1}, year = {2026}, keywords = {miR-10b; Transfection; mimic miRNA; gene expression; HOXD10 gene; PI3K gene}, abstract = { Breast cancer remains one of the leading causes of death in women worldwide, with high incidence and mortality rates. The abnormal expression of the small non-coding RNA, microRNA-10b (miR-10b), has been associated with breast cancer progression. miR-10b is involved in various biological processes, including proliferation, metastasis, and drug resistance. However, the underlying mechanism by which miR-10b contributes to breast cancer progression remains unclear. This study aimed to investigate the effect of miR-10b on the expression of HOXD10 and PI3K genes, as well as its impact on cell viability and proliferation in breast cancer cells. In this study, T47D breast cancer cells were transfected with mimic miR-10b using the FANA-oligo transfection method at concentrations of 1, 2.5, and 5 µM. Cell viability was assessed using the MTT assay, while HOXD10 and PI3K gene expression levels were measured using RT-qPCR and ELISA. Data were analysed using paired t-tests with SPSS, and results were considered statistically significant at p < 0.05. The results showed that mimic miR-10b induced a dose-dependent increase in cell proliferation. Notably, only HOXD10 gene expression was significantly affected by the transfection, while PI3K gene expression remained unchanged. Cells transfected with 5 µM miR-10b mimic exhibited the highest proliferation rate compared to non-transfected controls ( p < 0.05). In conclusion, miR-10b promotes breast cancer cell proliferation by downregulating HOXD10 expression, independent of PI3K, suggesting it is a potential target for further investigation. }, issn = {2597-9914}, pages = {58--63} doi = {10.14710/jksa.29.1.58-63}, url = {https://ejournal.undip.ac.id/index.php/ksa/article/view/73358} }
Refworks Citation Data :
Breast cancer remains one of the leading causes of death in women worldwide, with high incidence and mortality rates. The abnormal expression of the small non-coding RNA, microRNA-10b (miR-10b), has been associated with breast cancer progression. miR-10b is involved in various biological processes, including proliferation, metastasis, and drug resistance. However, the underlying mechanism by which miR-10b contributes to breast cancer progression remains unclear. This study aimed to investigate the effect of miR-10b on the expression of HOXD10 and PI3K genes, as well as its impact on cell viability and proliferation in breast cancer cells. In this study, T47D breast cancer cells were transfected with mimic miR-10b using the FANA-oligo transfection method at concentrations of 1, 2.5, and 5 µM. Cell viability was assessed using the MTT assay, while HOXD10 and PI3K gene expression levels were measured using RT-qPCR and ELISA. Data were analysed using paired t-tests with SPSS, and results were considered statistically significant at p < 0.05. The results showed that mimic miR-10b induced a dose-dependent increase in cell proliferation. Notably, only HOXD10 gene expression was significantly affected by the transfection, while PI3K gene expression remained unchanged. Cells transfected with 5 µM miR-10b mimic exhibited the highest proliferation rate compared to non-transfected controls (p < 0.05). In conclusion, miR-10b promotes breast cancer cell proliferation by downregulating HOXD10 expression, independent of PI3K, suggesting it is a potential target for further investigation.
Article Metrics:
Last update:
Last update: 2026-11-12 09:22:20
As an article writer, the author has the right to use their article for various purposes, including use by institutions that employ the author or institutions that provide funding for the research. These author rights are granted without special permission.
Authors who publish a paper in JKSA have broad rights to use their work for teaching and scientific purposes without the need to request permission, including: (i) teaching in the author's class or institution; (ii) presenting the work at meetings or conferences and distributing copies to participants; (iii) using the work in training conducted by the author or the author's institution; (iv) distributing copies to colleagues for research purposes; (v) using the work in the compilation of subsequent works by the author; (vi) including the work in a thesis or dissertation; (vii) reusing part of the article in another work, with appropriate citation; (viii) preparing derivative works, with appropriate citation; and (ix) voluntarily posting the work on open websites operated by the author or the author's institution for scientific purposes, in accordance with the CC BY-SA License.
Authors and readers may copy and redistribute the material in any medium or format, and may remix, transform, and build upon the material for any purpose, provided that they give appropriate credit by citing the article or its content, provide a link to the license, and indicate if changes were made.
The authors submitting a manuscript do so on the understanding that, if accepted for publication, the copyright of the article shall be assigned to Jurnal Kimia Sains dan Aplikasi (JKSA). Copyright encompasses the rights to reproduce and distribute the article in all forms and media, including reprints, photographs, microfilms, and any other similar reproductions, as well as translations.
Reproducing any part of this journal, storing it in a database, or transmitting it in any form or medium is permitted without written permission from JKSA. However, the original source must be properly cited in accordance with academic conventions.
JKSA, the Chemistry Department of Diponegoro University, and the Editor make every effort to ensure that no inaccurate, false, or misleading data, opinions, or statements are published in JKSA. However, the content of each article is the sole and exclusive responsibility of its authors.
The Copyright Transfer Form can be downloaded here: [Copyright Transfer Form - Indonesian] [Copyright Transfer Form - English]. The copyright form should bear the authors' original signatures and be sent to the Editor as a printed document, a scanned document sent via email, or by fax.
Prof. Adi Darmawan, Ph.D (Editor in Chief)
Editor in chief of Jurnal Kimia Sains dan Aplikasi (JKSA)
Chemistry Department, Faculty of Sciences and Mathematics, Diponegoro University
Visitor: View My Stats
Jurnal Kimia Sains dan Aplikasi is indexed in:
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
