Raghu Aarthy1, Arunagiri Kuha Deva Magendhra Rao1, Krishna Patel2,3, Velusami Sridevi4, Thangarajan Rajkumar1, Harsha Gowda2,3,5, Samson Mani6. 1. Department of Molecular Oncology, Cancer Institute (WIA), Chennai, 600036, India. 2. Institute of Bioinformatics, International Technology Park, Bangalore, 560066, India. 3. Amrita School of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, 691001, India. 4. Department of Surgical Oncology, Cancer Institute (WIA), Chennai, 600036, India. 5. Manipal Academy of Higher Education (MAHE), Manipal, Karnataka, 576104, India. 6. Department of Molecular Oncology, Cancer Institute (WIA), Chennai, 600036, India. samsonn.m@gmail.com.
Abstract
BACKGROUND: The heterogeneity of breast tumors presents a challenge in disease management, necessitating an understanding of the molecular mechanisms driving breast tumorigenesis. Aberrant expression of microRNAs is known to promote tumor growth and progression. Our previous RNA-sequencing dataset revealed the upregulation of miR-362-5p and miR-454-3p in breast tumors. We investigated potential role of miR-362-5p and miR-454-3p in breast cancer using MDAMB231 and MCF7 cell lines. METHODS AND RESULTS: The expression of miR-362-5p and miR-454-3p were altered in MCF7 and MDAMB231 using mimics and inhibitors. The effect on cell viability, cell cycle progression and migration was assessed using Alamar blue assay, flow cytometry and wound healing assay. Further, the expression of potential target genes were measured using real-time PCR. Our results indicated that an increased expression of miR-362-5p promoted cell growth and survival in MCF7, but decreased cell migration. In contrast, miR-362-5p overexpression reduced cancer cell growth, survival and migration in MDAMB231. Overexpression of miR-454-3p was oncogenic in both cell lines but suppressed migration in the aggressive cell line MDAMB231. CONCLUSION: Two microRNAs, miR-362-5p and miR-454-3p, were evaluated for functional activity in breast cancer cell lines and they showed increased proliferative signals and tumorigenic properties.
BACKGROUND: The heterogeneity of breast tumors presents a challenge in disease management, necessitating an understanding of the molecular mechanisms driving breast tumorigenesis. Aberrant expression of microRNAs is known to promote tumor growth and progression. Our previous RNA-sequencing dataset revealed the upregulation of miR-362-5p and miR-454-3p in breast tumors. We investigated potential role of miR-362-5p and miR-454-3p in breast cancer using MDAMB231 and MCF7 cell lines. METHODS AND RESULTS: The expression of miR-362-5p and miR-454-3p were altered in MCF7 and MDAMB231 using mimics and inhibitors. The effect on cell viability, cell cycle progression and migration was assessed using Alamar blue assay, flow cytometry and wound healing assay. Further, the expression of potential target genes were measured using real-time PCR. Our results indicated that an increased expression of miR-362-5p promoted cell growth and survival in MCF7, but decreased cell migration. In contrast, miR-362-5p overexpression reduced cancer cell growth, survival and migration in MDAMB231. Overexpression of miR-454-3p was oncogenic in both cell lines but suppressed migration in the aggressive cell line MDAMB231. CONCLUSION: Two microRNAs, miR-362-5p and miR-454-3p, were evaluated for functional activity in breast cancer cell lines and they showed increased proliferative signals and tumorigenic properties.
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