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LncRNA LOC610012 Inhibits Canine Mammary Tumor Activity via the PTGS2/EP3 and GSK3β Signaling Pathways
Bohan Zhang1, Lixin He1, Xiao Wang1
1Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
Abstract:
Canine mammary tumors (CMTs) are the common tumors in female dogs, and approximately 50% of CMTs are malignant tumors, with abnormal regulation of non-coding RNAs being a critical factor in disease progression. Currently, research on long non-coding RNAs (lncRNAs) regulating CMT development remains limited. This study identified a novel lncRNA, aiming to explore the role of lncRNA LOC610012 in CMTs. In this study, immunofluorescence and Western blot analyses were employed to detect protein expression. LncRNA LOC610012 is downregulated in CMT tissues and cells. Stable cells of LOC610012 were constructed by the lentivirus technique. Through a variety of experimental methods, LOC610012 inhibited the proliferation, invasion, and metastasis of CMT cells in in vitro and in vivo experiments conducted using cell culture and mouse models. Mechanistically, LOC610012 regulated the expression of EP3 and GSK-3β by targeting PTGS2, resulting in excessive production of reactive oxygen species (ROS), which inhibited cell viability. Similarly, through transmission electron microscopy, mitochondrial damage caused by LOC610012 was observed in CMT cells, which was manifested as mitochondrial swelling, membrane rupture, and mitochondrial ridge disappearance. PTGS2 could partially restore the inhibition of LOC610012 on cell activity. LOC610012 acts as a tumor suppressor gene in CMTs and as a potential biomarker for the disease.
Insights
A novel long non-coding RNA (lncRNA), LOC610012, was found to suppress canine mammary tumor (CMT) growth. This lncRNA inhibits proliferation, invasion, and metastasis, offering a potential biomarker for CMTs.
Area of Science:
- Veterinary Oncology
- Molecular Biology
- Non-coding RNA Research
Background:
- Canine mammary tumors (CMTs) are prevalent in female dogs, with malignant forms accounting for about 50%.
- Dysregulation of non-coding RNAs is implicated in CMT progression, yet research on long non-coding RNAs (lncRNAs) in CMTs is limited.
Purpose of the Study:
- To identify and characterize a novel long non-coding RNA (lncRNA), LOC610012, and investigate its role in canine mammary tumors (CMTs).
Main Methods:
- Immunofluorescence and Western blot analyses were used to assess protein expression.
- Lentivirus techniques were employed to create stable cell lines overexpressing LOC610012.
- In vitro and in vivo experiments utilized cell culture and mouse models to evaluate the functional impact of LOC610012.
- Transmission electron microscopy was used to examine mitochondrial morphology.
Main Results:
- LncRNA LOC610012 was found to be downregulated in CMT tissues and cells.
- Overexpression of LOC610012 significantly inhibited CMT cell proliferation, invasion, and metastasis in vitro and in vivo.
- Mechanistically, LOC610012 targets PTGS2, affecting EP3 and GSK-3β expression, leading to increased reactive oxygen species (ROS) production and mitochondrial damage, thereby inhibiting cell viability.
- PTGS2 partially rescued the inhibitory effects of LOC610012 on cell activity.
Conclusions:
- LncRNA LOC610012 functions as a tumor suppressor gene in canine mammary tumors.
- LOC610012 demonstrates potential as a diagnostic and prognostic biomarker for CMTs.
