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Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
LINC00152 knockdown exerts repressive effects on epithelial-mesenchymal transition in bladder cancer
Guoping Wang1, Meijun Han2, Fei Chen1
1Department of Urology, Hangzhou Ninth People's Hospital, 98 Yilong Road, Qiantang District, Hangzhou City, 311225 Zhejiang Province China.
Abstract:
Bladder cancer (BLCA) is a prevalent malignancy of the urinary tract. Long noncoding RNAs (lncRNAs) exert significant effects on various human cancers by targeting microRNAs (miRs). This study, therefore, probed the action of the LINC00152/miR-103a-3p axis in epithelial-mesenchymal transition (EMT) and progression of BLCA. LINC00152, miR-103a-3p, and ADORA3 expression in clinical BLCA tissues were tested. LINC00152 was knocked down in BLCA cells alone or combined with miR-103a-3p inhibition or ADORA3 overexpression. The level of EMT- and PI3K/AKT pathway-related genes was assessed with Western blot. Cell proliferation, invasion and migration, and apoptosis were examined with CCK8 and EdU, Transwell, and flow cytometry assays, respectively. Binding of miR-103a-3p to LINC00152 and ADORA3 was validated through RIP and dual-luciferase reporter gene assays. The action of LINC00152 in BLCA progression was verified in vivo. LINC00152 and ADORA3 expression was abundant and miR-103a-3p expression was poor in BLCA tissues. LINC00152 knockdown or PI3K/AKT pathway inhibition repressed malignant behaviors and EMT of BLCA cells. Mechanistically, LINC00152 bound specifically to miR-103a-3p, which targeted ADORA3 and then activated the PI3K/AKT pathway. miR-103a-3p inhibition or ADORA3 overexpression nullified the suppressive impacts of LINC00152 knockdown on EMT and malignant behaviors of BLCA cells. Furthermore, LINC00152 knockdown decreased ADORA3 expression and suppressed tumor growth in vivo. LINC00152 knockdown upregulates miR-103a-3p to reduce ADORA3 expression, thus protecting against the malignant biological behaviors and EMT of BLCA cells.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s10616-025-00829-0.
Insights
This study reveals that inhibiting LINC00152 in bladder cancer (BLCA) upregulates miR-103a-3p, reducing ADORA3 expression and suppressing tumor progression. This finding offers a potential therapeutic strategy for BLCA by targeting the LINC00152/miR-103a-3p/ADORA3 axis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bladder cancer (BLCA) is a significant urinary tract malignancy.
- Long noncoding RNAs (lncRNAs) play crucial roles in cancer development by interacting with microRNAs (miRs).
Purpose of the Study:
- To investigate the role of the LINC00152/miR-103a-3p axis in bladder cancer progression and epithelial-mesenchymal transition (EMT).
- To elucidate the molecular mechanism involving ADORA3 and the PI3K/AKT pathway.
Main Methods:
- Analysis of LINC00152, miR-103a-3p, and ADORA3 expression in BLCA tissues.
- In vitro experiments involving LINC00152 knockdown, miR-103a-3p inhibition, and ADORA3 overexpression in BLCA cells.
- Assessment of EMT markers, cell proliferation, invasion, migration, and apoptosis.
- Validation of molecular interactions using RIP and dual-luciferase reporter assays.
- In vivo tumor growth studies.
Main Results:
- LINC00152 and ADORA3 were highly expressed, while miR-103a-3p was poorly expressed in BLCA tissues.
- LINC00152 knockdown suppressed BLCA cell proliferation, invasion, migration, and EMT, partly by inhibiting the PI3K/AKT pathway.
- LINC00152 directly binds to miR-103a-3p, and miR-103a-3p targets ADORA3, thereby regulating the PI3K/AKT pathway.
- Restoring miR-103a-3p or overexpressing ADORA3 counteracted the suppressive effects of LINC00152 knockdown.
- In vivo, LINC00152 knockdown reduced ADORA3 expression and inhibited tumor growth.
Conclusions:
- The LINC00152/miR-103a-3p/ADORA3 axis is a key regulator of bladder cancer progression and EMT.
- LINC00152 promotes BLCA by downregulating miR-103a-3p and subsequently activating the PI3K/AKT pathway via ADORA3.
- Targeting LINC00152 may represent a promising therapeutic strategy for bladder cancer.
