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Updated: Jan 25, 2026

Quantitation of Intra-peritoneal Ovarian Cancer Metastasis
Published on: July 18, 2016
miR-340-FHL2 axis inhibits cell growth and metastasis in ovarian cancer
Zheng Huang1, Qiuxia Li1, Kaili Luo1
1Institute of Genomic Medicine, Wenzhou Medical University, 325000, Wenzhou, Zhejiang, P. R. China.
Abstract:
Although increasing evidence indicated that deregulation of microRNAs (miRNAs) contributed to tumor initiation and progression, but little is known about the biological role of miR-340 in ovarian cancer (OC). In this study, we found that miR-340 expression was downregulated in OC tissues compared with its expression in normal ovarian epithelium and endometrium, and treatment with 5-aza-2'-deoxycytidine (5-Aza-dC) or trichostatin A (TSA) increased miR-340 expression in OC cells. In addition, ectopic miR-340 expression inhibited OC cell growth and metastasis in vitro and in vivo. Four and a half LIM domains protein 2 (FHL2) was confirmed as a direct target of miR-340 and silencing FHL2 mimicked the effects of miR-340 in OC cells. Further mechanistic study showed that miR-340 inhibited the Wnt/β-catenin pathway by targeting FHL2, as well as downstream cell cycle and epithelial-to-mesenchymal transition (EMT) signals in OC cells. Moreover, the greatest association between miR-340 and FHL2 was found in 481 ovarian serous cystadenocarcinoma tissues via pan-cancer analysis. Finally, we revealed that lower miR-340 or higher FHL2 was associated with poor OC patient outcomes. Our findings indicate that the miR-340-FHL2 axis regulates Wnt/β-catenin signaling and is involved in tumorigenesis in OC. Therefore, manipulating the expression of miR-340 or its target genes is a potential strategy in OC therapy.
Insights
MicroRNA-340 (miR-340) is downregulated in ovarian cancer (OC), inhibiting tumor growth and metastasis by targeting FHL2. Restoring miR-340 may offer a new therapeutic strategy for OC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) play a role in cancer development.
- The specific function of miR-340 in ovarian cancer (OC) is not well understood.
Purpose of the Study:
- To investigate the role of miR-340 in ovarian cancer.
- To identify miR-340's molecular targets and pathways involved in OC progression.
Main Methods:
- Compared miR-340 expression in OC tissues and normal samples.
- Treated OC cells with epigenetic modifiers (5-Aza-dC, TSA).
- Overexpressed miR-340 and silenced FHL2 in OC cells.
- Analyzed Wnt/β-catenin pathway and downstream targets.
- Performed pan-cancer analysis on patient tissues.
Main Results:
- miR-340 expression was significantly downregulated in OC tissues.
- 5-Aza-dC and TSA treatments upregulated miR-340 expression.
- miR-340 overexpression inhibited OC cell growth and metastasis in vitro and in vivo.
- FHL2 was identified as a direct target of miR-340; silencing FHL2 mimicked miR-340's effects.
- miR-340 suppressed the Wnt/β-catenin pathway by targeting FHL2, affecting cell cycle and EMT.
- Low miR-340 and high FHL2 levels correlated with poor patient outcomes.
Conclusions:
- The miR-340-FHL2 axis regulates Wnt/β-catenin signaling and is implicated in ovarian cancer tumorigenesis.
- miR-340 acts as a tumor suppressor in OC.
- Targeting the miR-340-FHL2 pathway presents a potential therapeutic strategy for ovarian cancer.
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