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Updated: May 3, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
FOXP4-AS1 suppresses papillary thyroid carcinoma progression by binding to Lactate Dehydrogenase A and suppressing
Ning Ma1, Hai-Ying Tian2, Wei Zhao3
1Department of Vascular and Thyroid Surgery, Guizhou Provincial People's Hospital, No 83, Zhongshan East Road, Guiyang 550000, China; Guizhou Medical University, No 9, Beijing Road, Guiyang 550004, China.
Abstract:
Although FOXP4-AS1 exerts oncogenic effects in multiple cancers, this study reveals that it suppresses PTC progression. A series of experiments demonstrate that overexpression of FOXP4-AS1 inhibits PTC cell proliferation, migration, and invasion, whereas its knockdown promotes these malignant phenotypes and enhances tumorigenesis in nude mice. FOXP4-AS1 is distributed in both the nucleus and cytoplasm, enriched in the aerobic glycolysis pathway, and binds to Lactate Dehydrogenase A (LDHA)-a key enzyme in aerobic glycolysis with known links to tumor metabolic microenvironment. LDHA was primarily localized in the cytoplasm, and its downregulation suppressed the malignant behavior of PTC cells. Further mechanistic investigations reveal that knockdown of FOXP4-AS1 increases LDHA expression, and additional inhibition of LDHA partially reverses the pro-tumor effects induced by FOXP4-AS1 silencing. In conclusion, this study identifies FOXP4-AS1 as a tumor suppressor in PTC and elucidates the regulatory mechanism of the FOXP4-AS1/LDHA axis by which FOXP4-AS1 represses LDHA expression to attenuate aerobic glycolysis, providing novel insights into the mechanisms of PTC progression and potential therapeutic targets and diagnostic biomarkers relevant to metabolic modulation in PTC.
Insights
FOXP4-AS1 acts as a tumor suppressor in papillary thyroid cancer (PTC), inhibiting cell growth and metastasis. It represses Lactate Dehydrogenase A (LDHA) to reduce aerobic glycolysis, offering potential therapeutic strategies for PTC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metabolism
Background:
- Papillary thyroid cancer (PTC) progression involves complex molecular mechanisms.
- The role of long non-coding RNAs like FOXP4-AS1 in PTC is not fully understood.
- FOXP4-AS1 is known to have oncogenic roles in other cancers.
Purpose of the Study:
- To investigate the function of FOXP4-AS1 in papillary thyroid cancer.
- To elucidate the molecular mechanism by which FOXP4-AS1 regulates PTC progression.
- To identify potential therapeutic targets related to the FOXP4-AS1/LDHA axis.
Main Methods:
- In vitro experiments assessing cell proliferation, migration, and invasion.
- In vivo tumorigenesis assays in nude mice.
- Analysis of FOXP4-AS1 and Lactate Dehydrogenase A (LDHA) expression and localization.
- Mechanistic studies involving gene knockdown and inhibition.
Main Results:
- FOXP4-AS1 overexpression suppressed PTC cell proliferation, migration, and invasion.
- FOXP4-AS1 knockdown promoted malignant phenotypes and enhanced tumor growth in vivo.
- FOXP4-AS1 interacts with LDHA, a key enzyme in aerobic glycolysis.
- FOXP4-AS1 knockdown led to increased LDHA expression, which was partially reversed by LDHA inhibition.
Conclusions:
- FOXP4-AS1 functions as a tumor suppressor in papillary thyroid cancer.
- The FOXP4-AS1/LDHA axis regulates aerobic glycolysis in PTC.
- FOXP4-AS1 represses LDHA expression, attenuating aerobic glycolysis and PTC progression.
- This study provides insights into PTC mechanisms and identifies potential therapeutic and diagnostic targets.
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