Lnc-THAP7-AS1 suppresses the ovarian cancer progression by targeting miR-92b-5p/fatty acid 2-hydroxylase signal axis
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Updated: Sep 9, 2025

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Meili Pei1, Yanqi Yang2, Bing Su1
1Department of Gynecology and Obstetrics, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.
Background:
Ovarian cancer (OC) ranks among the most lethal gynecological malignancies. Research has highlighted long noncoding RNAs (lncRNAs) as promising novel molecular targets for cancer therapy. This study endeavors to identify novel lncRNAs, elucidate their specific roles, and unravel their regulatory mechanism in OC development.
Methods:
Utilizing LncRNA Microarray technology, we screened for differentially expressed RNAs, ultimately selecting THAP7-AS1 for in-depth investigation. RNA pull-down, luciferase assays and FISH were performed to validate the interaction among THAP7-AS1, miR-92b-5p and FA2H. qRT-PCR was conducted to assess the expression of THAP7-AS1, miR-92b-5p and FA2H in OC tissues and cell lines. Cellular biological effects were examined using proliferation CCK-8 and EdU assays, chamber Transwell migration assays, and flow cytometer for apoptosis analysis. Additionally, nude mice xenograft models were established to evaluate the in vivo effect of THAP7-AS1 on tumor growth.
Results:
Our findings revealed a downregulation of THAP7-AS1 in OC tissues and cells. Overexpression of THAP7-AS1 inhibited cell proliferation, migration, and induced apoptosis. miR-92b-5p was identified as a sponge target of THAP7-AS1, with its expression upregulated in OC tissues and cells. Forced expression of miR-92b-5p exhibited cellular effects opposite to those of THAP7-AS1 overexpression. Additionally, FA2H was confirmed as a direct target of miR-92b-5p Silencing FA2H suppressed apoptosis, promoted proliferation and migration. In vivo experiments showed overexpression of THAP7-AS1 significantly reduced tumor volume and weight.
Conclusion:
THAP7-AS1 is firstly reported as a tumor suppressor in OC by targeting the miR-92b-5p/FA2H axis. Our findings suggest that THAP7-AS1 holds potential as therapeutic target in OC treatment.
Insights
THAP7-AS1 acts as a tumor suppressor in ovarian cancer (OC) by inhibiting the miR-92b-5p/FA2H pathway. This long noncoding RNA (lncRNA) shows potential as a therapeutic target for OC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ovarian cancer (OC) is a leading cause of gynecological cancer mortality.
- Long noncoding RNAs (lncRNAs) are emerging as critical regulators in cancer and potential therapeutic targets.
Purpose of the Study:
- To identify novel lncRNAs involved in OC development.
- To elucidate the regulatory mechanism of THAP7-AS1 in OC.
- To investigate THAP7-AS1 as a potential therapeutic target for OC.
Main Methods:
- LncRNA Microarray screening identified THAP7-AS1.
- RNA pull-down, luciferase assays, and FISH validated molecular interactions.
- qRT-PCR assessed expression in OC tissues and cell lines.
- In vitro assays (proliferation, migration, apoptosis) and in vivo xenograft models evaluated functional roles.
Main Results:
- THAP7-AS1 was downregulated in OC tissues and cells.
- Overexpression of THAP7-AS1 suppressed proliferation and migration while inducing apoptosis.
- THAP7-AS1 sponged miR-92b-5p, which was upregulated in OC.
- FA2H was a direct target of miR-92b-5p; its silencing promoted proliferation and migration.
- In vivo, THAP7-AS1 overexpression reduced tumor growth.
Conclusions:
- THAP7-AS1 functions as a tumor suppressor in OC by targeting the miR-92b-5p/FA2H axis.
- THAP7-AS1 represents a promising therapeutic target for ovarian cancer.
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