ArticleBioengineered2021
Circular RNA PIP5K1A (circPIP5K1A) accelerates endometriosis progression by regulating the miR-153-3p/Thymosin Beta-4 X-Linked (TMSB4X) pathway.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- The role of TGF-β superfamily in endometriosis: a systematic review.Frontiers in immunology · 2025Pooled it
- Circular RNAs in Endometriosis: from Expression Pattern To Pathogenesis.Cell biochemistry and biophysics · 2026Review
- The Critical Roles of Circular RNAs in Basic Research and Clinical Application of Female Reproductive-Related Diseases.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Circular RNA PIP5K1A act as microRNA-552-3p sponge to regulates inflammation, oxidative damage in glucolipotoxicity-induced pancreatic INS-1 β-cells via Janus kinase 1.Bioengineered · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a common gynecologic disease, endometriosis (EM) poses a threat to the reproductive health of about 10% women globally. Recent studies have revealed that circular RNAs (circRNAs) are deeply implicated in EM pathogenesis. However, the functions of circPIP5K1A in EM have not been studied yet. Our study intended to uncover the molecular mechanism of circPIP5K1A in EM. In this work, gene and protein expressions were determined by RT-qPCR or Western blotting. CCK-8, wound healing, transwell, and flow cytometry assays were conducted to analyze cell viability, migration, invasion, cell cycle, and apoptosis. Additionally, bioinformatics analysis, dual-luciferase reporter assay, as well as RIP assay were performed to investigate the combination between miR-153-3p and circPIP5K1A or TMSB4X. Herein, we found remarkable high circPIP5K1A expression in EM tissues and cells. Silencing of circPIP5K1A suppressed proliferation, restrained cell cycle, increased cell apoptosis, and decreased migration and invasion in EM cells. In addition, miR-153-3p inhibition could abrogate the impacts of circPIP5K1A knockdown on EM progression in vitro. Also, we found that circPIP5K1A regulated TMSB4X level via interaction with miR-153-3p in EM cells. Besides, circPIP5K1A promoted EM progression via TMSB4X. Moreover, TMSB4X could activate the TGF-β signaling in hEM15A cells. To sum up, our study elucidated that circPIP5K1A accelerated EM progression in vitro by activating the TGF-β signaling pathway via the miR-153-3p/TMSB4X axis, providing a potential clinical target for EM treatment.
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