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Updated: Jul 28, 2025

Design and Validation of a Volumetric-extrusion Bioprinter for Bioprinting of Soluble Basement Membrane Extract for Translational Research
Published on: March 28, 2025
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Xiaolong Zhu1,2,3,4, Xingwei Wu1,2,3, Hui Yang1,2,3,4
1Central Laboratory, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, People's Republic of China.
This study reveals that the long non-coding RNA LINC01003 promotes glioma progression by regulating the focal adhesion pathway. Targeting LINC01003 offers a potential therapeutic strategy for glioma patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in glioma development.
- The specific role and regulatory mechanisms of LINC01003 in glioma remain largely uncharacterized.
Purpose of the Study:
- To investigate the functional significance of LINC01003 in glioma.
- To elucidate the molecular mechanisms underlying LINC01003's role in glioma progression.
Main Methods:
- Utilized GEPIA2 and Chinese Glioma Genome Atlas (CCGA) databases for expression and survival analysis.
- Performed in vitro and in vivo loss-of-function experiments to assess LINC01003's impact on glioma.
- Employed RNA sequencing, bioinformatics, and RNA immunoprecipitation (RIP) assays to identify pathways and regulatory mechanisms, including N6-methyladenine (m6A) modification.
Main Results:
- LINC01003 expression is significantly upregulated in glioma tissues and cell lines.
- Elevated LINC01003 levels correlate with poorer overall survival in glioma patients.
- Knockdown of LINC01003 suppressed glioma cell cycle, proliferation, and migration, mediated via the focal adhesion signaling pathway.
- LINC01003 upregulation is dependent on m6A modification regulated by METTL3.
Conclusions:
- LINC01003 acts as a oncogenic lncRNA promoting glioma tumorigenesis.
- The LINC01003-CAV1-FAK axis represents a promising therapeutic target for glioma treatment.
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