ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
LncRNA FAISL Inhibits Calpain 2-Mediated Proteolysis of FAK to Promote Progression and Metastasis of Triple Negative Breast Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- SNP rs7430456 mediated LINC00578 drives triple negative breast cancer through regulating miR-143-5p expression.Hereditas · 2026Article
- ST3GAL1 drives colorectal cancer metastasis by mediating NRF2-induced activation of the integrin-α6β4 signaling pathway via sialylation modification.Journal of translational medicine · 2026Article
- Long Non-Coding RNA VPS9D1-AS1 in Human Cancer: Functions, Mechanisms, and Clinical Utility.Anti-cancer agents in medicinal chemistry · 2026Review
- Ifebemtinib and paclitaxel synergistically inhibit the proliferation and metastasis of TNBC by blocking PI3K/Akt pathway through LSD1/PIK3IP1 axis.Scientific reports · 2025Article
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SLPI as a dedifferentiation biomarker in BRAFV600E-mutant papillary thyroid cancer.Endocrine connections · 2025Article
- Long Non-Coding RNAs: Key Regulators of Tumor Epithelial/Mesenchymal Plasticity and Cancer Stemness.Cells · 2025Review
- LncRNA SNHG15 acts as a ceRNA to promote breast cancer progression through the miR-153-3p/KLF5 signal axis.Journal of Cancer · 2025Article
- LncRNA FAISL Inhibits Calpain 2-Mediated Proteolysis of FAK to Promote Progression and Metastasis of Triple Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
12 authors.
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Abstract
Triple negative breast cancer (TNBC) is the most aggressive subtype in breast tumors. When re-analyzing TCGA breast cancer dataset, we found cell adhesion molecules are highly enriched in differentially expressed genes in TNBC samples, among which Focal Adhesion Kinase (FAK) is most significantly associated with poor survival of TNBC patients. FAK is precisely modulated in the focal adhesion dynamics. To investigate whether lncRNAs regulate FAK signaling, we performed RNA immunoprecipitation sequencing and found FAISL (FAK Interacting and Stabilizing LncRNA) abundantly enriched in FAK-interacting lncRNAs and frequently overexpressed in TCGA TNBC tissues. FAISL promotes TNBC cell adhesion, cytoskeleton spreading, proliferation, and anchor-independent survival. FAISL doesn't affect FAK mRNA but positively regulates FAK protein level by blocking Calpain 2-mediated proteolysis. FAISL interacts with the C-terminus domain of FAK, whereby masks the binding site of Calpain 2 and prevents FAK cleavage. High level of FAISL correlates with FAK expression in tumor tissues and poor prognosis of TNBC patients. A siRNA delivery system targeting FAISL using reduction-responsive nanoparticles effectively inhibits tumor growth and metastasis in TNBC mouse models. Together, these findings uncover a lncRNA-mediated mechanism of regulating FAK proteolysis in the TNBC progression, and highlight the potential of targeting lncRNA FAISL for TNBC treatment.
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