<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>18(6)</volume><submitter>Liao X</submitter><pubmed_abstract>&lt;h4>Background/aims&lt;/h4>: Colorectal cancer (CRC) is a common malignant tumor, and circular RNAs (circRNAs) are abnormally expressed in CRC. However, the function and underlying mechanism of circRNA pinin (circ-PNN; hsa_circ_0101802) in CRC remain unclear.&lt;h4>Methods&lt;/h4>: Exosomes were isolated from the plasma of CRC patients and identified by transmission electron microscopy and Western blotting. The RNA expression levels of circ-PNN, miR-1225-5p, and fibroblast growth factor 13 (FGF13) were measured by quantitative real-time polymerase chain reaction. Cell proliferation was detected by Cell Counting K-8, colony formation, and 5-ethynyl-2'-deoxyuridine assays. Cell apoptosis was assessed by flow cytometry. The expression of apoptosis and metastasis-related proteins was evaluated by Western blotting. The associations among circ-PNN, miR-1225-5p, and FGF13 were confirmed by dual-luciferase report assay and RNA immunoprecipitation assay. A xenograft model was used to verify the function of circ-PNN in tumor formation &lt;i>in vivo&lt;/i>.&lt;h4>Results&lt;/h4>: circ-PNN expression was upregulated in plasmic exosomes derived from CRC patients. The expression of circ-PNN and FGF13 was upregulated, while miR-1225-5p expression was downregulated in CRC cells incubated with plasmic exosomes derived from CRC patients. Tumor-derived exosomes promoted the proliferation, migration, and invasion but inhibited apoptosis of CRC cells. Moreover, the addition of tumor-derived exosomes partly reversed the inhibitory effect of circ-PNN knockdown on CRC tumor progression &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i>. Thus, circ-PNN acts as a sponge for miR-1225-5p to regulate FGF13 expression.&lt;h4>Conclusions&lt;/h4>: Tumor-derived exosomal circ-PNN promoted CRC progression through the regulation of the miR-1225-5p/FGF13 pathway, providing a potential therapeutic target for CRC.</pubmed_abstract><journal>Gut and liver</journal><pagination>1014-1025</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11565002</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Tumor-Derived Exosomal Circular RNA Pinin Induces FGF13 Expression to Promote Colorectal Cancer Progression through miR-1225-5p.</pubmed_title><pmcid>PMC11565002</pmcid><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Yang L</pubmed_authors><pubmed_authors>Li T</pubmed_authors><pubmed_authors>Liao X</pubmed_authors><pubmed_authors>Xie Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tumor-Derived Exosomal Circular RNA Pinin Induces FGF13 Expression to Promote Colorectal Cancer Progression through miR-1225-5p.</name><description>&lt;h4>Background/aims&lt;/h4>: Colorectal cancer (CRC) is a common malignant tumor, and circular RNAs (circRNAs) are abnormally expressed in CRC. However, the function and underlying mechanism of circRNA pinin (circ-PNN; hsa_circ_0101802) in CRC remain unclear.&lt;h4>Methods&lt;/h4>: Exosomes were isolated from the plasma of CRC patients and identified by transmission electron microscopy and Western blotting. The RNA expression levels of circ-PNN, miR-1225-5p, and fibroblast growth factor 13 (FGF13) were measured by quantitative real-time polymerase chain reaction. Cell proliferation was detected by Cell Counting K-8, colony formation, and 5-ethynyl-2'-deoxyuridine assays. Cell apoptosis was assessed by flow cytometry. The expression of apoptosis and metastasis-related proteins was evaluated by Western blotting. The associations among circ-PNN, miR-1225-5p, and FGF13 were confirmed by dual-luciferase report assay and RNA immunoprecipitation assay. A xenograft model was used to verify the function of circ-PNN in tumor formation &lt;i>in vivo&lt;/i>.&lt;h4>Results&lt;/h4>: circ-PNN expression was upregulated in plasmic exosomes derived from CRC patients. The expression of circ-PNN and FGF13 was upregulated, while miR-1225-5p expression was downregulated in CRC cells incubated with plasmic exosomes derived from CRC patients. Tumor-derived exosomes promoted the proliferation, migration, and invasion but inhibited apoptosis of CRC cells. Moreover, the addition of tumor-derived exosomes partly reversed the inhibitory effect of circ-PNN knockdown on CRC tumor progression &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i>. Thus, circ-PNN acts as a sponge for miR-1225-5p to regulate FGF13 expression.&lt;h4>Conclusions&lt;/h4>: Tumor-derived exosomal circ-PNN promoted CRC progression through the regulation of the miR-1225-5p/FGF13 pathway, providing a potential therapeutic target for CRC.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-06-06T17:37:54.889Z</modification><creation>2025-04-07T04:32:23.328Z</creation></dates><accession>S-EPMC11565002</accession><cross_references><pubmed>38384181</pubmed><doi>10.5009/gnl230304</doi></cross_references></HashMap>