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author Liu, Hui-Pu
Tai, Shun-Ban
Jiang, Jun-Lin
Tey, Shu-Farn
Liu, Pei-Feng
Lin, Ming-Wei
Wu, Shuen-Chiu
Chen, Yung-Che
Chen, Chun-Lin
author_facet Liu, Hui-Pu
Tai, Shun-Ban
Jiang, Jun-Lin
Tey, Shu-Farn
Liu, Pei-Feng
Lin, Ming-Wei
Wu, Shuen-Chiu
Chen, Yung-Che
Chen, Chun-Lin
Liu, Hui-Pu
Tai, Shun-Ban
Jiang, Jun-Lin
Tey, Shu-Farn
Liu, Pei-Feng
Lin, Ming-Wei
Wu, Shuen-Chiu
Chen, Yung-Che
Chen, Chun-Lin
collection PubMed - marine biology
contents Epac (RAPGEF3) promotes betaglycan expression to mediate ciprofloxacin-induced suppression of cancer cell migration and metastasis: Mechanistic insights and drug repurposing potential. Liu, Hui-Pu Tai, Shun-Ban Jiang, Jun-Lin Tey, Shu-Farn Liu, Pei-Feng Lin, Ming-Wei Wu, Shuen-Chiu Chen, Yung-Che Chen, Chun-Lin Cell Movement Humans Animals Ciprofloxacin Proteoglycans Drug Repositioning Guanine Nucleotide Exchange Factors Receptors, Transforming Growth Factor beta Cell Line, Tumor Mice Mice, Nude Neoplasm Metastasis Mice, Inbred BALB C Neoplasm Invasiveness Gene Expression Regulation, Neoplastic Signal Transduction Xenograft Model Antitumor Assays Fluoroquinolones (FQs), potent antimicrobials, have shown potential in curbing cancer invasion and metastasis by affecting cell migration and extracellular matrix reshaping. However, the molecular mechanisms behind their impact remain unclear. The type III TGF-β receptor (TβR3, also called betaglycan), a co-receptor in the TGF-β superfamily, is often found to be downregulated in various human cancers. This receptor plays a crucial role in suppressing cancer progression and metastasis, independent of TGF-β signaling. In this study, we investigated the effects of ciprofloxacin (a member of FQs) on TβR3 production in cancer cells and their subsequent impact on cancer cell migration and invasion. Our results demonstrated that ciprofloxacin and other FQs dose-dependently elevated TβR3 levels, which was associated with reduced cell migration and invasion. Gene silencing and pharmacological approaches confirmed that exchange protein directly activated by cAMP (Epac) and JNK/AP1 pathways are critical for FQ-induced TβR3 expression. In vivo studies showed that mice receiving clinically relevant doses of ciprofloxacin exhibited elevated TβR3 levels in the liver and lung, which were associated with inhibited tumor progression. Furthermore, histological analysis of human non-small cell lung cancer (NSCLC) tissues revealed that metastatic lung cancers had lower TβR3 protein expression compared to matched normal lung tissues. Overall; our findings indicate that cancer invasion and malignancy are associated with reduced TβR3 levels, and that FQs can inhibit cancer cell migration and invasion by upregulating TβR3 expression. These results elucidate the potential for repositioning FQs as a supplemental therapeutic strategy in cancer treatment.
format Artículo científico
id pubmed_40532572
institution PubMed
language en
publishDate 2025
publisher Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
record_format pubmed
spellingShingle Epac (RAPGEF3) promotes betaglycan expression to mediate ciprofloxacin-induced suppression of cancer cell migration and metastasis: Mechanistic insights and drug repurposing potential.
Liu, Hui-Pu
Tai, Shun-Ban
Jiang, Jun-Lin
Tey, Shu-Farn
Liu, Pei-Feng
Lin, Ming-Wei
Wu, Shuen-Chiu
Chen, Yung-Che
Chen, Chun-Lin
Cell Movement
Humans
Animals
Ciprofloxacin
Proteoglycans
Drug Repositioning
Guanine Nucleotide Exchange Factors
Receptors, Transforming Growth Factor beta
Cell Line, Tumor
Mice
Mice, Nude
Neoplasm Metastasis
Mice, Inbred BALB C
Neoplasm Invasiveness
Gene Expression Regulation, Neoplastic
Signal Transduction
Xenograft Model Antitumor Assays
Epac (RAPGEF3) promotes betaglycan expression to mediate ciprofloxacin-induced suppression of cancer cell migration and metastasis: Mechanistic insights and drug repurposing potential. Liu, Hui-Pu Tai, Shun-Ban Jiang, Jun-Lin Tey, Shu-Farn Liu, Pei-Feng Lin, Ming-Wei Wu, Shuen-Chiu Chen, Yung-Che Chen, Chun-Lin Cell Movement Humans Animals Ciprofloxacin Proteoglycans Drug Repositioning Guanine Nucleotide Exchange Factors Receptors, Transforming Growth Factor beta Cell Line, Tumor Mice Mice, Nude Neoplasm Metastasis Mice, Inbred BALB C Neoplasm Invasiveness Gene Expression Regulation, Neoplastic Signal Transduction Xenograft Model Antitumor Assays Fluoroquinolones (FQs), potent antimicrobials, have shown potential in curbing cancer invasion and metastasis by affecting cell migration and extracellular matrix reshaping. However, the molecular mechanisms behind their impact remain unclear. The type III TGF-β receptor (TβR3, also called betaglycan), a co-receptor in the TGF-β superfamily, is often found to be downregulated in various human cancers. This receptor plays a crucial role in suppressing cancer progression and metastasis, independent of TGF-β signaling. In this study, we investigated the effects of ciprofloxacin (a member of FQs) on TβR3 production in cancer cells and their subsequent impact on cancer cell migration and invasion. Our results demonstrated that ciprofloxacin and other FQs dose-dependently elevated TβR3 levels, which was associated with reduced cell migration and invasion. Gene silencing and pharmacological approaches confirmed that exchange protein directly activated by cAMP (Epac) and JNK/AP1 pathways are critical for FQ-induced TβR3 expression. In vivo studies showed that mice receiving clinically relevant doses of ciprofloxacin exhibited elevated TβR3 levels in the liver and lung, which were associated with inhibited tumor progression. Furthermore, histological analysis of human non-small cell lung cancer (NSCLC) tissues revealed that metastatic lung cancers had lower TβR3 protein expression compared to matched normal lung tissues. Overall; our findings indicate that cancer invasion and malignancy are associated with reduced TβR3 levels, and that FQs can inhibit cancer cell migration and invasion by upregulating TβR3 expression. These results elucidate the potential for repositioning FQs as a supplemental therapeutic strategy in cancer treatment.
title Epac (RAPGEF3) promotes betaglycan expression to mediate ciprofloxacin-induced suppression of cancer cell migration and metastasis: Mechanistic insights and drug repurposing potential.
topic Cell Movement
Humans
Animals
Ciprofloxacin
Proteoglycans
Drug Repositioning
Guanine Nucleotide Exchange Factors
Receptors, Transforming Growth Factor beta
Cell Line, Tumor
Mice
Mice, Nude
Neoplasm Metastasis
Mice, Inbred BALB C
Neoplasm Invasiveness
Gene Expression Regulation, Neoplastic
Signal Transduction
Xenograft Model Antitumor Assays
url https://pubmed.ncbi.nlm.nih.gov/40532572/