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pubmed, article, google, scholar, cancer, cas, colorectal, central, cells, claudin, lactobacillus, metastatic, expression, tight, junction, intestinal, colon, effects, fluorouracil, gut, plantarum, singh, physiol, microbiota, research, furesistant, proteins, cell, cldn, access, microbiol, barrier, dhawan, human, privacy, cookies, function, content, journal, metabolites, behavior, hctfur, metastasis, gastroenterol, sharma, information, publish, search, regulating, ldms,

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month download article/chapter lactobacillus-derived metabolites enhance hct-116/5-fur cell proliferation 5-fu suppressed chemoresistant ct26 tumour-bearing mice targeting chemotherapy-induced cldn1 host-microbe interaction published inhibit e-cadherin expression combination therapy epithelial-mesenchymal transition gut-heart-brain axis anti-tumour immune effect related subjects colorectal cancer cells full article pdf colorectal adenocarcinoma cells tight junction formation colon cancer cells tight junction proteins eun-mi ha metastatic colorectal cancer tight junction permeability privacy choices/manage cookies human intestinal microbiome downregulating cldn-1 expression lactobacillus plantarum supernatant colorectal cancer statistics human developmental biology fluorouracil-induced neurotoxicity inhibit metastatic behavior national research foundation check access instant access colorectal cancer incidence tumor-suppressive effects european economic area increase drug sensitivity 5-fluouracil increases chemosensitivity multicentre randomised trial early life shapes probiotic therapy inflammatory bowel diseases lasting commensal relationship sulfide-detoxifying enzymes article journal metastatic potential including increased migration regulating claudin-1 expression conditions privacy policy tumor metastasis

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• Intestinal microbiota development in the premature neonate: Establishment of a lasting commensal relationship?

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         headline:Lactobacillus-derived metabolites enhance the antitumor activity of 5-FU and inhibit metastatic behavior in 5-FU-resistant colorectal cancer cells by regulating claudin-1 expression
         description:Lactobacillus plantarum-derived metabolites (LDMs) increase drug sensitivity to 5-FU and antimetastatic effects in 5-FU-resistant colorectal cancer cells (HCT-116/5FUR). In this study, we evaluated the effects of LDMs on the regulation of genes and proteins involved in HCT-116/5-FUR cell proliferation and metastasis. HCT-116/5-FUR cells showed high metastatic potential, significantly reduced tight junction (TJ) integrity, including increased migration and paracellular permeability, and upregulation of claudin-1 (CLDN-1). The genetic silencing of CLDN-1 increased the sensitivity of HCT-116/5FUR to 5-FU and inhibited its metastatic potential by regulating the expression of epithelial-mesenchymal transition (EMT) related genes. Co-treatment of HCT-116/5FUR with LDMs and 5-FU suppressed chemoresistant and metastatic behavior by downregulating CLDN-1 expression. Finally, we designed LDMs-based therapeutic strategies to treatment for metastatic 5-FU-resistant colorectal cancer cells. These results suggested that LDMs and 5-FU cotreatments can synergistically target 5-FU-resistant cells, making it a candidate strategy to overcome 5-FU chemoresistance improve anticancer drug efficacy.
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      headline:Lactobacillus-derived metabolites enhance the antitumor activity of 5-FU and inhibit metastatic behavior in 5-FU-resistant colorectal cancer cells by regulating claudin-1 expression
      description:Lactobacillus plantarum-derived metabolites (LDMs) increase drug sensitivity to 5-FU and antimetastatic effects in 5-FU-resistant colorectal cancer cells (HCT-116/5FUR). In this study, we evaluated the effects of LDMs on the regulation of genes and proteins involved in HCT-116/5-FUR cell proliferation and metastasis. HCT-116/5-FUR cells showed high metastatic potential, significantly reduced tight junction (TJ) integrity, including increased migration and paracellular permeability, and upregulation of claudin-1 (CLDN-1). The genetic silencing of CLDN-1 increased the sensitivity of HCT-116/5FUR to 5-FU and inhibited its metastatic potential by regulating the expression of epithelial-mesenchymal transition (EMT) related genes. Co-treatment of HCT-116/5FUR with LDMs and 5-FU suppressed chemoresistant and metastatic behavior by downregulating CLDN-1 expression. Finally, we designed LDMs-based therapeutic strategies to treatment for metastatic 5-FU-resistant colorectal cancer cells. These results suggested that LDMs and 5-FU cotreatments can synergistically target 5-FU-resistant cells, making it a candidate strategy to overcome 5-FU chemoresistance improve anticancer drug efficacy.
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