We are analyzing https://link.springer.com/article/10.1186/s12943-020-01168-8.

Title:
CAF secreted miR-522 suppresses ferroptosis and promotes acquired chemo-resistance in gastric cancer | Molecular Cancer
Description:
Background Ferroptosis is a novel mode of non-apoptotic cell death induced by build-up of toxic lipid peroxides (lipid-ROS) in an iron dependent manner. Cancer-associated fibroblasts (CAFs) support tumor progression and drug resistance by secreting various bioactive substances, including exosomes. Yet, the role of CAFs in regulating lipid metabolism as well as ferroptosis of cancer cells is still unexplored and remains enigmatic. Methods Ferroptosis-related genes in gastric cancer (GC) were screened by using mass spectrum; exosomes were isolated by ultra-centrifugation and CAF secreted miRNAs were determined by RT-qPCR. Erastin was used to induce ferroptosis, and ferroptosis levels were evaluated by measuring lipid-ROS, cell viability and mitochondrial membrane potential. Results Here, we provide clinical evidence to show that arachidonate lipoxygenase 15 (ALOX15) is closely related with lipid-ROS production in gastric cancer, and that exosome-miR-522 serves as a potential inhibitor of ALOX15. By using primary stromal cells and cancer cells, we prove that exosome-miR-522 is mainly derived from CAFs in tumor microenvironment. Moreover, heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) was found to mediate miR-522 packing into exosomes, and ubiquitin-specific protease 7 (USP7) stabilizes hnRNPA1 through de-ubiquitination. Importantly, cisplatin and paclitaxel promote miR-522 secretion from CAFs by activating USP7/hnRNPA1 axis, leading to ALOX15 suppression and decreased lipid-ROS accumulation in cancer cells, and ultimately result in decreased chemo-sensitivity. Conclusions The present study demonstrates that CAFs secrete exosomal miR-522 to inhibit ferroptosis in cancer cells by targeting ALOX15 and blocking lipid-ROS accumulation. The intercellular pathway, comprising USP7, hnRNPA1, exo-miR-522 and ALOX15, reveals new mechanism of acquired chemo-resistance in GC. Graphical abstract
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Keywords {🔍}

cells, cafs, cancer, alox, exosomes, pubmed, fig, tumor, cell, hnrnpa, article, ferroptosis, usp, google, scholar, cas, analysis, levels, tissues, expression, supplemental, figure, gastric, lipidros, cisplatin, central, death, data, caf, resistance, exomir, zhang, role, microenvironment, wang, derived, treated, showed, promotes, isolated, nfs, protein, lipid, primary, exosomal, secretion, study, mice, sgc, min,

Topics {✒️}

caf-secreted exo-mir-146a caf-exosome delivered cys-mir-522 reporter plasmid p-mir-alox15 friedmann angeli jp suppressed erastin-induced ferroptosis stem-loop rt-pcr chemotherapy-induced damage responses mir-522-3p promotes tumorigenesis p53-mediated ferroptotic responses aif-mediated cell death δct = ct gene-ct control human hnrnp a2/b1 chemo-toxicity reduces ubiquitination synthetic single-stranded mir-522 article download pdf promotes acquired chemo-resistance leica uc6 ultra-microtome usp7/hnrnpa1/exo-mir-522 pathway chemo-toxicity treated cafs therapies search search ferroptosis-related signaling pathway gpx4 inhibitor-induced ferroptosis decreased lipid-ros accumulation decreasing lipid-ros levels exosomal mir-196a derived blocking lipid-ros accumulation classical tumor-promoting factors proteome-wide protein quantification high-sensitivity scmos camera mediating lipid-ros production caf-derived exosomal mir-522 beta-galactosidase expression vector exo-mir-522 positively correlated lenti-virus transduced cafs activating usp7/hnrnpa1 axis reverse chemotherapy resistance nano-tracking analysis showed immuno-precipitation immuno-precipitation guoguang ying designed activating usp7/hnrnpa1 pathway protein tyrosine phosphatases fibroblast cell strains clinical research center caf secreted mirnas toxic lipid peroxides paired para-carcinoma tissues promotes mir-522 secretion suppressed cell death demonstrative research platform iron dependent manner

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         headline:CAF secreted miR-522 suppresses ferroptosis and promotes acquired chemo-resistance in gastric cancer
         description:Ferroptosis is a novel mode of non-apoptotic cell death induced by build-up of toxic lipid peroxides (lipid-ROS) in an iron dependent manner. Cancer-associated fibroblasts (CAFs) support tumor progression and drug resistance by secreting various bioactive substances, including exosomes. Yet, the role of CAFs in regulating lipid metabolism as well as ferroptosis of cancer cells is still unexplored and remains enigmatic. Ferroptosis-related genes in gastric cancer (GC) were screened by using mass spectrum; exosomes were isolated by ultra-centrifugation and CAF secreted miRNAs were determined by RT-qPCR. Erastin was used to induce ferroptosis, and ferroptosis levels were evaluated by measuring lipid-ROS, cell viability and mitochondrial membrane potential. Here, we provide clinical evidence to show that arachidonate lipoxygenase 15 (ALOX15) is closely related with lipid-ROS production in gastric cancer, and that exosome-miR-522 serves as a potential inhibitor of ALOX15. By using primary stromal cells and cancer cells, we prove that exosome-miR-522 is mainly derived from CAFs in tumor microenvironment. Moreover, heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) was found to mediate miR-522 packing into exosomes, and ubiquitin-specific protease 7 (USP7) stabilizes hnRNPA1 through de-ubiquitination. Importantly, cisplatin and paclitaxel promote miR-522 secretion from CAFs by activating USP7/hnRNPA1 axis, leading to ALOX15 suppression and decreased lipid-ROS accumulation in cancer cells, and ultimately result in decreased chemo-sensitivity. The present study demonstrates that CAFs secrete exosomal miR-522 to inhibit ferroptosis in cancer cells by targeting ALOX15 and blocking lipid-ROS accumulation. The intercellular pathway, comprising USP7, hnRNPA1, exo-miR-522 and ALOX15, reveals new mechanism of acquired chemo-resistance in GC.
         datePublished:2020-02-27T00:00:00Z
         dateModified:2020-02-27T00:00:00Z
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            Ferroptosis
            Cancer-associated fibroblasts
            Exosomes
            miR-522
            GC
            Cancer Research
            Oncology
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ScholarlyArticle:
      headline:CAF secreted miR-522 suppresses ferroptosis and promotes acquired chemo-resistance in gastric cancer
      description:Ferroptosis is a novel mode of non-apoptotic cell death induced by build-up of toxic lipid peroxides (lipid-ROS) in an iron dependent manner. Cancer-associated fibroblasts (CAFs) support tumor progression and drug resistance by secreting various bioactive substances, including exosomes. Yet, the role of CAFs in regulating lipid metabolism as well as ferroptosis of cancer cells is still unexplored and remains enigmatic. Ferroptosis-related genes in gastric cancer (GC) were screened by using mass spectrum; exosomes were isolated by ultra-centrifugation and CAF secreted miRNAs were determined by RT-qPCR. Erastin was used to induce ferroptosis, and ferroptosis levels were evaluated by measuring lipid-ROS, cell viability and mitochondrial membrane potential. Here, we provide clinical evidence to show that arachidonate lipoxygenase 15 (ALOX15) is closely related with lipid-ROS production in gastric cancer, and that exosome-miR-522 serves as a potential inhibitor of ALOX15. By using primary stromal cells and cancer cells, we prove that exosome-miR-522 is mainly derived from CAFs in tumor microenvironment. Moreover, heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) was found to mediate miR-522 packing into exosomes, and ubiquitin-specific protease 7 (USP7) stabilizes hnRNPA1 through de-ubiquitination. Importantly, cisplatin and paclitaxel promote miR-522 secretion from CAFs by activating USP7/hnRNPA1 axis, leading to ALOX15 suppression and decreased lipid-ROS accumulation in cancer cells, and ultimately result in decreased chemo-sensitivity. The present study demonstrates that CAFs secrete exosomal miR-522 to inhibit ferroptosis in cancer cells by targeting ALOX15 and blocking lipid-ROS accumulation. The intercellular pathway, comprising USP7, hnRNPA1, exo-miR-522 and ALOX15, reveals new mechanism of acquired chemo-resistance in GC.
      datePublished:2020-02-27T00:00:00Z
      dateModified:2020-02-27T00:00:00Z
      pageStart:1
      pageEnd:17
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12943-020-01168-8
      keywords:
         Ferroptosis
         Cancer-associated fibroblasts
         Exosomes
         miR-522
         GC
         Cancer Research
         Oncology
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