We are analyzing https://link.springer.com/article/10.1007/s10863-023-09986-3.

Title:
USP10 suppresses ABCG2-induced malignant characteristics of doxorubicin-resistant thyroid cancer by inhibiting PI3K/AKT pathway | Journal of Bioenergetics and Biomembranes
Description:
Doxorubicin (DOX) is the most extensively used drug in the chemotherapy of thyroid cancer (TC). However, the existence of DOX resistance is not conducive to TC treatment. Here, we investigated the role of USP10 in DOX-resistant TC and explored the underlying molecular mechanism. CCK-8 assay was used to measure cell viability in thyroid cancer FTC133 and DOX-resistant FTC133-DOX cells. RT-qPCR and western blot were used to evaluate USP10 expression. Cell migration, invasion, and apoptotic assays were conducted. Western blot was used to detect cellular signaling proteins, EMT-related proteins, and apoptosis-related proteins. We found a lower expression of USP10 in the human TC cell line FTC133 as compared to the normal human thyroid Htori-3 cells. Notably, USP10 expression was further reduced in DOX-resistant (FTC133-DOX) cells compared to the FTC133 cells. FTC133-DOX cells had increased invasion, migration, and EMT properties while less apoptosis by activating the PI3K/AKT pathway. Interestingly, overexpressing USP10 increased the chemosensitivity of FTC133 cells to DOX therapy. Overexpressing USP10 inhibited invasion, migration, and EMT properties of FTC133-DOX cells and promoted apoptosis. Mechanistically, overexpressing USP10 inhibited PI3K/AKT pathway by activating PTEN. Furthermore, overexpressed USP10 controlled all these processes by downregulating ABCG2. This study demonstrates that USP10 could reduce DOX-induced resistance of TC cells to DOX therapy and could suppress TC malignant behavior by inhibiting the PI3K/AKT pathway. Furthermore, USP10 targeted ABCG2 to inhibit all these malignant processes, therefore, either increasing USP10 expression or inhibiting ABCG2 could be used as novel targets for treating DOX-resistant thyroid cancer.
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Keywords {🔍}

cells, cancer, usp, thyroid, ftcdox, pubmed, article, cell, expression, abcg, google, scholar, resistance, cas, dox, ftc, pathway, pcdnausp, drug, pikakt, compared, protein, fig, apoptosis, study, found, liu, group, central, overexpression, doxresistant, migration, signaling, pten, transfected, doxorubicin, invasion, regulating, chen, biological, tpc, results, malignant, assay, western, lower, human, pcdnaabcg, showed, role,

Topics {✒️}

pc-dna-usp10 + pc-dna-abcg2 group compared pten/pi3k/akt signaling pathway rtk-dependent pi3k/akt signalling emt-transcription factor slug/snai2 pten/pi3k/akt signalling pathway phosphoinositide 3-kinase/akt pathways pi3k/akt/mtor pathway involved pcdna-usp10 + pcdna-abcg2 group compared met-pi3k-akt signaling transfecting pc-dna-usp10 cells pi3k/akt pathway enhances stroma-induced drug tolerance pten/pi3k/akt pathway phosphatidylinositol 3-kinase/protein kinase drug-resistant cell lines dox-resistant ftc133-dox cells doxorubicin-resistant thyroid cancer inhibiting pi3k/akt pathway drug-resistant cell line thyroid cancer-related deaths article download pdf drug-resistant strains showed drug-resistant cancer cells abcg2-induced drug resistance pcdna-usp10 induced apoptosis pc-dna-usp10 group pro-apoptotic proteins elevated dual protein/lipid phosphatase reduce dox-induced resistance pro-apoptotic proteins p53 abcg2-mediated multidrug resistance abcg2-overexpressing cancer cells pc-dna-abcg2 compared malignant biological behavior ftc133-dox cells invaded important signaling pathway pi3k/akt pathway usp10-mediated biological properties pcdna-usp10 group compared full access β-actin forward primer activating erk pathway regulating mapks-related p53 thyroid cancer cell normal thyroid cells drug-resistant strains drug-resistant strains common endocrine malignancy privacy choices/manage cookies mediating drug resistance

Schema {🗺️}

WebPage:
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         headline:USP10 suppresses ABCG2-induced malignant characteristics of doxorubicin-resistant thyroid cancer by inhibiting PI3K/AKT pathway
         description:Doxorubicin (DOX) is the most extensively used drug in the chemotherapy of thyroid cancer (TC). However, the existence of DOX resistance is not conducive to TC treatment. Here, we investigated the role of USP10 in DOX-resistant TC and explored the underlying molecular mechanism. CCK-8 assay was used to measure cell viability in thyroid cancer FTC133 and DOX-resistant FTC133-DOX cells. RT-qPCR and western blot were used to evaluate USP10 expression. Cell migration, invasion, and apoptotic assays were conducted. Western blot was used to detect cellular signaling proteins, EMT-related proteins, and apoptosis-related proteins. We found a lower expression of USP10 in the human TC cell line FTC133 as compared to the normal human thyroid Htori-3 cells. Notably, USP10 expression was further reduced in DOX-resistant (FTC133-DOX) cells compared to the FTC133 cells. FTC133-DOX cells had increased invasion, migration, and EMT properties while less apoptosis by activating the PI3K/AKT pathway. Interestingly, overexpressing USP10 increased the chemosensitivity of FTC133 cells to DOX therapy. Overexpressing USP10 inhibited invasion, migration, and EMT properties of FTC133-DOX cells and promoted apoptosis. Mechanistically, overexpressing USP10 inhibited PI3K/AKT pathway by activating PTEN. Furthermore, overexpressed USP10 controlled all these processes by downregulating ABCG2. This study demonstrates that USP10 could reduce DOX-induced resistance of TC cells to DOX therapy and could suppress TC malignant behavior by inhibiting the PI3K/AKT pathway. Furthermore, USP10 targeted ABCG2 to inhibit all these malignant processes, therefore, either increasing USP10 expression or inhibiting ABCG2 could be used as novel targets for treating DOX-resistant thyroid cancer.
         datePublished:2023-11-03T00:00:00Z
         dateModified:2023-11-03T00:00:00Z
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            Organic Chemistry
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      headline:USP10 suppresses ABCG2-induced malignant characteristics of doxorubicin-resistant thyroid cancer by inhibiting PI3K/AKT pathway
      description:Doxorubicin (DOX) is the most extensively used drug in the chemotherapy of thyroid cancer (TC). However, the existence of DOX resistance is not conducive to TC treatment. Here, we investigated the role of USP10 in DOX-resistant TC and explored the underlying molecular mechanism. CCK-8 assay was used to measure cell viability in thyroid cancer FTC133 and DOX-resistant FTC133-DOX cells. RT-qPCR and western blot were used to evaluate USP10 expression. Cell migration, invasion, and apoptotic assays were conducted. Western blot was used to detect cellular signaling proteins, EMT-related proteins, and apoptosis-related proteins. We found a lower expression of USP10 in the human TC cell line FTC133 as compared to the normal human thyroid Htori-3 cells. Notably, USP10 expression was further reduced in DOX-resistant (FTC133-DOX) cells compared to the FTC133 cells. FTC133-DOX cells had increased invasion, migration, and EMT properties while less apoptosis by activating the PI3K/AKT pathway. Interestingly, overexpressing USP10 increased the chemosensitivity of FTC133 cells to DOX therapy. Overexpressing USP10 inhibited invasion, migration, and EMT properties of FTC133-DOX cells and promoted apoptosis. Mechanistically, overexpressing USP10 inhibited PI3K/AKT pathway by activating PTEN. Furthermore, overexpressed USP10 controlled all these processes by downregulating ABCG2. This study demonstrates that USP10 could reduce DOX-induced resistance of TC cells to DOX therapy and could suppress TC malignant behavior by inhibiting the PI3K/AKT pathway. Furthermore, USP10 targeted ABCG2 to inhibit all these malignant processes, therefore, either increasing USP10 expression or inhibiting ABCG2 could be used as novel targets for treating DOX-resistant thyroid cancer.
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      dateModified:2023-11-03T00:00:00Z
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         ABCG2
         Doxorubicin resistance
         Pathways
         Bioorganic Chemistry
         Biochemistry
         general
         Animal Anatomy / Morphology / Histology
         Animal Biochemistry
         Organic Chemistry
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      affiliation:
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