We are analyzing https://link.springer.com/article/10.1186/s13046-019-1159-2.

Title:
ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2 | Journal of Experimental & Clinical Cancer Research
Description:
Background ALKBH5 regulated the malignant behavior of breast cancer and glioblastoma. However, the expression and function of ALKBH5 in epithelial ovarian cancer have not yet been determined. In the present study, we investigated the expression and function of ALKBH5 in epithelial ovarian cancer with respect to its potential role in the tumorigenesis of the disease as well as an early diagnostic marker. Methods Immunohistochemistry and western blot were used to detect protein expression. Gene silencing and over-expression experiment were used to study gene function. Cell proliferation assay and Matrigel invasion assays were used to detect cell proliferation and invasion, respectively. The nude mouse tumor formation experiment was used to evaluate the growth of cells in vivo. Results The expression of ALKBH5 was found to be increased in epithelial ovarian cancer tissue as compared to the normal ovarian tissues. The silencing of ALKBH5 in SKOV3 cells enhanced the autophagy and inhibited the proliferation and invasion in vitro and in vivo, whereas the ectopic expression of ALKBH5 in A2780 cells exerted an opposite effect. Mechanical study revealed that ALKBH5 physically interacted with HuR. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. Also, ALKBH5 enhanced the stability of BCL-2 mRNA and promoted the interaction between Bcl-2 and Beclin1. Conclusion Overall, the present study identified ALKBH5 as a candidate oncogene in epithelial ovarian cancer and a potential target for ovarian cancer therapy.
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Keywords {🔍}

alkbh, cells, expression, cancer, autophagy, ovarian, bcl, infected, lvrup, skov, fig, article, mrna, atg, proliferation, beclin, lvrupnc, cell, google, scholar, regulated, inhibited, lvalkbh, study, tumor, hur, ulk, silencing, invasion, increased, lvnc, added, data, egfr, cas, epithelial, concentration, puromycin, mgml, pathway, interaction, rna, lcii, compared, promoted, mtor, protein, ectopic, pikc, luciferase,

Topics {✒️}

serine/threonine-protein kinase ulk1 plasmid encoding mrfp-gfp-lc3 monoclonal mouse anti-β-actin mutant luciferase-bcl-2-3′-utr reporter main anti-apoptotic protein bravo-san pedro jm milk-derived fusion peptide ampk/mtor signaling pathway pi3k/akt/mtor pathways therapy-driven anticancer immunosurveillance mrfp-gfp-lc3 reporter luciferase-bcl-2 3′-utr reporter pmir-report-bcl-2-3′-utr lv3-shalkbh5–1-infected group apoptosis-resistant prostate cancer article google scholar article download pdf egfr-pi3k-akt-mtor pathway a2780 cells-infected lv121-alkbh5 mtor-dependent autophagy contributes mrfp-gfp-lc3 distribution lv3-nc-infected group alkbh5-mediated m6a-demethylation alkbh5-lentiviral expression vector lvru6p-nc-infected skov3 cells mtor signaling pathway full access lv121-alkbh5-infected group alkbh5 silencing-induced autophagy protein kinase mtor privacy choices/manage cookies irrelevant primary antibodies lv121-nc-infected group luciferase reporter assay long 3′-utr mrnas phenol/chloroform extraction mrfp-gfp-lc3 flavopiridol-treated cells relative lvru6p-nc-infected group alkbh5-mediated bcl-2 regulation serous ovarian carcinoma alternative splicing events creative commons license ovarian cancer therapy epithelial ovarian cancer ovarian cancer tissue potential clinical significance b-cell lymphoma-2 common rna modifications lvru6p-02-infected skov3 cells

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WebPage:
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         headline:ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2
         description:ALKBH5 regulated the malignant behavior of breast cancer and glioblastoma. However, the expression and function of ALKBH5 in epithelial ovarian cancer have not yet been determined. In the present study, we investigated the expression and function of ALKBH5 in epithelial ovarian cancer with respect to its potential role in the tumorigenesis of the disease as well as an early diagnostic marker. Immunohistochemistry and western blot were used to detect protein expression. Gene silencing and over-expression experiment were used to study gene function. Cell proliferation assay and Matrigel invasion assays were used to detect cell proliferation and invasion, respectively. The nude mouse tumor formation experiment was used to evaluate the growth of cells in vivo. The expression of ALKBH5 was found to be increased in epithelial ovarian cancer tissue as compared to the normal ovarian tissues. The silencing of ALKBH5 in SKOV3 cells enhanced the autophagy and inhibited the proliferation and invasion in vitro and in vivo, whereas the ectopic expression of ALKBH5 in A2780 cells exerted an opposite effect. Mechanical study revealed that ALKBH5 physically interacted with HuR. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. Also, ALKBH5 enhanced the stability of BCL-2 mRNA and promoted the interaction between Bcl-2 and Beclin1. Overall, the present study identified ALKBH5 as a candidate oncogene in epithelial ovarian cancer and a potential target for ovarian cancer therapy.
         datePublished:2019-04-15T00:00:00Z
         dateModified:2019-04-15T00:00:00Z
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            Cancer Research
            Immunology
            Apoptosis
            Oncology
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      headline:ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2
      description:ALKBH5 regulated the malignant behavior of breast cancer and glioblastoma. However, the expression and function of ALKBH5 in epithelial ovarian cancer have not yet been determined. In the present study, we investigated the expression and function of ALKBH5 in epithelial ovarian cancer with respect to its potential role in the tumorigenesis of the disease as well as an early diagnostic marker. Immunohistochemistry and western blot were used to detect protein expression. Gene silencing and over-expression experiment were used to study gene function. Cell proliferation assay and Matrigel invasion assays were used to detect cell proliferation and invasion, respectively. The nude mouse tumor formation experiment was used to evaluate the growth of cells in vivo. The expression of ALKBH5 was found to be increased in epithelial ovarian cancer tissue as compared to the normal ovarian tissues. The silencing of ALKBH5 in SKOV3 cells enhanced the autophagy and inhibited the proliferation and invasion in vitro and in vivo, whereas the ectopic expression of ALKBH5 in A2780 cells exerted an opposite effect. Mechanical study revealed that ALKBH5 physically interacted with HuR. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. Also, ALKBH5 enhanced the stability of BCL-2 mRNA and promoted the interaction between Bcl-2 and Beclin1. Overall, the present study identified ALKBH5 as a candidate oncogene in epithelial ovarian cancer and a potential target for ovarian cancer therapy.
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         BCL-2
         Beclin1
         Autophagy
         miR-7, EGFR
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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      name:Department of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China
      name:Department of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China
      name:Department of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China
      name:Department of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China

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