We are analyzing https://link.springer.com/article/10.1186/s12935-021-01993-x.

Title:
LncRNA WDFY3-AS2 promotes cisplatin resistance and the cancer stem cell in ovarian cancer by regulating hsa-miR-139-5p/SDC4 axis | Cancer Cell International
Description:
Background Ovarian cancer (OC) is a high-mortality gynecological cancer that is typically treated with cisplatin, although such treatment often results in chemoresistance. Ovarian cancer resistance is usually related to cell stemness. Herein, we explored the function of lncRNA WDFY3-AS2 in OC cell resistance to cisplatin (DDP). Methods Cisplatin resistant OC A2780 cell lines (A2780-DDP) were established by long-term exposure to cisplatin. CCK-8 assay were performed to evaluate the viability of A2780, and A2780-DDP cells. Quantitative RT-PCR was used to examine the expression of lncRNA WDFY3-AS2, miR-139-5p, and SDC4 in A2780-DDP cell lines. After treatment with cisplatin, cell apoptosis and CD44+CD166+-positive cells were measured by flow cytometry. The transwell assays were employed to measure the effect of WDFY3-AS2 on cell migration, and invasion. In addition, tumorsphere formation assay was used to enrich OC cancer stem cells (CSCs) from A2780-DDP cells. The expression of CSC markers (SOX2, OCT4, and Nanog) was detected by western blotting. The regulatory mechanism was confirmed by RNA pull down, and luciferase reporter assays. Furthermore, xenograft tumor in nude mice was used to assess the impact of WDFY3-AS2 on cisplatin resistance in OC in vivo. Results WDFY3-AS2 was highly expressed in OC A2780-DDP cells, and silencing WDFY3-AS2 significantly inhibited proliferation, migration and invasion but increased apoptosis in OC A2780-DDP cells. Additionally, WDFY3-AS2 significantly promoted the A2780-DDP cells tumorspheres. WDFY3-AS2 was predicted to impact OC by sponging miR-139-5p and regulating SDC4. The xenografts inoculated with A2780-DDP cells additionally confirmed that tumor growth in vivo was reduced by si-WDFY3-AS2 transfection. MiR-139-5p inhibitor or SDC4 overexpression could restore the suppressive influence of silenced WDFY3-AS2 on tumor growth. Conclusions Together, WDFY3-AS2 may lead to change of cisplatin resistance by the expression of miR-139-5p/SDC4 in the OC A2870-DDP cells both in vitro and in vivo. Our finding may provide a drug target for the drug resistance of OC.
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Keywords {🔍}

cells, wdfyas, cancer, pubmed, cell, addp, mirp, cisplatin, sdc, google, scholar, expression, lncrna, ovarian, resistance, cas, siwdfyas, fig, stem, tumor, inhibitor, assay, central, treatment, cscs, rna, wang, analysis, data, zhang, invasion, article, transfection, transfected, migration, cisplatinresistant, usa, control, study, carcinoma, levels, regulating, axis, apoptosis, mice, targeting, long, noncoding, anhui, qrtpcr,

Topics {✒️}

regulating hsa-mir-139-5p/sdc4 axis label-free lc–ms/ms hsa-mir-139-5p seed region wdfy3-as2 sponged mir-139-5p regulating mir-2355-5p/socs2 axis targeting mir-491-5p/znf703 axis a2780-ddp sphere-forming cells si-wdfy3-as2 + pcdna-nc si-wdfy3-as2 significantly inhibited si-wdfy3-as2 + inhibitor-nc si-wdfy3-as2 + inhibitor nc wdfy3-as2-wt significantly suppressed si-wdfy3-as2 + mir-139 inhibitor si-wdfy3-as2 transfected cells mir-139-5p-biotin group compared mir-139-5p reverses cd44+/cd133+ cisplatin-resistant a2780-ddp cells induces wnt/pcp signaling a2780-ddp cell lines mature hsa-mir-139-5p transfected sphere-forming cells jak/stat signaling pathway mediating lncrna wdfy3-as2 lncrna wdfy3-as2 sirna wdfy3-as2 significantly promoted mir-143/fosl2-signaling pathway hsa-mir-139-5p inhibitor si-wdfy3-as2 inhibited hsa-mir-139-5p mimic inhibiting wnt/β-catenin wdfy3-as2 overexpression promoted spheroid-forming cell populations mir-139-5p/sdc4 axis cd133-positive cell numbers si-wdfy3-as2 group annexin v-fitc kit ting wang & mei zhang specific pathogen-free facility wdfy3-as2 expression patterns wdfy3-as2 expression rose wdfy3-as2 expression level serum-free dmem/f12 wdfy3-as2 biotin probe si-wdfy3-as2 + sdc4 si-wdfy3-as2 mice si-wdfy3-as2 transfection mir-139-5p inhibitor reversed high-mortality gynecological cancer wdfy3-as2 transfected cells mir-133a targets yes1

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         description:Ovarian cancer (OC) is a high-mortality gynecological cancer that is typically treated with cisplatin, although such treatment often results in chemoresistance. Ovarian cancer resistance is usually related to cell stemness. Herein, we explored the function of lncRNA WDFY3-AS2 in OC cell resistance to cisplatin (DDP). Cisplatin resistant OC A2780 cell lines (A2780-DDP) were established by long-term exposure to cisplatin. CCK-8 assay were performed to evaluate the viability of A2780, and A2780-DDP cells. Quantitative RT-PCR was used to examine the expression of lncRNA WDFY3-AS2, miR-139-5p, and SDC4 in A2780-DDP cell lines. After treatment with cisplatin, cell apoptosis and CD44+CD166+-positive cells were measured by flow cytometry. The transwell assays were employed to measure the effect of WDFY3-AS2 on cell migration, and invasion. In addition, tumorsphere formation assay was used to enrich OC cancer stem cells (CSCs) from A2780-DDP cells. The expression of CSC markers (SOX2, OCT4, and Nanog) was detected by western blotting. The regulatory mechanism was confirmed by RNA pull down, and luciferase reporter assays. Furthermore, xenograft tumor in nude mice was used to assess the impact of WDFY3-AS2 on cisplatin resistance in OC in vivo. WDFY3-AS2 was highly expressed in OC A2780-DDP cells, and silencing WDFY3-AS2 significantly inhibited proliferation, migration and invasion but increased apoptosis in OC A2780-DDP cells. Additionally, WDFY3-AS2 significantly promoted the A2780-DDP cells tumorspheres. WDFY3-AS2 was predicted to impact OC by sponging miR-139-5p and regulating SDC4. The xenografts inoculated with A2780-DDP cells additionally confirmed that tumor growth in vivo was reduced by si-WDFY3-AS2 transfection. MiR-139-5p inhibitor or SDC4 overexpression could restore the suppressive influence of silenced WDFY3-AS2 on tumor growth. Together, WDFY3-AS2 may lead to change of cisplatin resistance by the expression of miR-139-5p/SDC4 in the OC A2870-DDP cells both in vitro and in vivo. Our finding may provide a drug target for the drug resistance of OC.
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            lncRNA WDFY3-AS2
            Hsa-miR-139-5p
            SDC4
            Cisplatin resistance
            Cancer stem cells
            Ovarian cancer
            Cancer Research
            Cell Biology
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      description:Ovarian cancer (OC) is a high-mortality gynecological cancer that is typically treated with cisplatin, although such treatment often results in chemoresistance. Ovarian cancer resistance is usually related to cell stemness. Herein, we explored the function of lncRNA WDFY3-AS2 in OC cell resistance to cisplatin (DDP). Cisplatin resistant OC A2780 cell lines (A2780-DDP) were established by long-term exposure to cisplatin. CCK-8 assay were performed to evaluate the viability of A2780, and A2780-DDP cells. Quantitative RT-PCR was used to examine the expression of lncRNA WDFY3-AS2, miR-139-5p, and SDC4 in A2780-DDP cell lines. After treatment with cisplatin, cell apoptosis and CD44+CD166+-positive cells were measured by flow cytometry. The transwell assays were employed to measure the effect of WDFY3-AS2 on cell migration, and invasion. In addition, tumorsphere formation assay was used to enrich OC cancer stem cells (CSCs) from A2780-DDP cells. The expression of CSC markers (SOX2, OCT4, and Nanog) was detected by western blotting. The regulatory mechanism was confirmed by RNA pull down, and luciferase reporter assays. Furthermore, xenograft tumor in nude mice was used to assess the impact of WDFY3-AS2 on cisplatin resistance in OC in vivo. WDFY3-AS2 was highly expressed in OC A2780-DDP cells, and silencing WDFY3-AS2 significantly inhibited proliferation, migration and invasion but increased apoptosis in OC A2780-DDP cells. Additionally, WDFY3-AS2 significantly promoted the A2780-DDP cells tumorspheres. WDFY3-AS2 was predicted to impact OC by sponging miR-139-5p and regulating SDC4. The xenografts inoculated with A2780-DDP cells additionally confirmed that tumor growth in vivo was reduced by si-WDFY3-AS2 transfection. MiR-139-5p inhibitor or SDC4 overexpression could restore the suppressive influence of silenced WDFY3-AS2 on tumor growth. Together, WDFY3-AS2 may lead to change of cisplatin resistance by the expression of miR-139-5p/SDC4 in the OC A2870-DDP cells both in vitro and in vivo. Our finding may provide a drug target for the drug resistance of OC.
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         lncRNA WDFY3-AS2
         Hsa-miR-139-5p
         SDC4
         Cisplatin resistance
         Cancer stem cells
         Ovarian cancer
         Cancer Research
         Cell Biology
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