We are analyzing https://link.springer.com/article/10.1007/s10528-022-10201-y.

Title:
Downregulation of Circ-CEP128 Enhances the Paclitaxel Sensitivity of Cervical Cancer Through Regulating miR-432-5p/MCL1 | Biochemical Genetics
Description:
Chemoresistance is a common problem in cancer treatment, and circular RNA (circRNA) has been found to be associated with the progression of chemoresistance in cancer. However, the role and mechanism of circRNA centrosomal protein 128 (circ-CEP128) in the chemoresistance of cervical cancer (CC) are still unclear. The expression of circ-CEP128, microRNA (miR)-432-5p, and myeloid cell leukemia-1 (MCL1) was measured by quantitative real-time PCR. The paclitaxel resistance of cells was assessed using MTT assay. Cell proliferation, apoptosis, migration, and invasion were determined using MTT assay, colony formation assay, flow cytometry, and transwell assay. The protein levels of metastasis markers and MCL1 were examined using western blot analysis. Mice xenograft models were constructed to assess the effect of circ-CEP128 silencing on CC tumor growth and paclitaxel sensitivity. The interaction between miR-432-5p and circ-CEP128 or MCL1 was confirmed by dual-luciferase reporter assay and RIP assay. Circ-CEP128 had highly expression in CC tumor tissues and cells. Silencing of circ-CEP128 could enhance the paclitaxel sensitivity of CC cells by decreasing cell growth, migration, and invasion. Also, knockdown of circ-CEP123 reduced CC tumor growth and promoted the paclitaxel sensitivity of CC tumors. MiR-432-5p was found to be sponged by circ-CEP128, and its inhibitor could reverse the promoting function of circ-CEP128 silencing on the paclitaxel sensitivity of CC cells. Additionally, MCL1 was a target of miR-432-5p, and circ-CEP128 could sponge miR-432-5p to regulate MCL1. Besides, overexpressed MCL1 also could reverse the enhancing effect of miR-432-5p on the paclitaxel sensitivity of CC cells. In conclusion, the present study showed that circ-CEP128 silencing could increase the paclitaxel sensitivity of CC by regulating the miR-432-5p/MCL1 axis.
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Keywords {🔍}

pubmed, article, cancer, google, scholar, cas, cervical, zhang, circcep, mcl, central, rna, cell, mirp, wang, paclitaxel, circular, sensitivity, cells, regulating, chen, zhao, chemoresistance, progression, tumor, yang, circrna, resistance, assay, proliferation, invasion, huang, liu, med, privacy, cookies, content, access, httpsdoiorgs, zhou, information, publish, search, enhances, lan, expression, microrna, silencing, growth, sponging,

Topics {✒️}

regulating mir-432-5p/rab10 axis mir-128-3p/s100a14 pathway boping yang & chunyan ren month download article/chapter quantitative real-time pcr immune-related adverse event mir-320a/mcl1 axis regulating mir-145-5p/myd88 dual-luciferase reporter assay mir-432-5p/mcl1 axis paclitaxel modulate tumor-infiltrating regulating mir-432-5p/mcl1 chemotherapy-resistant cervical cancer full article pdf bladder cancer progression circ-cep128 enhances privacy choices/manage cookies regulating mir-145-5p myeloid cell leukemia-1 cell cycle progression cc tumor growth tumorigenic circular rnas circular rnas act human cervical cancer decreasing cell growth circmto1 promotes tumorigenesis enhance cisplatin resistance cc tumor tissues inhibit cell proliferation related subjects targeting mir-432-5p promotes cell apoptosis circcrim1 inhibits hdac4 mapk signaling pathway maintaining tumor microenvironment affiliated tumor hospital sponge mir-432-5p circ-cep128 silencing sponging mir-5047 european economic area mice xenograft models present study showed persistent complete response de menezes rx de kroon cd improves cytotoxic efficacy directly targets fn1 del rio ha conditions privacy policy article zhao

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         description:Chemoresistance is a common problem in cancer treatment, and circular RNA (circRNA) has been found to be associated with the progression of chemoresistance in cancer. However, the role and mechanism of circRNA centrosomal protein 128 (circ-CEP128) in the chemoresistance of cervical cancer (CC) are still unclear. The expression of circ-CEP128, microRNA (miR)-432-5p, and myeloid cell leukemia-1 (MCL1) was measured by quantitative real-time PCR. The paclitaxel resistance of cells was assessed using MTT assay. Cell proliferation, apoptosis, migration, and invasion were determined using MTT assay, colony formation assay, flow cytometry, and transwell assay. The protein levels of metastasis markers and MCL1 were examined using western blot analysis. Mice xenograft models were constructed to assess the effect of circ-CEP128 silencing on CC tumor growth and paclitaxel sensitivity. The interaction between miR-432-5p and circ-CEP128 or MCL1 was confirmed by dual-luciferase reporter assay and RIP assay. Circ-CEP128 had highly expression in CC tumor tissues and cells. Silencing of circ-CEP128 could enhance the paclitaxel sensitivity of CC cells by decreasing cell growth, migration, and invasion. Also, knockdown of circ-CEP123 reduced CC tumor growth and promoted the paclitaxel sensitivity of CC tumors. MiR-432-5p was found to be sponged by circ-CEP128, and its inhibitor could reverse the promoting function of circ-CEP128 silencing on the paclitaxel sensitivity of CC cells. Additionally, MCL1 was a target of miR-432-5p, and circ-CEP128 could sponge miR-432-5p to regulate MCL1. Besides, overexpressed MCL1 also could reverse the enhancing effect of miR-432-5p on the paclitaxel sensitivity of CC cells. In conclusion, the present study showed that circ-CEP128 silencing could increase the paclitaxel sensitivity of CC by regulating the miR-432-5p/MCL1 axis.
         datePublished:2022-04-07T00:00:00Z
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      description:Chemoresistance is a common problem in cancer treatment, and circular RNA (circRNA) has been found to be associated with the progression of chemoresistance in cancer. However, the role and mechanism of circRNA centrosomal protein 128 (circ-CEP128) in the chemoresistance of cervical cancer (CC) are still unclear. The expression of circ-CEP128, microRNA (miR)-432-5p, and myeloid cell leukemia-1 (MCL1) was measured by quantitative real-time PCR. The paclitaxel resistance of cells was assessed using MTT assay. Cell proliferation, apoptosis, migration, and invasion were determined using MTT assay, colony formation assay, flow cytometry, and transwell assay. The protein levels of metastasis markers and MCL1 were examined using western blot analysis. Mice xenograft models were constructed to assess the effect of circ-CEP128 silencing on CC tumor growth and paclitaxel sensitivity. The interaction between miR-432-5p and circ-CEP128 or MCL1 was confirmed by dual-luciferase reporter assay and RIP assay. Circ-CEP128 had highly expression in CC tumor tissues and cells. Silencing of circ-CEP128 could enhance the paclitaxel sensitivity of CC cells by decreasing cell growth, migration, and invasion. Also, knockdown of circ-CEP123 reduced CC tumor growth and promoted the paclitaxel sensitivity of CC tumors. MiR-432-5p was found to be sponged by circ-CEP128, and its inhibitor could reverse the promoting function of circ-CEP128 silencing on the paclitaxel sensitivity of CC cells. Additionally, MCL1 was a target of miR-432-5p, and circ-CEP128 could sponge miR-432-5p to regulate MCL1. Besides, overexpressed MCL1 also could reverse the enhancing effect of miR-432-5p on the paclitaxel sensitivity of CC cells. In conclusion, the present study showed that circ-CEP128 silencing could increase the paclitaxel sensitivity of CC by regulating the miR-432-5p/MCL1 axis.
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         MCL1
         Human Genetics
         Biochemistry
         general
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         Medical Microbiology
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