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Research Paper Volume 12, Issue 8 pp 6756-6773
Exosomal miR-200c suppresses chemoresistance of docetaxel in tongue squamous cell carcinoma by suppressing TUBB3 and PPP2R1B
Relevance score: 9.116299Jun Cui, Haiyan Wang, Xiaohe Zhang, Xiaodong Sun, Jin Zhang, Jinji Ma
Keywords: tongue squamous cell carcinoma, docetaxel, chemoresistance, miR-200c, TUBB3, PPP2R1B
Published in Aging on April 20, 2020
Docetaxel-resistant HSC-3 (HSC-3DR) cells exhibited increased cell viability and inhibited apoptosis. (A) Cell viability in response to different concentrations of DTX in tongue squamous cell carcinoma cell lines was determined by CCK8 assays. (B) Cell viability of HSC-3 and HSC-3DR cells in response to different concentrations of DTX was determined by CCK8 assays. (C) The morphology of HSC-3 and HSC-3DR cells (scale bars = 50 μm). (D) Apoptosis of HSC-3 and HSC-3DR cells was determined by flow cytometry. (E) Invasion ability of HSC-3 and HSC-3DR cells was determined by Transwell assays (scale bars = 50 μm). (F) Migration ability of HSC-3 and HSC-3DR cells was determined by Transwell assays (scale bars = 50 μm). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
Docetaxel resistance in HSC-3 cells (HSC-3DR) was associated with EMT and elevated drug efflux. (A) Migration ability of HSC-3 and HSC-3DR cells was determined by wound healing assays (scale bars = 100 μm). (B) The expressions of EMT-associated proteins in HSC-3DR cells were determined by western blots. (C) The expression of nuclear γ-H2AX of HSC-3 and HSC-3DR cells was determined by fluorescence assays (scale bars = 10 μm). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
Downregulation of miR-200c was involved in docetaxel resistance in HSC-3 cells (HSC-3DR). (A) volcano plot of RNA-Seq analysis. Red and green points represent significantly upregulated and downregulated miRNAs, respectively, according to fold change > 2 and adjusted p < 0.05. (B) Expressions of downregulated miRNAs in RNA-Seq analysis were verified by qRT-PCR. (C) The expression of miR-200c in tongue squamous cell carcinoma cell lines was determined by qRT-PCR. (D) The expression of miR-200c in HSC-3 and HSC-3DR cells was determined by qRT-PCR. (E) The efficiency of miR-200c-encoding lentiviral vectors in HSC-3DR cells was determined by qRT-PCR. (F) Cell viability in HSC-3DR cells treated with miR-200c-encoding lentiviral vector (LV-200c) was determined by CCK8 assays. (G) Apoptosis of HSC-3DR cells treated with miR-200c-encoding lentiviral vectors (LV-200c) was determined by flow cytometry. (H) Invasion ability of HSC-3DR cells treated with miR-200c-encoding lentiviral vector (LV-200c) was determined by Transwell assays (scale bars = 50 μm). (I) Migration ability of HSC-3DR cells treated with miR-200c-encoding lentiviral vector (LV-200c) was determined by Transwell assays (scale bars = 50 μm). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
Effect of miR-200c on docetaxel resistance in in vitro and in vivo. (A) Migration ability of HSC-3DR cells treated with miR-200c-encoding lentiviral vectors (LV-200c) was determined by wound healing assays (scale bars = 100 μm). (B) The expressions of EMT-associated proteins in HSC-3DR cells treated with miR-200c-encoding lentiviral vectors (LV-200c) were determined by western blots. (C) The expression of nuclear γ-H2AX in HSC-3DR cells treated with miR-200c-encoding lentiviral vectors (LV-200c) was determined by fluorescence assays (scale bars = 10 μm). (D) Tumor volume of xenograft mice treated with HSC-3DR cells treated with miR-200c-encoding lentiviral vectors (LV-200c) and DTX. (E) Representative images of tumors. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
Characteristics and effects of exosomes derived from normal tongue epithelial cells (NTEC) transfected with miR-200c. (A) The morphology and size distribution of exosomes were determined by electron microscopy and nanoparticle tracking analysis (left figure: scale bars = 200 μm and middle figure: scale bars = 100 μm). (B) The expressions of exosome markers were determined by western blots. (C) The internalization of exosomes was determined by fluorescence assays. Blue: nuclei labeled with DAPI. Green: miR-200c-carrying exosomes labeled with PKH67. (D) The expression of miR-200c was determined by qRT-PCR in NTEC transfected with miR-200c-encoding lentiviral vectors (LV-200c) and their exosomes. (E) The expression of miR-200c was determined by qRT-PCR in exosomes treated with RNase A or the combination of RNase A and Triton X-100. (F) The expression of miR-200c was determined by qRT-PCR in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor. (G) Cell viability was determined by CCK8 assays in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
MiR-200c-carrying exosomes promoted apoptosis and inhibited migration ability in docetaxel-resistant HSC-3 (HSC-3DR) cells. (A) Apoptosis was determined by flow cytometry in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor. (B) Invasion ability was determined by Transwell assays in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor (scale bars = 50 μm). (C) Migration ability was determined by Transwell assays in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor (scale bars = 50 μm). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
MiR-200c-carrying exosomes regulated docetaxel resistance in in vitro and in vivo. (A) Migration ability was determined by wound healing assays in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor (scale bars = 100 μm). (B) The expression of nuclear γ-H2AX was determined by fluorescence assays in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor (scale bars = 10 μm). (C) The expressions of EMT-associated proteins were determined by western blots in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor. (D) Tumor volume of xenograft mice treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor. (E) Representative images of tumors. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
MiR-200c regulated docetaxel resistance in HSC-3 (HSC-3DR) cells via targeting TUBB3 and PPP2R1B. (A) Putative binding sites of miR-200c in 3’UTR of TUBB3 and PPP2R1B. (B) Relative luciferase activity was determined by luciferase reporter assays in HSC-3DR cells transfected with miR-200c mimics and luciferase vectors containing wild-type or mutant 3’UTR of TUBB3. (C) Relative luciferase activity was determined by luciferase reporter assays in HSC-3DR cells transfected with miR-200c mimics and luciferase vectors containing wild-type or mutant 3’UTR of PPP2R1B. (D) The mRNA expressions of TUBB3 and PPP2R1B were determined by qRT-PCR in HSC-3DR cells transfected with miR-200c-encoding lentiviral vectors (LV-200c). (E) The protein expressions of TUBB3 and PPP2R1B were determined by western blots in HSC-3DR cells transfected with miR-200c-encoding lentiviral vectors (LV-200c). (F) The protein expression of TUBB3 was determined by western blots in HSC-3DR cells transfected with TUBB3-carrying vectors with the wild-type or mutant miR-200c sequence. (G) The protein expression of PPP2R1B was determined by western blots in HSC-3DR cells transfected with PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence. (H) Cell viability was determined by CCK8 assays in HSC-3DR cells transfected with TUBB3 or PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence. (I) Apoptosis was determined by flow cytometry in HSC-3DR cells transfected with TUBB3 or PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence. (J) Invasion ability was determined by Transwell assays in HSC-3DR cells transfected with TUBB3 or PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence (scale bars = 50 μm). (K) Migration ability was determined by Transwell assays in HSC-3DR cells transfected with TUBB3 or PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence (scale bars = 50 μm). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
MiR-200c-carrying exosomes regulated expressions of TUBB3 and PPP2R1B. (A) Migration ability was determined by wound healing assays in HSC-3DR cells transfected with TUBB3 or PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence (scale bars = 100 μm). (B) The expression of nuclear γ-H2AX was determined by fluorescence assays in HSC-3DR cells transfected with TUBB3 or PPP2R1B-carrying vectors with the wild-type or mutant miR-200c sequence (scale bars = 10 μm). (C) The protein expressions of TUBB3 and PPP2R1B were determined by western blots in HSC-3DR cells treated with miR-200c-carrying exosomes or miR-200c-carrying exosomes with the miR-200c inhibitor. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Retraction pp undefined-undefined
Retraction of: Exosomal miR-200c suppresses chemoresistance of docetaxel in tongue squamous cell carcinoma by suppressing TUBB3 and PPP2R1B
Relevance score: 9.175945Jun Cui, Haiyan Wang, Xiaohe Zhang, Xiaodong Sun, Jin Zhang, Jinji Ma
Keywords: tongue squamous cell carcinoma, docetaxel, chemoresistance, miR-200c, TUBB3, PPP2R1B
Published in Aging on Invalid Date