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    TaKaRa pmr zsgreen1 plasmid vector
    <t>miR-141</t> promotes ovarian cancer cell growth and tumor seeding by enhancing anoikis resistance of ovarian cancer cells. a Experimental overview of anoikis assay. b The relative apoptosis rates of miR-141 stable clones and KLF12 knockdown cells were measured using TUNEL assay. Green signals represent DAPI positive cells and red signals represent TUNEL positive cells. Both overexpression of miR-141 or knockdown of KLF12 resulted in lower apoptotic rates of ovarian cancer cells after treated by anoikis assay. c Flow cytometry cell cycle analysis revealed that percentages of sub-G1 phase in either KLF12 knockdown OVCA433 cells or miR-141 overexpressed SKOV3 cells were reduced as compared with their negative controls. d Western blotting showed that either knockdown of KLF12 or overexpression of miR-141 could suppress ovarian cancer cell apoptosis through reduction of cleaved-PARP and cleaved-caspase 3 expression in anoikis treated ovarian cancer cells ( Upper : KLF12 knockdown clones in OVCA433, Lower ; miR-141 stable expressing clones in SKOV3). Bar, 50 μM. e Effects of miR-141 on ovarian cancer growth and tumor seeding were revealed using in vivo model by i.p. injecting miR-141 and the scrambled control clones into 5-weeks old female nude mice. Average number of tumor nodules ( Left ) and the tumor burden ( Right ) formed by miR-141 clones were much higher than the scrambled control and they were observed across the peritoneal cavity as photographed on Day 28 (4 weeks). The white arrows indicate the location of tumor nodules
    Pmr Zsgreen1 Plasmid Vector, supplied by TaKaRa, used in various techniques. Bioz Stars score: 95/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    miR-141 promotes ovarian cancer cell growth and tumor seeding by enhancing anoikis resistance of ovarian cancer cells. a Experimental overview of anoikis assay. b The relative apoptosis rates of miR-141 stable clones and KLF12 knockdown cells were measured using TUNEL assay. Green signals represent DAPI positive cells and red signals represent TUNEL positive cells. Both overexpression of miR-141 or knockdown of KLF12 resulted in lower apoptotic rates of ovarian cancer cells after treated by anoikis assay. c Flow cytometry cell cycle analysis revealed that percentages of sub-G1 phase in either KLF12 knockdown OVCA433 cells or miR-141 overexpressed SKOV3 cells were reduced as compared with their negative controls. d Western blotting showed that either knockdown of KLF12 or overexpression of miR-141 could suppress ovarian cancer cell apoptosis through reduction of cleaved-PARP and cleaved-caspase 3 expression in anoikis treated ovarian cancer cells ( Upper : KLF12 knockdown clones in OVCA433, Lower ; miR-141 stable expressing clones in SKOV3). Bar, 50 μM. e Effects of miR-141 on ovarian cancer growth and tumor seeding were revealed using in vivo model by i.p. injecting miR-141 and the scrambled control clones into 5-weeks old female nude mice. Average number of tumor nodules ( Left ) and the tumor burden ( Right ) formed by miR-141 clones were much higher than the scrambled control and they were observed across the peritoneal cavity as photographed on Day 28 (4 weeks). The white arrows indicate the location of tumor nodules

    Journal: Molecular Cancer

    Article Title: MicroRNA-141 enhances anoikis resistance in metastatic progression of ovarian cancer through targeting KLF12/Sp1/survivin axis

    doi: 10.1186/s12943-017-0582-2

    Figure Lengend Snippet: miR-141 promotes ovarian cancer cell growth and tumor seeding by enhancing anoikis resistance of ovarian cancer cells. a Experimental overview of anoikis assay. b The relative apoptosis rates of miR-141 stable clones and KLF12 knockdown cells were measured using TUNEL assay. Green signals represent DAPI positive cells and red signals represent TUNEL positive cells. Both overexpression of miR-141 or knockdown of KLF12 resulted in lower apoptotic rates of ovarian cancer cells after treated by anoikis assay. c Flow cytometry cell cycle analysis revealed that percentages of sub-G1 phase in either KLF12 knockdown OVCA433 cells or miR-141 overexpressed SKOV3 cells were reduced as compared with their negative controls. d Western blotting showed that either knockdown of KLF12 or overexpression of miR-141 could suppress ovarian cancer cell apoptosis through reduction of cleaved-PARP and cleaved-caspase 3 expression in anoikis treated ovarian cancer cells ( Upper : KLF12 knockdown clones in OVCA433, Lower ; miR-141 stable expressing clones in SKOV3). Bar, 50 μM. e Effects of miR-141 on ovarian cancer growth and tumor seeding were revealed using in vivo model by i.p. injecting miR-141 and the scrambled control clones into 5-weeks old female nude mice. Average number of tumor nodules ( Left ) and the tumor burden ( Right ) formed by miR-141 clones were much higher than the scrambled control and they were observed across the peritoneal cavity as photographed on Day 28 (4 weeks). The white arrows indicate the location of tumor nodules

    Article Snippet: To confirm the oncogenic functions of miR-141, a miR-141 precursor-expressing plasmid (pmR-ZsGreen1 vector, Clontech) was stably transfected into three advanced ovarian cancer cell lines: A2780CP (p53 mutated) (141-C2 and 141-C8), OVCA433 (p53 wildtype) (141-C5 and 141-C10) and SKOV3 (p53 deleted) (141-C1 and 141-C4) (Fig. , left panel ).

    Techniques: Clone Assay, TUNEL Assay, Over Expression, Flow Cytometry, Cytometry, Cell Cycle Assay, Western Blot, Expressing, In Vivo, Mouse Assay

    Increased anoikis resistance in ovarian cancer cells is involved intrinsic apoptotic pathway. a The Affymetrix GeneChip 3' Expression Array revealed a panel of apoptosis-related genes (Fold change > 2) induced in KLF12 knockdown OVCA433 cells which showed increased anoikis resistance. b Proteome Profiler (Human Apoptosis Array Kit) showed that 8 out of 35 Intrinsic Apoptosis-related factors were commonly upregulated in miR-141 enforced expression or KLF12 knockdown OVCA433 cells. c A schematic diagram illustrates that there are several Sp1 binding sites located along the promoter of survivin, confirming Sp1 is able to transcriptionally upregulate survivin. KLF12 is able to interfere the interaction of Sp1 with the promoter of survivin and the transcriptional activity. d ChIP assay showed the competitive occupancy of Sp1 by KLF12 on the promoter of survivin . ( Upper ) Position weight matrix (PWM) for SP1-binding sequence motif derived from Jaspar database. ChIP assays showed the occupancy of Sp1 on 3 SBEs ( Red color ) of the Survivin promoter in A2780cp cells were inhibited by KLF12. ( Lower ) Schematic diagram shows the positions of seven higher binding affinity SBEs on the survivin promoter. e Luciferase reporter assay using Survivin promoter luciferase reporter construct (luc-Survivin) demonstrated that Sp1 could significantly elevate the luciferase reporter signals from ~3-5.5 folds in HEK293 and ~48 to 70% in A2780cp by Sp1 dose dependently (200 to 1000 ng/well) ( Upper ). Using luc-survivin and pCMV6-AC-GFP-Sp1 (600 ng/well) and co-transfected with varied amount of pCMV6-KLF12 (200–800 ng/well), results showed that the Sp1-upregulated survivin signals were remarkably reduced from 5 to 2 folds in HEK293, and from 158% to 45% in A2780cp by KLF12 in a dose-dependent manner (200 – 1000 ng/well). f Western blot analysis showed that transient transfection of Sp1 could upregulate, while KLF12 could inhibit, survivin and XIAP expressions in A2780cp and OVCA433 cells. g Western blot analysis confirmed that knockdown of Sp1 had no effect on KLF12 expression but significantly reduced the expression of survivin and XIAP in two Sp1-enriched ovarian cancer cell lines, OVCA433 and SKOV3

    Journal: Molecular Cancer

    Article Title: MicroRNA-141 enhances anoikis resistance in metastatic progression of ovarian cancer through targeting KLF12/Sp1/survivin axis

    doi: 10.1186/s12943-017-0582-2

    Figure Lengend Snippet: Increased anoikis resistance in ovarian cancer cells is involved intrinsic apoptotic pathway. a The Affymetrix GeneChip 3' Expression Array revealed a panel of apoptosis-related genes (Fold change > 2) induced in KLF12 knockdown OVCA433 cells which showed increased anoikis resistance. b Proteome Profiler (Human Apoptosis Array Kit) showed that 8 out of 35 Intrinsic Apoptosis-related factors were commonly upregulated in miR-141 enforced expression or KLF12 knockdown OVCA433 cells. c A schematic diagram illustrates that there are several Sp1 binding sites located along the promoter of survivin, confirming Sp1 is able to transcriptionally upregulate survivin. KLF12 is able to interfere the interaction of Sp1 with the promoter of survivin and the transcriptional activity. d ChIP assay showed the competitive occupancy of Sp1 by KLF12 on the promoter of survivin . ( Upper ) Position weight matrix (PWM) for SP1-binding sequence motif derived from Jaspar database. ChIP assays showed the occupancy of Sp1 on 3 SBEs ( Red color ) of the Survivin promoter in A2780cp cells were inhibited by KLF12. ( Lower ) Schematic diagram shows the positions of seven higher binding affinity SBEs on the survivin promoter. e Luciferase reporter assay using Survivin promoter luciferase reporter construct (luc-Survivin) demonstrated that Sp1 could significantly elevate the luciferase reporter signals from ~3-5.5 folds in HEK293 and ~48 to 70% in A2780cp by Sp1 dose dependently (200 to 1000 ng/well) ( Upper ). Using luc-survivin and pCMV6-AC-GFP-Sp1 (600 ng/well) and co-transfected with varied amount of pCMV6-KLF12 (200–800 ng/well), results showed that the Sp1-upregulated survivin signals were remarkably reduced from 5 to 2 folds in HEK293, and from 158% to 45% in A2780cp by KLF12 in a dose-dependent manner (200 – 1000 ng/well). f Western blot analysis showed that transient transfection of Sp1 could upregulate, while KLF12 could inhibit, survivin and XIAP expressions in A2780cp and OVCA433 cells. g Western blot analysis confirmed that knockdown of Sp1 had no effect on KLF12 expression but significantly reduced the expression of survivin and XIAP in two Sp1-enriched ovarian cancer cell lines, OVCA433 and SKOV3

    Article Snippet: To confirm the oncogenic functions of miR-141, a miR-141 precursor-expressing plasmid (pmR-ZsGreen1 vector, Clontech) was stably transfected into three advanced ovarian cancer cell lines: A2780CP (p53 mutated) (141-C2 and 141-C8), OVCA433 (p53 wildtype) (141-C5 and 141-C10) and SKOV3 (p53 deleted) (141-C1 and 141-C4) (Fig. , left panel ).

    Techniques: Expressing, Binding Assay, Activity Assay, Chromatin Immunoprecipitation, Sequencing, Derivative Assay, Luciferase, Reporter Assay, Construct, Transfection, Western Blot

    Mir-141 is frequently upregulated in advanced ovarian cancers. a A graph showing 18 miRNAs with the highest expression in microRNA profiling analysis which was performed using the miRCURY LNA™ miRNA array (Exiqon) on two types of ovarian cancer cell lines; anchorage-growth independent (A2780s, A2780cp, SKOV3, C13*), and anchorage-growth dependent (HOSEs). The dot line shows the miRNAs with more than 2 folds of Delta LogMedianRatios were selected for further functional analysis using transfection of their pre-miRNA expressing plasmids in ovarian cancer cell lines e.g. A2780cp and SKOV3 and performing of soft agar assay. b Real time qPCR analysis showed that miR-141 is upregulated in ovarian cancer cell lines ( N = 12) as compared with the immortalized cell lines, HOSEs, ( N = 3). Samples were normalized with SNORD48 . c Graphical representation of qPCR analysis showing that miR-141 is elevated in ovarian cancer ( N = 65) when compare to the control normal ovary tissues ( N = 26) and immortalized cell lines ( N = 3). d Representative pictures showing miR-141 ISH expression signal (dark blue staining) is gradually increased along the tumor stages of epithelial ovarian cancer. (Magnification × 10; scale bar, 100 μm)

    Journal: Molecular Cancer

    Article Title: MicroRNA-141 enhances anoikis resistance in metastatic progression of ovarian cancer through targeting KLF12/Sp1/survivin axis

    doi: 10.1186/s12943-017-0582-2

    Figure Lengend Snippet: Mir-141 is frequently upregulated in advanced ovarian cancers. a A graph showing 18 miRNAs with the highest expression in microRNA profiling analysis which was performed using the miRCURY LNA™ miRNA array (Exiqon) on two types of ovarian cancer cell lines; anchorage-growth independent (A2780s, A2780cp, SKOV3, C13*), and anchorage-growth dependent (HOSEs). The dot line shows the miRNAs with more than 2 folds of Delta LogMedianRatios were selected for further functional analysis using transfection of their pre-miRNA expressing plasmids in ovarian cancer cell lines e.g. A2780cp and SKOV3 and performing of soft agar assay. b Real time qPCR analysis showed that miR-141 is upregulated in ovarian cancer cell lines ( N = 12) as compared with the immortalized cell lines, HOSEs, ( N = 3). Samples were normalized with SNORD48 . c Graphical representation of qPCR analysis showing that miR-141 is elevated in ovarian cancer ( N = 65) when compare to the control normal ovary tissues ( N = 26) and immortalized cell lines ( N = 3). d Representative pictures showing miR-141 ISH expression signal (dark blue staining) is gradually increased along the tumor stages of epithelial ovarian cancer. (Magnification × 10; scale bar, 100 μm)

    Article Snippet: To confirm the oncogenic functions of miR-141, a miR-141 precursor-expressing plasmid (pmR-ZsGreen1 vector, Clontech) was stably transfected into three advanced ovarian cancer cell lines: A2780CP (p53 mutated) (141-C2 and 141-C8), OVCA433 (p53 wildtype) (141-C5 and 141-C10) and SKOV3 (p53 deleted) (141-C1 and 141-C4) (Fig. , left panel ).

    Techniques: Expressing, Functional Assay, Transfection, Soft Agar Assay, Real-time Polymerase Chain Reaction, In Situ Hybridization, Staining

    miR-141 enhances ovarian cancer cell survival. QPCR analyses showed the expressions of miR-141 in, ( a ) ( left ) miR-141-overexpressing clones of A2780cp, OVCA433 and SKOV3; ( right ) and anti-miR141 treated cell lines; OVCA433 and SKOV3. VC: empty control and SC: scrambled control. b ( left ) XTT cell proliferation demonstrated that overexpression of miR-141 could remarkably enhanced the cell proliferation in A2780cp, OVCA433 and SKOV3 cell lines; ( right ) while inhibition of miR-141 significantly attenuated the cell proliferation in OVCA433 and SKOV3 cells with treatment of anti-miR141. The foci formation assay demonstrated that, ( c ) ( left ) overexpression of miR-141 could increase the cell viability in low-serum medium (0.1% FBS) compared with the vector control, ( right ) while depletion of miR-141 led to a reduction of cell viability

    Journal: Molecular Cancer

    Article Title: MicroRNA-141 enhances anoikis resistance in metastatic progression of ovarian cancer through targeting KLF12/Sp1/survivin axis

    doi: 10.1186/s12943-017-0582-2

    Figure Lengend Snippet: miR-141 enhances ovarian cancer cell survival. QPCR analyses showed the expressions of miR-141 in, ( a ) ( left ) miR-141-overexpressing clones of A2780cp, OVCA433 and SKOV3; ( right ) and anti-miR141 treated cell lines; OVCA433 and SKOV3. VC: empty control and SC: scrambled control. b ( left ) XTT cell proliferation demonstrated that overexpression of miR-141 could remarkably enhanced the cell proliferation in A2780cp, OVCA433 and SKOV3 cell lines; ( right ) while inhibition of miR-141 significantly attenuated the cell proliferation in OVCA433 and SKOV3 cells with treatment of anti-miR141. The foci formation assay demonstrated that, ( c ) ( left ) overexpression of miR-141 could increase the cell viability in low-serum medium (0.1% FBS) compared with the vector control, ( right ) while depletion of miR-141 led to a reduction of cell viability

    Article Snippet: To confirm the oncogenic functions of miR-141, a miR-141 precursor-expressing plasmid (pmR-ZsGreen1 vector, Clontech) was stably transfected into three advanced ovarian cancer cell lines: A2780CP (p53 mutated) (141-C2 and 141-C8), OVCA433 (p53 wildtype) (141-C5 and 141-C10) and SKOV3 (p53 deleted) (141-C1 and 141-C4) (Fig. , left panel ).

    Techniques: Real-time Polymerase Chain Reaction, Clone Assay, Over Expression, Inhibition, Tube Formation Assay, Plasmid Preparation

    KLF12 expression inversely correlates with miR-141 and exerts inhibitory effects on ovarian cancer tumorigenicity. a Representative pictures showing miR-141 expressions examined by ISH (dark blue staining) is inversely correlated with KLF12 expression detected by IHC (brown staining) in early and advanced ovarian cancers. (Magnification × 10; scale bar, 100 μm). b Overexpression of KLF12 in two ovarian cancer cells; OVCA433 and SKOV3 ( Upper ), significantly suppresses their cell growth rates (Day 3 vs Day 1) examined by XTT cell proliferation assay when compared the cell growth rate of their empty vector controls, VC. c Focus formation assay revealed that overexpression of KLF12 significantly inhibit the number of foci in OVCA433 and SKOV3 cultured in low serum medium for 14 days. d The soft agar assay showed that overexpression of KLF12 remarkably reduce the number and size of colonies formed in soft agar in OVCA433 and SKOV3 cells as compared with their empty vector controls. The above assays represent the error bars with mean ± SD of at least 3 independent experiments. e Western blot analysis revealed that three KLF12 stable clones were obtained from transfection of shRNAi of KLF12 in OVCA433. SC represents scrambled control. These results were obtained from at least three experiments. f XTT cell proliferation assay showed that there was a significant increase of cell growth rate in all three KLF12 knockdown clones as compared with the scramble control (SC). g The focus formation assay showed that there were two KLF12 knockdown clones (KD2 and KD4) had a significant increase in the number of foci

    Journal: Molecular Cancer

    Article Title: MicroRNA-141 enhances anoikis resistance in metastatic progression of ovarian cancer through targeting KLF12/Sp1/survivin axis

    doi: 10.1186/s12943-017-0582-2

    Figure Lengend Snippet: KLF12 expression inversely correlates with miR-141 and exerts inhibitory effects on ovarian cancer tumorigenicity. a Representative pictures showing miR-141 expressions examined by ISH (dark blue staining) is inversely correlated with KLF12 expression detected by IHC (brown staining) in early and advanced ovarian cancers. (Magnification × 10; scale bar, 100 μm). b Overexpression of KLF12 in two ovarian cancer cells; OVCA433 and SKOV3 ( Upper ), significantly suppresses their cell growth rates (Day 3 vs Day 1) examined by XTT cell proliferation assay when compared the cell growth rate of their empty vector controls, VC. c Focus formation assay revealed that overexpression of KLF12 significantly inhibit the number of foci in OVCA433 and SKOV3 cultured in low serum medium for 14 days. d The soft agar assay showed that overexpression of KLF12 remarkably reduce the number and size of colonies formed in soft agar in OVCA433 and SKOV3 cells as compared with their empty vector controls. The above assays represent the error bars with mean ± SD of at least 3 independent experiments. e Western blot analysis revealed that three KLF12 stable clones were obtained from transfection of shRNAi of KLF12 in OVCA433. SC represents scrambled control. These results were obtained from at least three experiments. f XTT cell proliferation assay showed that there was a significant increase of cell growth rate in all three KLF12 knockdown clones as compared with the scramble control (SC). g The focus formation assay showed that there were two KLF12 knockdown clones (KD2 and KD4) had a significant increase in the number of foci

    Article Snippet: To confirm the oncogenic functions of miR-141, a miR-141 precursor-expressing plasmid (pmR-ZsGreen1 vector, Clontech) was stably transfected into three advanced ovarian cancer cell lines: A2780CP (p53 mutated) (141-C2 and 141-C8), OVCA433 (p53 wildtype) (141-C5 and 141-C10) and SKOV3 (p53 deleted) (141-C1 and 141-C4) (Fig. , left panel ).

    Techniques: Expressing, In Situ Hybridization, Staining, Immunohistochemistry, Over Expression, Proliferation Assay, Plasmid Preparation, Tube Formation Assay, Cell Culture, Soft Agar Assay, Western Blot, Clone Assay, Transfection

    KLF12 is a direct target of miR-141. a The downstream targets of miR-141 were predicted by an in silico study using three bioinformatics algorithms (PicTar, Miranda, and TargetScanHuman 6.0). b Ontology analysis using miRNA_Targets database 22 identified those predicted targets are involved in metabolic process, biological regulation, localization and cellular process etc. c The putative miR-141 targets which may be associated with anoikis resistance of ovarian cancer cells are categorized into six functional aspects. The red highlighted genes are the novel targets, while the black color genes have been reported as the miR-141 direct targets. d Western blot analysis showed that enforced expression of miR-141 (+) could reduce, while depletion of endogenous miR-141 by anti-miR-141 (+) could enhance the expressions of KLF12 and SIK1 only as compared with their controls (−) in ovarian cancer cells. But the expressions of other putative downstream targets; FUS, E2F3 and MAP2K4 had little or no change when the level of miR-141 was altered. e Luciferase reporter assay was performed in HEK293 cells and showed that the 3’ UTR of KLF12 luciferase activity was significantly inhibited by miR-141 expression dependently. f A schematic diagram shows the putative binding sites for miR-141 on the whole 3'UTR region of KLF12. Transient transfection of miR-141 mitigated the expression of KLF12 3’UTR-luciferase reporter activity. The KLF12 3’UTR with C1 binding site showed the highest suppression by miR-141. g ( Left panel ) The schematic diagram shows the most conserved and common pairing of wild-type and its mutant target regions of KLF12 and miR-141. ( Right panel ) The bar chart shows that miR-141 remarkably reduced the wild-type, whereas the KLF12_3’UTR mutant showed no change in luciferase reporter activity. h QPCR showed that miR-141 could reduce the expression of KLF12 mRNA in ovarian cancer cell lines. i Stable expression of miR-141 significantly reduced the expression of KLF12 in A2780cp and OVCA433 cells, while depletion of miR-141 using anti-miR-141 restored the expression of KLF12 in SKOV3 cells

    Journal: Molecular Cancer

    Article Title: MicroRNA-141 enhances anoikis resistance in metastatic progression of ovarian cancer through targeting KLF12/Sp1/survivin axis

    doi: 10.1186/s12943-017-0582-2

    Figure Lengend Snippet: KLF12 is a direct target of miR-141. a The downstream targets of miR-141 were predicted by an in silico study using three bioinformatics algorithms (PicTar, Miranda, and TargetScanHuman 6.0). b Ontology analysis using miRNA_Targets database 22 identified those predicted targets are involved in metabolic process, biological regulation, localization and cellular process etc. c The putative miR-141 targets which may be associated with anoikis resistance of ovarian cancer cells are categorized into six functional aspects. The red highlighted genes are the novel targets, while the black color genes have been reported as the miR-141 direct targets. d Western blot analysis showed that enforced expression of miR-141 (+) could reduce, while depletion of endogenous miR-141 by anti-miR-141 (+) could enhance the expressions of KLF12 and SIK1 only as compared with their controls (−) in ovarian cancer cells. But the expressions of other putative downstream targets; FUS, E2F3 and MAP2K4 had little or no change when the level of miR-141 was altered. e Luciferase reporter assay was performed in HEK293 cells and showed that the 3’ UTR of KLF12 luciferase activity was significantly inhibited by miR-141 expression dependently. f A schematic diagram shows the putative binding sites for miR-141 on the whole 3'UTR region of KLF12. Transient transfection of miR-141 mitigated the expression of KLF12 3’UTR-luciferase reporter activity. The KLF12 3’UTR with C1 binding site showed the highest suppression by miR-141. g ( Left panel ) The schematic diagram shows the most conserved and common pairing of wild-type and its mutant target regions of KLF12 and miR-141. ( Right panel ) The bar chart shows that miR-141 remarkably reduced the wild-type, whereas the KLF12_3’UTR mutant showed no change in luciferase reporter activity. h QPCR showed that miR-141 could reduce the expression of KLF12 mRNA in ovarian cancer cell lines. i Stable expression of miR-141 significantly reduced the expression of KLF12 in A2780cp and OVCA433 cells, while depletion of miR-141 using anti-miR-141 restored the expression of KLF12 in SKOV3 cells

    Article Snippet: To confirm the oncogenic functions of miR-141, a miR-141 precursor-expressing plasmid (pmR-ZsGreen1 vector, Clontech) was stably transfected into three advanced ovarian cancer cell lines: A2780CP (p53 mutated) (141-C2 and 141-C8), OVCA433 (p53 wildtype) (141-C5 and 141-C10) and SKOV3 (p53 deleted) (141-C1 and 141-C4) (Fig. , left panel ).

    Techniques: In Silico, Functional Assay, Western Blot, Expressing, Luciferase, Reporter Assay, Activity Assay, Binding Assay, Transfection, Mutagenesis, Real-time Polymerase Chain Reaction