scholarly journals miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundMicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.MethodsThe miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed. ResultsIn vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.ConclusionsIn summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals MiR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jinchun Cong ◽  
Jian Gong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract Background MicroRNA (miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer. Methods The miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed. Results In vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study. Conclusions In summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundMicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.MethodsThe miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed.ResultsIn vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.ConclusionsIn summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals MiR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract Background: MicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer. Methods: The miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo , tumour growth and Wnt/β-catenin pathway-related proteins were also analysed. Results: In vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study. Conclusions: In summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals miR-200c /FUT4 axis prevents the migration, invasion and proliferation of colon cancer cells by downregulating Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Negative Control ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Ki 67 ◽  
Sw480 Cells ◽  
Related Proteins

Abstract Background To investigate the effects of miR-200c targeting fucosyltransferase 4 (FUT4) on the proliferation, migration and invasion of colon cancer cells and further to explore its mechanism. Methods The expression of miR-200c and FUT4 mRNA in Lovo and SW480 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analyzed by Pearson. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into Lovo and SW480 cells, and RT-PCR was used to analyze the effect of transfection. Cell counting kitcck-8 (CCK-8), cloning and transwell assays were used to detect the migration, invasion and proliferation of Lovo and SW480 cells, respectively. Immunofluorescence was used to analyze the expression of Ki-67 protein. Moreover, the expression of Wnt/β-catenin signaling pathway-related proteins were detected by western blot. Double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. Results Pearson results showed that miR-200c and FUT4 were negatively correlated in Lovo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibits the proliferation, migration and invasion of Lovo cells by down-regulating FUT4. The expression of Ki67 positive cells and Wnt/β-catenin signaling pathway-related proteins were reduced in miR-200c overexpression and FUT4 silencing groups. The scientific search and dual luciferase reporting system identified FUT4 was the target of miR-200c. Conclusion In conclusion, miR-200c overexpression inhibits FUT4 expression and down-regulates the Wnt/β-catenin signaling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

scholarly journals CircHMGCS1 is upregulated in colorectal cancer and promotes proliferation of colorectal cancer cells by targeting microRNA-503-5p

2019 ◽  
Vol 17 ◽  
pp. 205873921986955 ◽  
Author(s):  
Jingqing Dong ◽  
Jun Li ◽  
Jihui Luo ◽  
Weiqiang Wu
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Clinical Parameter ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Apoptosis Pathway ◽  
Colorectal Cancer Cells ◽  
And Migration ◽  
Related Proteins

This study aims to explore the regulatory mechanism of circHMGCS1/microRNA-503-5p (miR-503-5p) axis during colorectal cancer (CRC) development and progression. Real-time quantitative polymerase chain reaction (RT-qPCR) was applied to evaluate the expression of circHMGCS1 and miR-503-5p in CRC samples and their adjacent non-tumor specimen. Then, cell proliferation and cell apoptosis and migration and invasion of circHMGCS1-knocked down cells were further detected, using cell counting kit-8 (CCK-8), flow cytometry, Transwell assay, and western blotting assays. CircHMGCS1 was found to be significantly upregulated in CRC, and its high expression was closely correlated with the poor clinical parameter. In addition, the knockdown of circHMGCS1 could significantly inhibit CRC cells’ growth promoting apoptosis, as suggested by the expression of apoptosis pathway-related proteins, which changed consistently. Furthermore, miR-503-5p inhibitors were able to reverse the suppression of cell proliferation induced by silencing circHMGCS1. Therefore, circHMGCS1 might serve as a promising bio-marker and treatment target for CRC.

scholarly journals The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Correlation Analysis ◽  
Cancer Cells ◽  
Pearson Correlation ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Pearson Correlation Analysis ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundTo investigate the effects of miR-200c, which targets fucosyltransferase 4 (FUT4), on the proliferation, migration and invasion of colon cancer cells and to further explore its mechanism.MethodsWe assessed the miR-200c and FUT4 mRNA levels in LoVo and SW480 cells by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analysed by Pearson correlation analysis. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into LoVo and SW480 cells, and RT-PCR was used to analyse the transfection efficiency. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to detect the migration, invasion and proliferation of LoVo and SW480 cells. Immunofluorescence was used to analyse the expression of the Ki-67 protein. Moreover, the expression of Wnt/β-catenin signalling pathway-related proteins was detected by western blots. A double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin signalling pathway-related proteins were also analysed. ResultsPearson correlation analysis showed that miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A bioinformatics analysis and a dual luciferase reporting system identified FUT4 as the target of miR-200c. ConclusionsIn conclusion, miR-200c overexpression inhibits FUT4 expression and downregulates the Wnt/β-catenin signalling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

scholarly journals Long noncoding RNA AFAP1-AS1 promotes tumor progression and invasion by regulating the miR-2110/Sp1 axis in triple-negative breast cancer

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Xiaohui Zhang ◽  
Fangyuan Li ◽  
Yidong Zhou ◽  
Feng Mao ◽  
Yan Lin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Noncoding Rna ◽  
Triple Negative ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion

AbstractLong noncoding ribonucleic acids (LncRNAs) have been found to be involved in the proliferation, apoptosis, invasion, migration, and other pathological processes of triple-negative breast cancer (TNBC). Expression of the lncRNA actin filament-associated protein 1 antisense RNA1 (AFAP1-AS1) has been found to be significantly higher in TNBC than in other subtypes or in normal tissue samples, but the specific mechanism by which AFAP1-AS1 affects the occurrence and development of TNBC is yet to be revealed. In this study, we used Cell Counting Kit-8 (CCK-8), colony formation, wound healing migration, Transwell invasion, and nude mouse xenograft assays to confirm the role of AFAP1-AS1 in the proliferation, migration of TNBC cells in vitro and in vivo. In addition, we performed bioinformatics analyses, reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), western blot (WB), and dual-luciferase reporter assays (dual-LRA) to confirm interaction among AFAP1-AS1, micro-RNA 2110 (miR-2110), and Sp1 transcription factor (Sp1). We found that silencing AFAP1-AS1 and Sp1 or upregulating miR-2110 suppressed the proliferation, migration, and invasion of MDA–MB-231 and MDA–MB-468 cells in vitro as well as tumor growth in vivo. Mechanistically, the dual-LRA highlighted that miR-2110 was an inhibitory target of AFAP1-AS1, and that AFAP1-AS1 functioned as a miR-2110 sponge to increase Sp1 expression. AFAP1-AS1 silencing led to a reduction in Sp1 mRNA and protein levels, which could be reversed by joint transfection with miR-2110 inhibitor. Our findings demonstrated that AFAP1-AS1 could modulate the progression of breast cancer cells and affect tumorigenesis in mice by acting as a miR-2110 sponge, resulting in regulation of Sp1 expression. Therefore, AFAP1-AS1 could play a pivotal role in the treatment of TNBC.

scholarly journals circ_0000467 promotes the proliferation, metastasis, and angiogenesis in colorectal cancer cells through regulating KLF12 expression by sponging miR-4766-5p

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1415-1427
Author(s):  
Hui Chen ◽  
Chen Wu ◽  
Liang Luo ◽  
Yuan Wang ◽  
Fangxing Peng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Reaction Cell ◽  
Western Blot Assay

Abstract Background Circular RNAs have been identified as crucial players in the initiation and progression of cancers, including colorectal cancer (CRC). The Has_circ_0000467 (circ_0000467) expression has been found to be upregulated in CRC, but its function and mechanism remain unclear. Methods The expression levels of circ_0000467, microRNA-4766-5p (miR-4766-5p), and Krueppel-like factor 12 (KLF12) were examined using reverse transcription-quantitative polymerase chain reaction. Cell proliferation was analyzed by cell counting kit-8 assay and colony formation assay. The apoptosis was measured by flow cytometry. Transwell migration and invasion assays were applied to evaluate cell metastatic ability. Angiogenesis was detected using tube formation assay. All protein expressions were quantified by western blot assay. Dual-luciferase reporter assay was used to analyze intergenic binding. Xenograft models were constructed for the experiment of circ_0000467 in vivo. Results The expression of circ_0000467 was upregulated in CRC tissues and cells. Knockdown of circ_0000467 repressed cell proliferation, metastasis, and angiogenesis, but it induced apoptosis in CRC cells. circ_0000467 targeted miR-4766-5p and inhibited the expression of miR-4766-5p. Silencing of circ_0000467 inhibited CRC progression by upregulating miR-4766-5p. miR-4766-5p suppressed the expression of target gene KLF12 and KLF12 overexpression reversed the effects of miR-4766-5p on CRC cell behaviors. circ_0000467 positively regulated the expression of KLF12 by targeting miR-4766-5p. circ_0000467 downregulation in vivo reduced CRC tumorigenesis by regulating miR-4766-5p and KLF12. Conclusion circ_0000467 acted as an oncogene in CRC through regulating KLF12 expression by sponging miR-4766-5p. Therefore, circ_0000467 can be used as an effective target in CRC diagnosis and therapy.

scholarly journals MicroRNA-937 is overexpressed and predicts poor prognosis in patients with colon cancer

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Huiya Liu ◽  
Lin Ma ◽  
Ling Wang ◽  
Yizuo Yang
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cox Regression ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Prognostic Impact ◽  
Cancer Tissues

Abstract Background Colon cancer is a heterogeneous tumor and a leading cause of cancer-related mortality. MicroRNA (miRNA) has been proposed as the biomarker in cancers. The aim of this study was to investigate the clinical significance and potential functional role of miR-937 in colon cancer. Methods In the present study, reverse transcription-quantitative polymerase chain reaction (qRT-PCR) was conducted to examine the expression levels of miR-937 in colon cancer tissues and cell lines. Kaplan-Meier curve and Cox regression analyses were used to determine the prognostic impact of miR-937 on survival. Cell Counting Kit-8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. Results miR-937 was significantly upregulated in colon cancer tissues and cell lines. Clinical analysis results showed that miR-937 expression was associated with lymph node metastasis and TNM stage. Patients with high miR-937 expression predicted a shorter overall survival rate. Functionally, overexpression of miR-937 promoted cell proliferation, migration, and invasion, while inhibition of miR-937 inhibited these cellular behaviors in vitro. Conclusions These results suggested that miR-937 may act as a prognostic biomarker and a potential target for therapeutic strategy, as well as promote proliferation, migration, and invasion of colon cancer.

scholarly journals Long non-coding RNA AFAP1-AS1 promotes tumor progression and invasion by regulating the miR-2110/Sp1 axis in triple negative breast cancer

2020 ◽  
Author(s):  
Xiaohui Zhang ◽  
Fangyuan Li ◽  
Yidong Zhou ◽  
Feng Mao ◽  
Yan Lin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Bioinformatics Analyses

Abstract Background: LncRNAs have been proved to be involved in the proliferation, apoptosis, invasion, migration and other pathological processes of triple negative breast cancer (TNBC). And the expression level of LncRNA AFAP1-AS1 in TNBC was found to be significantly higher than that in other subtypes and normal tissue samples, but the specific mechanism of LncRNA AFAP1-AS1 affecting the occurrence and development of TNBC needs to be revealed.Methods: Cell Counting Kit-8 assays, colony formation assays, wound-healing migration, transwell invasion assays and nude mouse xenograft assays were used to confirm the role of LncRNA AFAP1-AS1 in the proliferation, migration of TNBC cells in vitro and in vivo. Bioinformatics analyses, quantitative polymerase chain reaction (qRT-PCR), western blot, and dual-luciferase assays were performed to confirm the interaction between between LncRNA AFAP1-AS1, miR-2110 and Sp1.Results: In the present study, the silencing of AFAP1-AS1 and Sp1 or the upregulation of miR-2110 would result in the suppression of proliferation, migration and invasion of MDA-MB-231 and MDA-MB-468 cells in vitro as well as tumor growth in vivo. Mechanistically, the dual-luciferase reporter assay highlighted that AFAP1-AS1 functioned as a miR-2110 sponge to increase Sp1 expression. AFAP1-AS1 silencing led to a reduction in Sp1 mRNA and protein levels, which could be reverse by the joint transfection of miR-2110 inhibitor.Conclusions: Our findings demonstrated that AFAP1-AS1 acts as a miR-2110 sponge in TNBC cells, resulting in the regulation of Sp1 expression. And the AFAP1-AS1/miR-2110/Sp1 axis modulated the proliferation, migration and invasion of breast cancer cells and affected the tumorigenesis in mice.

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