LncRNA LUCAT1/miR-181a-5p axis promotes proliferation and invasion of breast cancer via targeting KLF6 and KLF15

Abstract Background Long non-coding RNAs (lncRNAs) are novel regulatory molecules in breast cancer development. LncRNA LUCAT1 is a potential tumor promoter in human cancers. In this study, we aimed to explore the role of LUCAT1 in human breast cancer tissues and cells. Methods A total of 31 breast cancer patients who underwent tumor resection, but without chemo- or radiotherapy or acute lung/heart/kidney diseases, provided tumor and adjacent normal tissues. Bioinformatic analysis, qRT-PCR, and luciferase reporter assay were carried out during the study. Results qRT-PCR analysis indicated that, compared with the adjacent tissues and MCF-10A normal breast epithelial cells, LUCAT1 was markedly up-regulated in the breast cancer tissues and five BC cell lines, including MDA-MB-231, MDA-MB-468, MDA-MB-435, SKBR3, and MCF-7. The knockdown of LUCAT1, through the transfection of small interfering RNA (siRNA) specific to LUCAT1, resulted in inhibition of proliferation in breast cancer cells. The expression levels of miR-181a-5p were decreased in the breast cancer tissues and five BC cell lines. Bioinformatic analysis and luciferase reporter assay suggested the interaction between miR-181a-5p and LUCAT1. In addition, the effects of LUCAT1 on promoting cell proliferation were attenuated by overexpression of miR-181a-5p through the transfection of miR-181a-5p mimic. Moreover, bioinformatics and luciferase reporter assay confirmed that miR-181a-5p targeted the 3′-UTR region of KLF6 and KLF15 mRNA, which were two tumor suppressor genes. LUCAT1/miR-181a-5p axis regulated the expression of KLF6 and KLF15 both in vitro and in vivo. Conclusions Our data indicate that LUCAT1/miR-181a-5p axis can serve as a novel therapeutic target in breast cancer.

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Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression

Breast Cancer Research ◽

10.1186/s13058-021-01497-6 ◽

2022 ◽

Vol 24 (1) ◽

Author(s):

Lingjiao Meng ◽

Sheng Chang ◽

Yang Sang ◽

Pingan Ding ◽

Liuxin Wang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Cancer Progression ◽

Breast Cancer Cells ◽

Breast Cancer Progression ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Qrt Pcr ◽

Cancer Tissues

Abstract Background A growing body of evidence indicates that abnormal expression of circular RNAs (circRNAs) plays a crucial role by acting as molecular sponges of microRNAs (miRNAs) in various diseases, including cancer. In this study, we explored whether circCCDC85A could function as a miR-550a-5p sponge and influence breast cancer progression. Methods We detected the expression of circCCDC85A in breast cancer tissues and cells using fluorescence in situ hybridization (FISH) and quantitative reverse transcription polymerase chain reaction (qRT-PCR). CCK-8 and colony formation assay were used to detect the proliferative ability of breast cancer cells. Wound healing assay and transwell migration and invasion assays were used to detect the migrative and invasive abilities of breast cancer cells. We also examined the interactions between circCCDC85A and miR-550a-5p using FISH, RNA-binding protein immunoprecipitation (RIP), and luciferase reporter assay. Moreover, we performed luciferase reporter assay, qRT-PCR, and Western blot to confirm the direct targeting of miR-550a-5p to MOB1A. Results The expression of circCCDC85A in breast cancer tissues was obviously lower than that in normal breast tissues. Over-expression of circCCDC85A substantially inhibited the proliferative, migrative, and invasive ability of breast cancer cells, while knocking down of circCCDC85A enhanced the aforementioned properties of breast cancer cells. Moreover, enforced expression of circCCDC85A inhibits the oncogenic activity of miR-550a-5p and increases the expression of MOB1A targeted by miR-550a-5p. Further molecular mechanism research showed that circCCDC85A may act as a molecular sponge for miR-550a-5p, thus restoring miR-550a-5p-mediated targeting repression of tumor suppressor MOB1A in breast cancer cells. Conclusion Our findings provide novel evidence that circCCDC85A inhibits the progression of breast cancer by functioning as a molecular sponge of miR-550a-5p to enhance MOB1A expression.

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Long Non-Coding RNA ANRIL Promotes Doxorubicin Resistance in Triple-Negative Breast Cancer via Suppressing Glycolysis Through the MicroRNA-125a/ENO Pathway

10.21203/rs.3.rs-1062354/v1 ◽

2021 ◽

Author(s):

Jianli Ma ◽

Wenhui Zhao ◽

Han Zhang ◽

Zhong Chu ◽

Huili Liu ◽

...

Keyword(s):

Breast Cancer ◽

Drug Resistance ◽

Cell Lines ◽

Triple Negative Breast Cancer ◽

Triple Negative ◽

Active Role ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Tnbc Cell

Abstract BackgroundBreast cancer is the main cause of death among women worldwide. More and more long non-coding RNAs (lncRNAs) have been identified as oncogenes or tumor suppressors during cancer development. However, whether ANRIL is involved in drug resistance in triple-negative breast cancer (TNBC) has not been investigated. MethodsLuciferase reporter assay was conducted to verify the binding of miR-125a and ANRIL. RT-PCR and western blot were performed to detect the expression of miR-125a, ANRIL and ENO1. Gene silence and overexpression experiments as well as CCK-8 and colony formation assays on TNBC cell lines were performed to determine the regulation of molecular pathways. Glycolysis analysis was performed with Seahorse extracellular flux methodology. ResultsANRIL expression in TNBC patients and TNBC cells was examined and we found that ANRIL expression was upregulated in both TNBC patients and TNBC cell lines. Knockdown of ANRIL increased the cytotoxic effect of ADR and inhibited HIF-1α-dependent glycolysis in TNBC cells. In addition, we found that ANRIL negatively regulated miR-125a expression in TNBC cell lines. Besides, a dual-luciferase reporter assay proved ANRIL functioned as a sponger of miR-125a. Further investigation revealed that ENO1 was a target of miR-125a and positively regulated by ANRIL in TNBC cells. Additionally, ANRIL upregulation reversed miR-125-mediated inhibition on HIF-1α-dependent glycolysis in TNBC cells. More notably, 2-deoxy-glucose (2-DG) attenuated ANRIL-induced increase of drug resistance in TNBC cells. ConclusionsTaken together, our study was the first to identify that knockdown of ANRIL plays an active role in overcoming the drug resistance in TNBC by inhibiting glycolysis through the miR-125a/ENO1 pathway, which maybe serve useful for the development of novel therapeutic targets.

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miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4

10.21203/rs.3.rs-36644/v2 ◽

2020 ◽

Author(s):

Bo Lin ◽

Enyi Shi ◽

Qiu Jin ◽

Wenhui Zhao ◽

Juan Wang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Quantitative Polymerase Chain Reaction ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Proliferation And Metastasis ◽

Cancer Tissues ◽

Mcf 7

Abstract Background:Dysregulation of miRNAs is involved in carcinogenesis of breast and may be used as prognostic biomarkers and therapeutic targets during cancer process. The purpose of this study was to explore the effect of miR-105-3p on tumourigenicity of breast cancer and its underlying molecular mechanisms.Methods:Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was applied to detect the expression of miR-105-3p in breast cancer tissues and cell lines. The impacts of miR-105-3p on proliferation, migration, invasion and apoptosis of human breast cancer cells (MCF-7 and ZR-75-30) were evaluated by CCK-8, transwell chamber assay, TUNEL assay and western blot assay, respectively. Besides, bioinformatics and luciferase reporter assay were used to find out the target genes of miR-105-3p.Results:The expression of miR-105-3p was elevated in breast cancer tissues and increased along with tumor severity. Downregulation of miR-105-3p could inhibit cell proliferation, suppress cell migration/invasion, and promote cell apoptosis in MCF-7 and ZR-75-30 cells. Furthermore, Golgi integral membrane protein 4 (GOLIM4) was identified to be the direct target gene of miR-105-3p by bioinformatics and luciferase reporter assay. In addition, silencing of GOLIM4 could restore the anti-breast cancer effects induced by miR-105-3p downregulation.Conclusions:miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4, which provides a new target for the prevention and treatment of breast cancer.

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miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4

10.21203/rs.3.rs-36644/v3 ◽

2021 ◽

Author(s):

Bo Lin ◽

Enyi Shi ◽

Qiu Jin ◽

Wenhui Zhao ◽

Juan Wang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Quantitative Polymerase Chain Reaction ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Proliferation And Metastasis ◽

Cancer Tissues ◽

Mcf 7

Abstract Background: Dysregulation of miRNAs is involved in carcinogenesis of breast and may be used as prognostic biomarkers and therapeutic targets during cancer process. The purpose of this study was to explore the effect of miR-105-3p on tumourigenicity of breast cancer and its underlying molecular mechanisms.Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was applied to detect the expression of miR-105-3p in breast cancer tissues and cell lines. The impacts of miR-105-3p on proliferation, migration, invasion and apoptosis of human breast cancer cells (MCF-7 and ZR-75-30) were evaluated by CCK-8, transwell chamber assay, TUNEL assay and western blot assay, respectively. Besides, bioinformatics and luciferase reporter assay were used to find out the target genes of miR-105-3p.Results: The expression of miR-105-3p was elevated in breast cancer tissues and increased along with tumor severity. Downregulation of miR-105-3p could inhibit cell proliferation, suppress cell migration/invasion, and promote cell apoptosis in MCF-7 and ZR-75-30 cells. Furthermore, Golgi integral membrane protein 4 (GOLIM4) was identified to be the direct target gene of miR-105-3p by bioinformatics and luciferase reporter assay. In addition, silencing of GOLIM4 could restore the anti-breast cancer effects induced by miR-105-3p downregulation.Conclusions: MiR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4, which provides a new target for the prevention and treatment of breast cancer.

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Mcl-1 Is a Novel Target of miR-26b That Is Associated with the Apoptosis Induced by TRAIL in HCC Cells

BioMed Research International ◽

10.1155/2015/572738 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 10

Author(s):

Chunlin Jiang ◽

Jianting Long ◽

Baoxian Liu ◽

Xiaoyan Xie ◽

Ming Kuang

Keyword(s):

Cell Lines ◽

Bioinformatic Analysis ◽

Negative Regulator ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Mrna Transfection ◽

Novel Target ◽

Hcc Cells

Aim. To investigate the role of miR-26b and Mcl-1 in TRAIL-inducing cell death in hepatocellular carcinoma.Methods. The expression of miR-26b and Mcl-1 in HCC was detected by RT-qPCR and western blot. The regulation of Mcl-1 by miR-26b was determined by luciferase reporter assay. MTT and flow cytometry were employed to detect the cell viability and apoptosis.Results. miR-26b is commonly downregulated in HCC cell lines compared with the LO2 cell line. In contrast, the Mcl-1 expression is upregulated in HCC cell lines. Bioinformatic analysis identified a putative target site in the Mcl-1 mRNA for miR-26b and luciferase reporter assay showed that miR-26b directly targeted the 3′-UTR (3′-Untranslated Regions) of Mcl-1 mRNA. Transfection of miR-26b mimics suppressed Mcl-1 expression in HCC cells and sensitized the cancer cells to TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) cytotoxicity. In addition, transfection of HCC cells with Mcl-1 expression plasmid abolished the sensitization effect of miR-26b to TRAIL-inducing apoptosis.Conclusions. Our study showed that miR-26b was a negative regulator of Mcl-1 gene and sensitized TRAIL-inducing apoptosis in HCC cells, suggesting that the miR-26b-Mcl-1 pathway might be a novel target for the treatment of HCC.

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MicroRNA-449b-5p suppresses cell proliferation, migration and invasion by targeting TPD52 in nasopharyngeal carcinoma

The Journal of Biochemistry ◽

10.1093/jb/mvz057 ◽

2019 ◽

Vol 166 (5) ◽

pp. 433-440 ◽

Cited By ~ 6

Author(s):

Wei Yin ◽

Lei Shi ◽

Yanjiao Mao

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Cell Lines ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Reporter Assay ◽

Western Blot Assay ◽

Qrt Pcr ◽

Dual Luciferase Reporter Assay

Abstract Nasopharyngeal carcinoma (NPC) is an important type of head and neck malignant cancer with geographical distribution. MicroRNA-449b-5p (miR-449b-5p) is related to the development of various cancers, while its function in NPC remains unknown. The present study aimed to investigate the role and target gene of miR-449b-5p in NPC. Expressions of miR-449b-5p in NPC cell lines and clinical tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was determined by MTT and colony formation assays. Migration and invasion abilities after different treatment were evaluated by wound healing and Transwell assays, respectively. Dual-luciferase reporter assay was performed to explore the relationship between miR-449b-5p and tumour protein D52 (TPD52). TPD52 expression was determined by qRT-PCR and western blot assay. miR-449b-5p was significantly downregulated in NPC cell lines and clinical tissues than the matched control. Overexpression of miR-449b-5p inhibited proliferation, migration and invasion of NPC cells. Dual-luciferase reporter assay indicated that miR-449b-5p directly targeted TPD52. Furthermore, shRNA-mediated downregulation of TPD52 rectified the promotion of cell migration and invasion by miR-449b-5p inhibition. In conclusion, the present study suggests that miR-449b-5p, as a novel tumour-suppressive miRNA against NPC, inhibits proliferation, migration and invasion of NPC cells via inhibiting TPD52 expression.

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MicroRNA-665 facilitates cell proliferation and represses apoptosis through modulating Wnt5a/β-Catenin and Caspase-3 signaling pathways by targeting TRIM8 in LUSC

Cancer Cell International ◽

10.1186/s12935-021-01913-z ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Tian-Jun Chen ◽

Qi Zheng ◽

Fei Gao ◽

Tian Yang ◽

Hui Ren ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Cell Growth ◽

Signaling Pathway ◽

Cell Lines ◽

Caspase 3 ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Qrt Pcr

Abstract Background MicroRNAs (miRNAs) are involved in the oncogenesis, development and transformation of lung squamous cell carcinoma (LUSC). miR-665 is clinically significant and acts as a pivotal function in some cancers. Nevertheless, the effects and the potential mechanisms of miR-665 in human LUSC are still unknown. Methods To analyse the clinical significant of miR-665 in human LUSC, quantitative real-time PCR (qRT-PCR) was use to measure miR-665 expression in LUSC specimen tissues and cell lines. Tripartite motif 8 (TRIM8) was verified a target of miR-665 by performing bioinformatic prediction and luciferase reporter assay. The expression levels of TRIM8 were examined through qRT-PCR and Western blotting in LUSC specimen tissues. CCK8 assay was fulfilled for analyzing the function in LUSC cell proliferation. Flow cytometry was used to detect cell and apoptosis. TRIM8 silencing and overexpression further verified the biological effects as those caused by miR-665. Results Here we reported that miR-665 expression was upregulated in LUSC specimen tissues and cell lines. High miR-665 levels were related to differentiation, tumor size and TNM stage. miR-665 mimics facilitated LUSC cell growth and cell cycle G1-S transition and repressed apoptosis. miR-665 inhibitor suppressed cell proliferation and G1-S transition and promoted apoptosis. miR-665 expression was negatively correlated with TRIM8 mRNA expression in LUSC. Luciferase reporter assay confirmed that TRIM8 was a direct target gene of miR-665. miR-665 mimics downregulated the TRIM8 levels, and miR-665 inhibitor upregulated the TRIM8 levels in LUSC cells. Particularly, silencing TRIM8 led to the similar effects of miR-665 mimics in LUSC cells. Overexpression of TRIM8 inhibited LUSC cell proliferation in vitro and in vivo. Furthermore, miR-665 promoted LUSC cell proliferation through facilitating the Wnt5a/β-catenin signaling pathway and restrained apoptosis via inhibiting Caspase-3 signaling pathway, whereas TRIM8 suppressed cell growth by repressing the Wnt5a/β-catenin signaling pathway and induced apoptosis through activating Caspase-3 signaling pathway. Conclusions The current study demonstrates that miR-665 facilitates LUSC cell proliferation and cell cycle transition by regulation of the Wnt5a/β-Catenin signaling pathway and represses cell apoptosis via modulation of Caspase-3 signaling pathway by directly targeting TRIM8. These findings suggest that miR-665 might be a potential new target for LUSC therapy.

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Silencing of miR-200a-3p Inhibits Proliferation, Invasion and Migration of Breast Cancer Cells by Targeting Ephrin-A5

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2690 ◽

2021 ◽

Vol 11 (7) ◽

pp. 1227-1235

Author(s):

Yongmei Zhang ◽

Huayi Zhang ◽

Gang Guo

Keyword(s):

Breast Cancer ◽

Cell Proliferation ◽

Cell Lines ◽

The Cancer Genome Atlas ◽

Luciferase Reporter Assay ◽

Cell Counting ◽

Luciferase Reporter ◽

Reporter Assay ◽

Invasion And Migration ◽

And Migration

Increasing evidence suggests microRNAs (miRs/miRNAs) exert considerable functions in the pathogenesis of malignancies, including breast cancer (BC). The miR-200a-3p has previously been reported to promote tumorigenesis in different types of cancers. The present study aimed to investigate the potential role of and possible mechanisms of miR-200a-3p in BC. In this study miR-200a-3p and ephrin-A5 (EFNA5) expression in tissues of patients with BC was analyzed using The Cancer Genome Atlas (TCGA) database. And several BC cell lines were employed to determine the expression levels of miR-200a-3p and EFNA5. Then, miR-200a-3p expression was silenced by transfection with miR-200a-3p inhibitor. Cell proliferation was evaluated using a cell counting kit-8 kit and colony formation assay, whilst cell invasion and migration were detected using Transwell and wound healing assays, respectively. Then, the potential interaction between miR-200a-3p and EFNA5 was verified using luciferase reporter assay. Subsequently, rescue assays were conducted by co-transfection with miR-200a-3p inhibitor and short hairpin RNA (shRNA) targeted against EFNA5 (shRNA-EFNA5) to study the effects of TTN-AS1 and miR-211-5p on BC development. Results indicated that miR-200a-3p expression was significantly upregulated while EFNA5 was notably downregulated in BC tissues and cell lines. Cells transfected with miR-200a-3p inhibitor presented lower abilities of cell proliferation, invasion and migration. Moreover, the luciferase reporter assay confirmed that EFNA5 was a direct target of miR-200a-3p. And EFNA5 silencing reversed the inhibitory effects of miR-200a-3p inhibitor on proliferation, invasion and migration of BC cells. Taken together, these findings revealed that miR-200a-3p silencing inhibits proliferation, invasion and migration of BC cells by targeting EFNA5, which provides insights into the regulatory mechanism of BC and new strategies for developing therapeutic interventions for this disease.

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LncRNA MIR4435-2HG Promotes Proliferation, Migration, Invasion and EMT Via Targeting miR-22- 3p/TMEM9B in Breast Cancer

10.21203/rs.3.rs-860533/v1 ◽

2021 ◽

Author(s):

Jing Ke ◽

Quhui Wang ◽

Wei Zhang ◽

Haijun Mei

Keyword(s):

Breast Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Cancer Cell Lines ◽

Luciferase Reporter ◽

Breast Cancer Cell Lines ◽

Reporter Assay ◽

Cancer Tissues ◽

Dual Luciferase Reporter Assay

Abstract Background: Breast cancer, as the malignancy with the highest incidence rate and mortality rate in women, seriously threatens human life and health. Pieces of evidence have suggested that long non-coding RNAs (lncRNAs) possess important effects on regulating the occurrence and development of breast cancer.Results: In the present study, MIR4435-2HG was highly expressed in breast cancer tissues and cells. Down-regulation of MIR4435-2HG inhibited the viability, proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of breast cancer cell lines by Cell Counting Kit-8 (CCK-8), colony formation, transwell migration and invasion, immunofluorescence and western blot assays. Dual-luciferase reporter assay and RNA pull-down analysis confirmed that miR-22-3p was a target of MIR4435-2HG. Over-expression of MicroRNA-22-3p (miR-22-3p) obviously inhibited the viability, proliferation, migration, invasion and EMT of breast cancer cell lines. Transmembrane protein 9 domain family member B (TMEM9B) was up-regulated in breast cancer tissues and cell lines. Dual-luciferase reporter assay confirmed that TMEM9B was a target of miR-22-3p. TMEM9B inhibition partially restored the effects of MIR4435-2HG/miR-22-3p on the viability, proliferation, migration, invasion and EMT of breast cancer cell lines.Conclusions: MIR4435-2HG potentially played a tumor-promoting role in the occurrence and development of breast cancer, which might be achieved by regulating the miR-22-3p/TMEM9B axis.

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miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4

10.21203/rs.3.rs-36644/v1 ◽

2020 ◽

Author(s):

Bo Lin ◽

Enyi Shi ◽

Qiu Jin ◽

Wenhui Zhao ◽

Juan Wang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Quantitative Polymerase Chain Reaction ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Proliferation And Metastasis ◽

Cancer Tissues ◽

Mcf 7

Abstract Background: Dysregulation of miRNAs is involved in carcinogenesis of breast cancer and may be used to prognostic biomarkers and therapeutic target during cancer process. The purpose of this study was to explore the effects of miR-105-3p on tumourigenicity of breast cancer and its underlying molecular mechanisms.Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was applied to detect the miR-105-3p in breast cancer tissues. The impacts of miR-105-3p on proliferation, migration, invasion and apoptosis of human breast cancer lines (MCF-7 and ZR-75-30) were evaluated by CCK-8, transwell chamber assay, TUNEL assay and western blot assay, respectively. Besides, bioinformatics and luciferase reporter assay were used find out the targeted gene of miR-105-3p.Results: The expression of miR-105-3p was elevated in breast cancer tissues and increased with tumor severity. Downregulation of miR-105-3p could inhibit cell proliferation, suppress cell migration/invasion, and promote cell apoptosis in MCF-7 and ZR-75-30 cells. Furthermore, Golgi integral membrane protein 4 (GOLIM4) was identified to be the direct target gene of miR-105-3p by bioinformatics and luciferase reporter assay. In addition, silencing of GOLIM4 could restore the anti-breast cancer effects induced by miR-105-3p downregulation.Conclusions: miR-105-3p acts an oncogene to promote proliferation and metastasis of breast cancer cell by targeting GOLIM4, which provides a new target for the prevention and treatment of breast cancer.

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