scholarly journals HAND2-AS1 Works as a ceRNA of miR-3118 to Suppress Proliferation and Migration in Breast Cancer by Upregulating PHLPP2

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Guolei Dong ◽  
Xiaorui Wang ◽  
Yan Jia ◽  
Yongsheng Jia ◽  
Weipeng Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Antisense Rna ◽  
Migration And Invasion ◽  
Downstream Target ◽  
Vital Functions ◽  
And Migration ◽  
Detailed Function ◽  
Selection Of ◽  
Proliferation And Migration

Large quantities of long noncoding RNAs (lncRNAs) have been verified to exert vital functions in the process of breast cancer (BC). lncRNA heart and neural crest derivatives expressed 2-antisense RNA 1 (HAND2-AS1) was reported to suppress the development of several cancers. However, its detailed function in BC remained unclear. In the current study, HAND2-AS1 was discovered to be low expressed in BC cell lines, and overexpression of HAND2-AS1 could repress proliferation, migration, and invasion but facilitate apoptosis in BC cells. Moreover, HAND2-AS1 was found to act as a sponge of miR-3118 which was detected to be upregulated in BC cell lines. miR-3118 depletion could constrict the progression of BC. HAND-AS1 hindered the course of BC by reducing the expression of miR-3118. Besides, PHLPP2 was treated as a downstream target of miR-3118 under the selection of RNA pull-down assays. HAND2-AS1 inhibited the process of BC by enhancing expression of PHLPP2. In summary, our study testified that HAND2-AS1 suppressed BC growth by targeting the miR-3118/PHLPP2 axis, indicating that HAND2-AS1 could be regarded as a potential target for BC treatment.

scholarly journals USP13 Regulates the Breast Tumor Proliferation and Migration through the Stabilization of PDCD4 Protein

2021 ◽  
Author(s):  
Jun Tian ◽  
Bei Li ◽  
Jing Qiao ◽  
Xinfeng Pang ◽  
Xiaojing Yue
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Tumor ◽  
Soft Agar ◽  
Tumor Proliferation ◽  
Soft Agar Assay ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Abstract Background: Programmed cell death protein 4 (PDCD4), which serves as a tumor suppressor protein, plays a important role in cell proliferation,apoptosis, cell migration and DNA-damage response.However, the exact mechanism for the deubiquitination of PDCD4 remain unclear.Methods: Western blotting was used to detect the expression of PDCD4 in the breast cancer tissues and BC cell lines. We identified the potential PDCD4 associated deubiquitinase by RNAi screening. GST-Pull down and domain-mapping analysis were used to reveal that USP13 and PDCD4 directly interact with each other.Flow cytometry was used to detect the changes of G1 to S phase. Soft agar assay was used to measure the changes of the cell proliferation efficiency.Results: The expression of PDCD4 was decreased in the breast cancer tissues and BC cell lines. USP13 as a potential PDCD4 associated deubiquitinase. USP13 physically interacted with PDCD4 and greatly increased the steady state of PDCD4 through the ubiquitin-proteasome pathway.Importantly, silencing of the USP13 facilitated cell cycle from G1 to Sphase, promoted breast tumor cells proliferation and migration through downregulation of PDCD4. Conclusions: Together, these results suggest that USP13 plays an important role in the breast tumor proliferation and migration through modulating PDCD4 stability.

Sprouty4 interferes with cell proliferation and migration of breast cancer-derived cell lines

Tumor Biology ◽  
2014 ◽  
Vol 35 (5) ◽  
pp. 4447-4456 ◽  
Author(s):  
Vanita Vanas ◽  
Elsa Mühlbacher ◽  
Rosana Kral ◽  
Hedwig Sutterlüty-Fall
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Knockdown of lncRNA FEZF1-AS1 Inhibits metastasis of Osteosarcoma Cells by miR-4456/GALNT10

2020 ◽  
Author(s):  
Zhenxing Si ◽  
Shifeng Zhou ◽  
Zilong Shen ◽  
Feiyu Luan ◽  
jinglong yan
Keyword(s):  
Cell Lines ◽  
Antisense Rna ◽  
Malignant Tumors ◽  
Luciferase Assay ◽  
Cell Infiltration ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Therapeutic Development ◽  
And Migration ◽  
Tissue Specimens

Abstract Background: Osteosarcoma (OS) is among the malignant tumors with high mortality and low survival, especially in children and adolescents. Research shows that LncRNA FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) enhances osteosarcoma progression. Nevertheless, the function and mechanism of FEZF1-AS1 in metastasis of OS remains unclear.Methods: We used qRT-PCR to assay for the expression of FEZF1-AS1, miR-4456, and GALNT10 in OS tissue specimens and cell lines. We also investigated the progression of OS through metastasis using the wound healing and Transwell assays. Moreover, we used the dual-luciferase reporter test, RIP assays, and western blot to validate whether FEZF1-AS1 serves as a competing endogenous RNA (ceRNA), modulating the expression of GALNT10 through sponging miR-4456 in OS.Results: FEZF1-AS1 was up modulated in OS tissues. Silencing FEZF1-AS1 repressed OS cell migration and invasion. microRNA-4456 (miR-4456) was involved in FEZF1-AS1-induced migration and invasion. miR-4456 was down modulated in OS tissue specimens and cell lines. Functionally, the up modulation of miR-4456 reversed the facilitative influence of FEZF1-AS1 on OS cell infiltration and migration. Mechanically, FEZF1-AS1 interacted with miR-4456 in a reciprocal suppressed manner. Moreover, miR-4456 targets GALNT10 via the Luciferase assay. Besides, the up modulation of GALNT10 reversed the migration and invasion inhibited by FEZF1-AS1 knockdown. Silencing of FEZF1-AS1 inhibits OS cell infiltration and migration through miR-4456 /GALNT10 sponging.Conclusion: Herein, we demonstrated that FEZF1-AS1 is a prospective bio signature of metastasis in OS patients. Mechanistically, we showed that the FEZF1-AS1/miR-4456/GALNT10 axis is a target for novel therapeutic development for OS.

scholarly journals LncRNA RNA Component of Mitochondrial RNA-Processing Endoribonuclease Promotes AKT-Dependent Breast Cancer Growth and Migration by Trapping MicroRNA-206

2021 ◽  
Vol 9 ◽  
Author(s):  
Yingdan Huang ◽  
Bangxiang Xie ◽  
Mingming Cao ◽  
Hua Lu ◽  
Xiaohua Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Rna Processing ◽  
Cancer Development ◽  
Mitochondrial Rna ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Downstream Target ◽  
And Migration ◽  
Proliferation And Migration

The RNA component of mitochondrial RNA-processing endoribonuclease (RMRP) was recently shown to play a role in cancer development. However, the function and mechanism of RMRP during cancer progression remain incompletely understood. Here, we report that RMRP is amplified and highly expressed in various malignant cancers, and the high level of RMRP is significantly associated with their poor prognosis, including breast cancer. Consistent with this, ectopic RMRP promotes proliferation and migration of TP53-mutated breast cancer cells, whereas depletion of RMRP leads to inhibition of their proliferation and migration. RNA-seq analysis reveals AKT as a downstream target of RMRP. Interestingly, RMRP indirectly elevates AKT expression by preventing AKT mRNA from miR-206-mediated targeting via a competitive sequestering mechanism. Remarkably, RMRP endorses breast cancer progression in an AKT-dependent fashion, as knockdown of AKT completely abolishes RMRP-induced cancer cell growth and migration. Altogether, our results unveil a novel role of the RMRP-miR-206-AKT axis in breast cancer development, providing a potential new target for developing an anti-breast cancer therapy.

Silibinin Inhibit Cell Migration through Downregulation of RAC1 Gene Expression in Highly Metastatic Breast Cancer Cell Line

Drug Research ◽  
2020 ◽  
Vol 70 (10) ◽  
pp. 478-483
Author(s):  
Hamed Esmaeil Lashgarian ◽  
Vahid Adamii ◽  
Vajihe Ghorbanzadeh ◽  
Leila Chodari ◽  
Fayze Kamali ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Migration And Invasion ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Triple negative breast cancer is the most invasive breast cancer subtype and possesses poor prognosis and survival. Rho GTPase famil, especially Rac1 participates in a number of signaling events in cells with crucial roles in malignancy, migration and invasion of tumor cells. Silibinin, a flavonoid antioxidant from milk thistle has attracted attention in the recent decades for chemoprevention and chemotherapy of tumor cells. In this study, the effect of silibinin on the migration capacity of MDA-MB-231 cells, a highly metastatic human breast cancer cell line was investigated by evaluation of Rac1 expression. Method MTT wound healing and transwell assays were performed to evaluate the effects of silibinin on proliferation and migration of MDA-MB-231 cells. In addition, the influence of the silibinin on the expression of Rac1mRNAs was assessed by RT-PCR. Results Results indicated significant dose-dependent inhibitory effect of silibinin on proliferation and migration of MDA-MB-231 cells. It significantly inhibited the expression of Rac1 mRNA. Conclusion In conclusion, the results demonstrate that the silibinin can be used as an experimental therapeutic for the management of TNBC metastatic cancer.

scholarly journals The evaluation of Melatonin and EGF interaction on breast cancer metastasis

2021 ◽  
Author(s):  
Maryam Akbarzadeh
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Metastasis ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Breast Cancer Patients ◽  
Mcf7 Cells ◽  
And Migration

Abstract Background Breast cancer is currently one of the most common types of cancer in women, and metastasis is the first cause of death in breast cancer patients. The epidermal growth factor (EGF) increases the invasion, growth, and migration of cancer cells. In the present study, melatonin, as a natural hormone, in EGF-induced tumor metastasis, was investigated. Methods First, MDA-MB-231 and MCF7 cells were cultured, and then the effects of melatonin on cell viability were determined by MTT assay. Transwell invasion assay was employed to identify the invasiveness of these breast cancer cell lines. Real-time RT-PCR then investigated the expression of MMP9 and MMP2. Cell proliferation was also determined under EGF and melatonin treatment using Ki67 assessment by flow cytometry. Results The rate of invasion and migration of EGF-treated cells increased in both groups, in which melatonin caused increased invasion by EGF in MCF7 cells. MMP9 and MMP2 expression increased significantly in both cell lines under EGF treatment, and melatonin increased these genes' expression in both cell lines (p <0.05). EGF increased the MMP9 and MMP2 gene expression, and melatonin increases EGF-induced expression(p <0.05). The EGF reduced the expression of the Ki67 protein in the MCF7 cell line, which was negatively affected by Melatonin and EGF. In contrast, along with Melatonin, EGF did not affect the proliferation of the MDA-MB-231 cell line. Conclusions Our results show that melatonin, as a natural compound, can increase the effects of EGF in the proliferation, migration, and invasion of cancer cells at low dosages.

scholarly journals miR-425 suppresses EMT and inhibits the development of TNBC (triple-negative breast cancer) by targeting TGF-β 1/SMAD 3 signaling pathway

2018 ◽  
Author(s):  
Yingping Liu ◽  
Hongfei Qiao ◽  
Jinglong Chen
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Mesenchymal Cell ◽  
Cell Proliferation And Migration ◽  
Tnbc Cell ◽  
Tumor Tissues ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

AbstractBackgroundEMT has the crucial effect on the progression and metastasis of tumor. This work will elucidate the role of miR-425 in EMT and development of TNBC.MethodsThe differential miRNA expression among non-tumor, para-tumor (adjacent tissue of tumor) and tumor tissues was analyzed. The luciferase activities of TGF-β1 3’ UTR treated with miR-425 were determined. Then human breast cancer cell lines were dealt with mimics or inhibitors of miR-425, and then the cell proliferation and migration, invasion ability were assessed. The expression of TGF-β1 and markers of epithelial cell and mesenchymal cell were analyzed. The influences of miR-425 on development of TNBC through inducing EMT by targeting TGF-β 1 and TGF-β1/SMAD3 signaling pathway in TNBC cell lines were investigated. Furthermore, Xenograft mice were used to explore the potential roles of miR-425 on EMT and development of TNBC in vivo.ResultsCompared with non-tumor tissues, 9 miRNAs were upregulated and 3 miRNAs were down-regulated in tumor tissues. The relative expression of miR-425 in tumor tissues was obviously much lower than that in para-tumor and non-tumor tissues. MiR-425 suppressed TGF-β1 expression, additionally inhibited expression of mesenchymal cell markers, while exerted effects on cell proliferation and migration of TNBC cell lines. Moreover, the agomir of miR-425 could protect against development process in murine TNBC xenogarft model.ConclusionsOur results demonstrated that miR-425 targets to TGF-β1, and was a crucial suppressor on EMT and development of TNBC through inhibiting TGF-β1/SMAD3 signaling pathway. It suggested that aim at TGF-β1/SMAD3 signaling pathway by enhancing relative miR-425 expression, was a feasible therapy strategy for TNBC.

scholarly journals ARSD, a novel ERα downstream target gene, inhibits proliferation and migration of breast cancer cells via activating Hippo/YAP pathway

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Yun Lin ◽  
Chun Li ◽  
Wei Xiong ◽  
Liping Fan ◽  
Hongchao Pan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cpg Islands ◽  
Systematic Investigation ◽  
Good Prognosis ◽  
Hippo Signaling ◽  
Loop Formation ◽  
Downstream Target ◽  
Potential Marker ◽  
And Migration ◽  
Proliferation And Migration

AbstractAdvanced breast cancer (BC), especially basal like triple-negative BC (TNBC), is a highly malignant tumor without viable treatment option, highlighting the urgent need to seek novel therapeutic targets. Arylsulfatase D (ARSD), localized at Xp22.3, is a female-biased gene due to its escaping from X chromosome inactivation (XCI). Unfortunately, no systematic investigation of ARSD on BC has been reported. In this study, we observed that ARSD expression was positively related to ERα status either in BC cells or tissue specimens, which were associated with good prognosis. Furthermore, we found a set of hormone-responsive lineage-specific transcription factors, FOXA1, GATA3, ERα, directly drove high expression of ARSD through chromatin looping in luminal subtype BC cells. Opposingly, ARSD still subjected to XCI in TNBC cells mediated by Xist, CpG islands methylation, and inhibitory histone modification. Unexpectedly, we also found that ectopic ARSD overexpression could inhibit proliferation and migration of TNBC cells by activating Hippo/YAP pathway, indicating that ARSD may be a molecule brake on ERα signaling pathway, which restricted ERα to be an uncontrolled active status. Combined with other peoples’ researches that Hippo signaling maintained ER expression and ER + BC growth, we believed that there should exist a regulative feedback loop formation among ERα, ARSD, and Hippo/YAP pathway. Collectively, our findings will help filling the knowledge gap about the influence of ARSD on BC and providing evidence that ARSD may serve as a potential marker to predict prognosis and as a therapeutic target.

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