scholarly journals LIFR-AS1 modulates Sufu to inhibit cell proliferation and migration by miR-197-3p in breast cancer

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Fangfang Xu ◽  
Hui Li ◽  
Chengjiu Hu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Colony Formation ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Wide Range

AbstractNumerous evidence has recently demonstrated that long non-coding RNAs (lncRNAs) play vital roles in the oncogenesis and development of a wide range of human neoplasms. Leukemia inhibitory factor receptor antisense RNA 1 (LIFR-AS1), a novel cancer-related lncRNA, has been reported to be under-expressed in breast cancer and associated with poor prognosis. However, the exact role of LIFR-AS1 in breast cancer remains largely unclear. The present study aimed to investigate the biological role of LIFR-AS1 in breast cancer and clarify the potential molecular mechanisms. In the present study, we found that LIFR-AS1 was significantly down-regulated in both tissues and cell lines. Furthermore, over-expression of LIFR-AS1 inhibited breast cancer cell proliferation, colony formation, migration and invasion, whereas knockdown of LIFR-AS1 promoted breast cancer cell proliferation, colony formation, migration and invasion. Moreover, LIFR-AS1 was observed to up-regulate suppressor of fused gene (Sufu) expression by competitively binding to miR-197-3p in breast cancer cells. Notably, miR-197-3p inhibitor reversed the promoting effects of LIFR-AS1 knockdown on breast cancer cell proliferation, colony formation, migration and invasion. Additionally, LIFR-AS1 knockdown promoted tumor growth in vivo. To sum up, our results imply the tumor-suppressing role of LIFR-AS1 in breast cancer.

scholarly journals Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion

2018 ◽  
Vol Volume 11 ◽  
pp. 3195-3203 ◽  
Author(s):  
Shudong Gu ◽  
Haibin Liang ◽  
Donghui Qi ◽  
Liyan Mao ◽  
Guoxin Mao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation

Abelson Interactor Protein-1 Positively Regulates Breast Cancer Cell Proliferation, Migration, and Invasion

2007 ◽  
Vol 5 (10) ◽  
pp. 1031-1039 ◽  
Author(s):  
Chunjie Wang ◽  
Roya Navab ◽  
Vladimir Iakovlev ◽  
Yan Leng ◽  
Jinyi Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation

scholarly journals p53–GSDME Elevation: A Path for CDK7 Inhibition to Suppress Breast Cancer Cell Survival

2021 ◽  
Vol 8 ◽  
Author(s):  
Yueyuan Wang ◽  
Jingyu Peng ◽  
Xuguang Mi ◽  
Ming Yang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Survival ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Colony Formation ◽  
Dependent Manner ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Cell Survival

Higher cyclin-dependent kinase (CDK7) expression is a character of breast cancer and indicates poor prognosis. Inhibiting CDK7 exhibited effective cancer cell suppression which implies the potential of CDK7 inhibition to be a method for anti-cancer treatment. Our study aimed to explore a novel mechanism of CDK7 inhibition for suppressing breast cancer cell survival. Here, we proved inhibiting CDK7 repressed breast cancer cell proliferation and colony formation and increased the apoptotic cell rate, with p53 and GSDME protein level elevation. When p53 was suppressed in MCF-7 cells, the decline of GSDME expression and associated stronger proliferation and colony formation could be observed. Since downregulation of GSDME was of benefit to breast cancer cells, p53 inhibition blocked the elevation of GSDME induced by CDK7 inhibition and retrieved cells from the tumor suppressive effect of CDK7 inhibition. Therefore, CDK7 inhibition exerted a negative effect on breast cancer cell proliferation and colony formation in a p53–GSDME dependent manner. These results revealed the CDK7–p53–GSDME axis could be a pathway affecting breast cancer cell survival.

scholarly journals Knock Down of LINC00504 Represses Proliferation and Invasion via Regulation of miR-140-5p in Breast Cancer

2020 ◽  
Author(s):  
Tieying Hou ◽  
Long Ye ◽  
Qingsong Qin ◽  
Shulin Wu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background: Breast cancer is one of the most common cancer in the world. Emerging evidence has demonstrated the critical role of long noncoding RNAs (lncRNAs) in the development of breast cancer. In this study, we aimed to investigate the role of LINC00504 in breast cancer progression. Methods: Quantification real-time PCR was used to analyzed the expression levels of LINC00504 and miR‐140-5p in breast cancer tissues and cell lines. Cell proliferation, migration and invasion were assessed by Cell Counting Kit‐8, transwell assay and Immunofluorescence. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were performed to verify the interaction between LINC00504 and miR‐140-5p. The expression levels of VEGFA, CDH1 and VIM were demonstrated by western blot assays. Result: Here, we found that LINC00504 is up regulated in breast cancer tissues and cell lines. Down regulation of LINC00504 mediated by shRNA suppressed the proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Furthermore, LINC00504 was found to competitively regulate miR‐140-5p via targeting VEGFA. Inhibition of miR‐140-5p attenuated the knockdown-LINC00504 induced inhibition of breast cancer cell proliferation and invasion.Conclusion: Taken together, our results demonstrated the mechanism of the LINC00504–miR‐140-5p–VEGFA axis in breast cancer cell proliferation and invasion and may lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

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