Wild-type p53 upregulates an early onset breast cancer-associated gene GAS7 to suppress metastasis via GAS7–CYFIP1-mediated signaling pathway

Chang, Jui-Chi; Kuo, Wen‐Hung; Lin, Chiao-Mei; Chen, Wenling; Chan, Shih-Hsuan; Chiu, Meng-Fan; Chang, I–Shou; Jiang, Shih–Sheng; Tsai, Fang‐Yu; Chen, Chung–Hsing; Huang, Pei‐Hsin; Chang, King‐Jen; Lin, Kai-Ti; Lin, Sheng-Chieh; Wang, Mingyang; Uen, Yih-Huei; Tu, Chi‐Wen; Hou, Ming‐Feng; Tsai, Shih‐Feng; Shen, Chen‐Yang; Tung, Shiao-Lin; Wang, Lu‐Hai

doi:10.1038/s41388-018-0253-9

Cited by 471 publications

(1,006 citation statements)

References 42 publications

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“…Lastly, we will discuss the category "regulation of key signaling pathways and actin cytoskeletal pathways" based on the expression profiles of PCNA, CDK4, cyclin D1, and p21 of THP-1 cells following silencing of miR-362-5p or induction of GAS7. Previous work has revealed that, some events, such as Stat5-, AKT-, Erk-, and CYFIP1mediated signaling pathways can be affected by GAS7 in some particular types of cells [34,35]. Chang et al [34] indicated that p53 upregulate GAS7, thus attenuating breast cancer cells metastasis through regulating CYFIP1 and WAVE2 complex.…”

Section: Discussionmentioning

confidence: 99%

“…Previous work has revealed that, some events, such as Stat5-, AKT-, Erk-, and CYFIP1mediated signaling pathways can be affected by GAS7 in some particular types of cells [34,35]. Chang et al [34] indicated that p53 upregulate GAS7, thus attenuating breast cancer cells metastasis through regulating CYFIP1 and WAVE2 complex. On the contrary, GAS7 has a proproliferative role in pre-B acute lymphoblastic leukemia cells, possibly through regulating Stat5, AKT, and Erk proliferation signals [35,36].…”

Section: Discussionmentioning

confidence: 99%

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miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia

Chen

et al. 2020

Human Cell

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Recently, miR-362-5p has attracted special interest as a novel prognostic predictor in acute myeloid leukemia (AML). However, its biological function and underlying molecular mechanism in AML remain to be further defined. Herein, we found that a significant increase in miR-362-5p expression was observed in AML patients and cell lines using quantitative realtime PCR. The expression of miR-362-5p was altered in THP-1 and HL-60 cells by transfecting with miR-362-5p mimic or inhibitor. A series of experiments showed that inhibition of miR-362-5p expression significantly suppressed cell proliferation, induced G0/G1 phase arrest and attenuated tumor growth in vivo. On the contrary, ectopic expression of miR-362-5p resulted in enhanced cell proliferation, cell cycle progression and tumor growth. Moreover, growth arrest-specific 7 (GAS7) was confirmed as a direct target gene of miR-362-5p and was negatively modulated by miR-362-5p. GAS7 overexpression imitated the tumor suppressive effect of silenced miR-362-5p on THP-1 cells. Furthermore, miR-362-5p knockdown or GAS7 overexpression obviously down-regulated the expression levels of PCNA, CDK4 and cyclin D1, but up-regulated p21 expression. Collectively, our findings demonstrate that miR-362-5p exerts oncogenic effects in AML by directly targeting GAS7, which might provide a promising therapeutic target for AML.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia

Chen

et al. 2020

Human Cell

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“…FOXN4 mainly function as transcriptional repressor to suppress P53 expression from mRNA and protein levels. P53, the most famous tumor suppressor, which controls several biological processes such as cell cycle, EMT, cell survival, metastasis and metabolism, [21][22][23] is frequently inactivation in breast cancer and is considered a constant feature of cancer. [24][25][26] In this study, we explored molecular changes associated with loss of p53 in breast cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

<p>FOXN4 Inhibits Breast Cancer Progression By Direct Activation Of P53</p>

Duan

2020

OTT

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Background: Fork head domain-containing gene family (Fox) transcription factors, consisting of over 20 members, are involved in the progression of certain types of tumor. However, whether FOXN4 is involved in carcinogenesis and tumor progression is still unclear. Purpose: In this study, we investigated the clinicopathological significance and the underlying mechanism of FOXN4 in breast cancer. Methods and results: We examined the lower expression of FOXN4 in breast cancer tissues and cancer cell lines. The expression of FOXN4 is negatively correlated with tumor size and lymph node metastasis. Using CCK-8 assay, colony formation assay, wound healing assay, and Transwell assay, we revealed that FOXN4 notably decreased breast cancer cell proliferation, epithelial-mesenchymal transition and invasion in vitro. In addition, quantitative chromatin immunoprecipitation and luciferase assays determined that FOXN4 was able to directly bind with the promoter of P53. RT-qPCR and Western blotting analysis showed that FOXN4 could directly activate P53 expression. Functionally, P53 knockdown rescued the tumor inhibition effects of FOXN4 in breast cancer cells. Conclusion: The present study provides new insights into the role of FOXN4 in breast cancer progression and suggests FOXN4 might represent a potential therapeutic target in breast cancer by modulating P53.

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“…GAS7 is expressed primarily in terminally differentiated brain cells and plays a putative role in neuronal development [27]. Recent researches supported that GAS7 involves cancer development and metastasis [28,29]. Moreover, GAS7 was also reported to associate with drug resistance.…”

Section: Discussionmentioning

confidence: 99%

Low expression of lncRNA CTB-104H12.5 induces resistance to adriamycin in HER2 negative breast cancer by downregulating GAS7C

Nian

Xue³

et al. 2020

Preprint

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Abstract Background Adriamycin-based neoadjuvant chemotherapy is widely used in HER2- breast cancer patients, however, some patients have no response or acquire resistance to these regimens. Therefore, it is important to screen patients who respond to adriamycin with biomarkers. Methods A human lncRNA microarray analysis followed by a quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to identify the differentially expressed lncRNAs. The proliferation viability of cells transfected with or without CTB 104H12.5 was measured by CCK-8 and clone formation assay, cell apoptosis and cell cycle were evaluated by Flow cytometry. And the expression of RNA and proteins was tested by qRT-PCR and Western blot, respectively. Results Ten whole blood samples from HER2- breast cancer patients who received docetaxel combined with adriamycin regimen were enrolled, a human lncRNA microarray analysis showed that the low expression of CTB-104H12.5 was associated unfavorable prognosis. And the mRNA and protein level of CTB-104H12.5 is much lower in MCF-7/ADR cells than that of MCF-7 cells while CTB-104H12.5 knockdown in MCF cells induces cell resistance to adriamycin, while CTB-104H12.5 overexpression in MCF7/ADR cells reversed their resistance to adriamycin. Also, the mRNA and protein levels of GAS7C were associated with CTB-104H12.5. Conclusions Low expression of CTB-10412.5 predicted resistance to adriamycin in HER2 negative breast cancer, which may serve as a potential biomarker to dynamically monitor adriamycin resistance for breast cancer patients.

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Wild-type p53 upregulates an early onset breast cancer-associated gene GAS7 to suppress metastasis via GAS7–CYFIP1-mediated signaling pathway

Cited by 471 publications

References 42 publications

miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia

miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia

<p>FOXN4 Inhibits Breast Cancer Progression By Direct Activation Of P53</p>

Low expression of lncRNA CTB-104H12.5 induces resistance to adriamycin in HER2 negative breast cancer by downregulating GAS7C

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