The Notch Pathway in Breast Cancer Progression

Kontomanolis, Emmanuel N; Kalagasidou, Sofia; Pouliliou, Stamatia; Anthoulaki, Xanthoula; Georgiou, Nikolaos; Papamanolis, Valentinos; Fasoulakis, Zacharias

doi:10.1155/2018/2415489

Cited by 108 publications

(91 citation statements)

References 123 publications

(149 reference statements)

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“…Three independent experiments. *P < 0.05, **P < 0.01 vs control (Si-ctrl) like HES1 [39]. In our study, the siRNA-mediated JAG1 knockdown or STAT3 knockdown significantly reduced HES1 expression, and STAT3 knockdown reduced JAG1 and HES1 expressions which were raised by linc00514 overexpression.…”

Section: Discussionsupporting

confidence: 55%

Linc00514 promotes breast cancer metastasis and M2 polarization of tumor-associated macrophages via Jagged1-mediated notch signaling pathway

Tao

Chen

et al. 2020

J Exp Clin Cancer Res

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Background Tumor-associated macrophages (TAMs) and tumor cells are important components of the tumor microenvironment. M2 polarization of TAMs, which is a major actor in breast cancer malignancy and metastasis, can be induced by breast cancer cells. However, the potential mechanisms of the interaction between breast cancer cells and TAMs remain unclear. Methods The candidate breast cancer-associated long non-coding RNAs (lncRNAs) were analyzed using the GEO database. Functional assays, including MTT assay, Transwell assay, and EdU labeling detection, were performed to investigate the oncogenic role of linc00514 in breast cancer progression. The co-culture and ELISA assays were used to assess the role of linc00514 in macrophage recruitment and M2 polarization. RNA immunoprecipitation, RNA pull-down, and luciferase reporter assays were applied to determine the mechanism of linc00514 in breast cancer metastasis. Mouse xenograft models, mouse pulmonary metastatic models, and mouse primary tumor models were used to assess the role of linc00514 in M2 macrophage polarization and breast cancer tumorigenicity. Results Linc00514 was highly expressed in clinical breast cancer tissues and breast cancer cell lines. Overexpression of linc00514 promoted the proliferation and invasion of breast cancer cells and increased xenograft tumor volumes and pulmonary metastatic nodules. Overexpression of linc00514 also increased the percentage of macrophages expressing M2 markers CD206 and CD163. Mechanistically, linc00514 promoted Jagged1 expression in a transcriptional manner by increasing the phosphorylation of a transcription factor STAT3. Subsequently, Jagged1-mediated Notch signaling pathway promoted IL-4 and IL-6 secretions in breast cancer cells and ultimately inducing M2 polarization of macrophages. Conclusion Linc00514 plays an important role in regulating breast cancer tumorigenicity and M2 macrophage polarization via Jagged1-mediated Notch signaling pathway.

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Section: Discussionsupporting

confidence: 55%

Linc00514 promotes breast cancer metastasis and M2 polarization of tumor-associated macrophages via Jagged1-mediated notch signaling pathway

Tao

Chen

et al. 2020

J Exp Clin Cancer Res

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“…Interestingly, effect of Notch2 on BC cell proapoptotic and anti-migratory response has been revealed to be inhibited when it was activated by zerumbone [31]. Furthermore, Notch signaling pathway has been found to play a significant role in breast epithelial cell differentiation and participated in BC growth by Notch receptors and ligands [45].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA SNHG3 promotes breast cancer cell proliferation and metastasis by binding to microRNA-154-3p and activating the notch signaling pathway

Jiang

Wang

et al. 2020

BMC Cancer

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Background: Breast cancer (BC) is a malignant tumor that occurs in the epithelial tissue of the breast gland. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) has been found to promote BC cell proliferation and invasion by regulating the microRNA (miR)-101/zinc-finger enhancer binding axis in BC. Herein, the objective of the present study is to evaluate the effect of lncRNA SNHG3 on BC cell proliferation and metastasis with the Notch signaling pathway. Methods: Differentially expressed lncRNA in BC tissues and normal breast tissues was analyzed. SNHG3 si-RNA-1 and SNHG3 si-RNA-2 were constructed to detect the mechanism of SNHG3 interference in BC cell proliferation, viability, migration and invasion. Then, dual-luciferase reporter gene assay was utilized to verify the binding relation between SNHG3 and miR-154-3p as well as miR-154-3p and Notch2. Moreover, xenograft transplantation was applied to confirm the in vitro experiments. Results: Highly expressed SNHG3 was observed in BC tissues. The growth of BC cells in vivo and in vitro was evidently repressed after silencing SNHG3. BC cell invasion and migration were inhibited by silencing SNHG3 in vitro. SNHG3 could act as a competing endogenous RNA of miR-154-3p and upregulate the Notch signaling pathway to promote BC cell development. Activation of the Notch signaling pathway can partly reverse the inhibition of cell activity induced by silencing SNHG3. Conclusion: Our study demonstrated that interfered lncRNA SNHG3 promoted BC cell proliferation and metastasis by activating the Notch signaling pathway. This investigation may offer new insight for BC treatment.

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“…The Notch signaling pathway has the dual effects of promoting cancer and anti-cancer [15,16] . Numerous research results show that it could exhibit the cancer progression in ovarian cancer, cholangiocarcinoma, lung cancer and breast cancer [17,18] , while this effect would be totally reversed in skin cancer and neuroendocrine tumors [9] .…”

Section: Discussion:-mentioning

confidence: 99%

Changes in the Expression of Notch and Hif-1α Signaling Molecules in Prostate Cancer Progression

Chen¹,

He²,

He³

et al. 2020

IJAR

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Objective: To explore the expression and clinical significance of Notch and HIF-1α signaling molecules in the progression of prostate cancer. Method: A total of 68 cases with prostate cancer were enrolled to detecting the expression level of Notch1, HIF-1α and Hes1 mRNA by qRT-PCR, in which the protein expression was measured by western blotting and immunohistochemistry staining, respectively. Correlation between molecules above and clinical pathological parameters were further analyzed. Results: Both Notch signaling and HIF-1α signaling molecules were overexpressed in prostate cancer on the protein level as well as mRNA level when compared to the para-caner tissues (P<0.05). The expression of these molecules were positive related to local lymphatic metastasis (P<0.05). However, this difference was not significant both in tumor volume and patient's age. Conclusion: Both Notch signaling and HIF-1α signaling pathway related molecules were overexpressed in prostate cancer, which might play an important role in the progression of prostate cancer.

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The Notch Pathway in Breast Cancer Progression

Cited by 108 publications

References 123 publications

Linc00514 promotes breast cancer metastasis and M2 polarization of tumor-associated macrophages via Jagged1-mediated notch signaling pathway

Linc00514 promotes breast cancer metastasis and M2 polarization of tumor-associated macrophages via Jagged1-mediated notch signaling pathway

Long non-coding RNA SNHG3 promotes breast cancer cell proliferation and metastasis by binding to microRNA-154-3p and activating the notch signaling pathway

Changes in the Expression of Notch and Hif-1α Signaling Molecules in Prostate Cancer Progression

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