scholarly journals The Hippo Signaling Pathway Coordinately Regulates Cell Proliferation and Apoptosis by Inactivating Yorkie, the Drosophila Homolog of YAP

Cell ◽  
2005 ◽  
Vol 122 (3) ◽  
pp. 421-434 ◽  
Author(s):  
Jianbin Huang ◽  
Shian Wu ◽  
Jose Barrera ◽  
Krista Matthews ◽  
Duojia Pan
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Hippo Signaling ◽  
Hippo Signaling Pathway ◽  
Proliferation And Apoptosis ◽  
Drosophila Homolog

scholarly journals Crosstalk Among YAP, LncRNA, and Tumor-Associated Macrophages in Tumorigenesis Development

2022 ◽  
Vol 11 ◽  
Author(s):  
Jing Xu ◽  
Xin-Yuan Liu ◽  
Qi Zhang ◽  
Hua Liu ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Close Association ◽  
Hippo Signaling ◽  
Internal Environment ◽  
Tumor Associated Macrophages ◽  
Hippo Signaling Pathway ◽  
Proliferation And Apoptosis ◽  
Non Coding Rnas

Long non-coding RNAs (ncRNAs), which do not encode proteins, regulate cell proliferation, tumor angiogenesis, and metastasis and are closely associated with the development, progression, and metastasis of many cancers. Tumor-associated macrophages (TAMs) in the tumor microenvironment play an important role in cancer progression. The Hippo signaling pathway regulates cell proliferation and apoptosis, maintains tissue and organ size, and homeostasis of the internal environment of organisms. Abnormal expression of Yes-associated protein (YAP), the Hippo signaling pathway key component, is widely observed in various malignancies. Further, TAM, lncRNA, and YAP are currently valuable targets for cancer immunotherapy. In this review, we have logically summarized recent studies, clarified the close association between the three factors and tumorigenesis, and analyzed the outlook of tumor immunotherapy.

scholarly journals SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway

2020 ◽  
Vol Volume 13 ◽  
pp. 1737-1749 ◽  
Author(s):  
Zhiqiang Wu ◽  
Chunmeng Wang ◽  
Yong Chen ◽  
Zhengwang Sun ◽  
Wangjun Yan
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Hippo Signaling ◽  
Hippo Signaling Pathway ◽  
Proliferation And Invasion

scholarly journals LTBP4 Inhibits the Proliferation and Metastasis in Melanoma by Activating Hippo-YAP Signaling

2020 ◽  
Author(s):  
Li na Wang ◽  
Dong run Tang ◽  
Tong Wu ◽  
Feng yuan Sun
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Nuclear Translocation ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Hippo Signaling ◽  
Ppi Network ◽  
Hippo Signaling Pathway ◽  
Proliferation And Metastasis

Abstract Background: Malignant melanoma is the deadliest of skin cancer. The present study aimed to elucidate potential key candidate genes in melanoma and its molecular mechanism. Methods: Three gene expression profile data sets (GSE46517, GSE52882 and GSE54493) were downloaded from the GEO database, which included data from melanoma tissue samples and cell lines. DEGs were subsequently investigated by GO analysis via using DAVID website. PPI network was constructed using the STRING database and visualized by Cytoscape software and MCODE were utilized to PPI network to pick out meaningful DEGs. Cell proliferation, apoptosis, migration and invasion were measured using CCK-8, colony formation, flow cytometry, transwell and wound healing assays. RT-PCR, western blotting and immunohistochemistry assays were used to detect mRNA and protein expressions. TCGAportal and GEPIA databases were used to perform the bioinformatics analysis of LTBP4 in melanoma. Results: LTBP4 both is the DEG and a key gene from the most significant module of the PPI network. LTBP4 expression was down-regulation in melanoma tissues and cells relative to controls, which showed positive correlation with invasion, TNM stage, distal metastasis and lymph node metastasis, and predicted the poor prognosis for patients with melanoma. Cox analysis identified LTBP4 low-expression as an independent prognostic variable for overall survival (OS) in patients with melanoma. The results revealed that LTBP4 inhibition reduced cell apoptosis, promoted cell proliferation and metastasis. These changes were correlated caspase-3, ki67 and E-cadherin expressions by western blotting assay. Further in vivo tumor formation study in nude mice indicated that LTBP4 inhibition promoted the progress of tumor formation. LTBP4 gene knockout reduced the phosphorylation level of YAP, MST1 and MOB1 and promoted the nuclear translocation of YAP to inhibit the activation of Hippo signaling pathway. The functions of LTBP4 overexpression (OE) inhibiting the expressions of CTGF, Cyr61 and Birc5, promoting the apoptosis, and inhibiting the metastasis and proliferation of melanoma cells were reversed by YAP/or MST1 OE.Conclusions: LTBP4 OE suppressed the proliferation and metastasis in melanoma via inhibiting the nuclear translocation of YAP to activating Hippo signaling pathway, thereby inhibiting the development and progression of melanoma.

scholarly journals Linc00887 suppresses tumorigenesis of cervical cancer through regulating the miR-454-3p/FRMD6-Hippo axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Pei Li ◽  
Jinsheng Wang ◽  
Lingran Zhi ◽  
Fengmei Cai
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Hippo Signaling ◽  
Luciferase Reporter Gene ◽  
Hippo Signaling Pathway ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background Emerging evidence suggested that long intergenic noncoding RNA (lincRNA) 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation. However, the role and regulatory mechanism of linc00887 in the progression of cervical cancer remain largely unknown. Methods In vivo or vitro, RT-qPCR assay was used to detect the expression of linc00887 in human normal (N = 30), cervical cancer tissues (N = 30), human normal cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (HeLa, C33A). Then, CCK-8 and Transwell assays were used to examine cell proliferation and invasion when linc00887 was overexpressed or knocked down. In addition, bioinformatics, luciferase reporter gene and pull-down assays were used to predict and validate the relationship between linc00887 and miR-454-3p. Moreover, we detected the expression of miR-454-3p in Ect1/E6E7, HeLa and C33A cells when linc00887 was overexpressed or knocked down. Cell proliferation and invasion were also measured when pcDNA-linc00887 and miR-454-3p were transfected alone or together. Next, miR-454-3p target gene was predicted and validated by bioinformatics and luciferase reporter gene assays. Gain- and loss-of-function experiments were performed in HeLa cells to evaluate the effect of miR-454-3p or linc00887 on the expression of FERM domain containing protein 6 (FRMD6) protein and several key proteins in the FRMD6-Hippo signaling pathway. Results Linc00887 was downregulated in cervical cancer tissues or human cervical cancer cell lines (Hela, C33A) compared with normal tissues or cell lines. Overexpression of linc00887 inhibited proliferation and invasion HeLa and C33A cells, while linc00887 knockdown had the opposite effect. Linc00887 bound with miR-454-3p, and overexpression of miR-454-3p rescued linc00887-induced inhibition proliferation and invasion of HeLa cells. MiR-454-3p targeted and suppressed the expression of FRMD6, and linc00887 suppressed tumorigenesis of cervical cancer through activating the FRMD6-Hippo signaling pathway. Conclusions Linc00887, sponging miR-454-3p, inhibited the progression of cervical cancer by activating the FRMD6-Hippo signaling pathway.

scholarly journals miR-24-3p Promotes Cell Proliferation, Migration, and Invasion of Human Cervical Cancer Cells through/via Targeting AMOTL2 and Attenuating the YAP/Hippo Pathway

2021 ◽  
Author(s):  
Yiyun Huang ◽  
Lijun Hu ◽  
Lu Lin ◽  
Yan Liu ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Hippo Signaling ◽  
Hippo Signaling Pathway ◽  
Cervical Cancer Cells

Abstract BackgroundmiR-24-3p promotes the development of the majority of malignancies.However, its function in cervical cancer is not clearly elucidated so far.MethodsIn this study, cell proliferation, migration, and invasion were measured by the CCK8 and transwell assays. Bioinformatic methods were used to predict the target genes of miR-24-3p, verifying by luciferase reporter assay and western blotting. The target genes set was also used for KEGG pathway enrichment analysis. ResultsThen we obsrved higher miR-24-3p level in cervical cancer cells and faster growth of tumor in a xenograft model. The function assays demonstrated that miR-24-3p promoted proliferation, migration, and invasion of cervical cancer cells in vitro. It was confirmed that miR-24-3p directly targeted AMOTL2 and the recovery of AMOTL2 reversed the function of miR-24-3p in cervical cancer cell line CaSki. Besides, miR-24-3p suppressed the Hippo signaling pathway in CaSki and SiHa cells. ConclusionsIn conclusion, our results reminded that miR-24-3p could boost the migration and proliferation of cervical cancer cells via down-regulating AMOTL2 and attenuating YAP/Hippo signaling pathway activity.

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