MicroRNA‐329‐mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

2018 ◽  
Vol 120 (6) ◽  
pp. 9964-9978 ◽  
Author(s):  
Zhi‐Gao Hu ◽  
Chao‐Wen Zheng ◽  
Hui‐Zhao Su ◽  
Yong‐Lian Zeng ◽  
Cheng‐Jie Lin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Suppress Cell Proliferation

scholarly journals miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway

2018 ◽  
Vol 26 (3) ◽  
pp. 363-372 ◽  
Author(s):  
Xiaowen Chen ◽  
Jianli Chen
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Luciferase Reporter ◽  
And Migration ◽  
Mcf 7

This study intended to investigate the effects of miR-3188 on breast cancer and to reveal the possible molecular mechanisms. miR-3188 was upregulated and TUSC5 was downregulated in breast cancer tissues and MCF-7 cells compared to normal tissue and MCF-10 cells. After MCF-7 cells were transfected with miR-3188 inhibitor, cell proliferation and migration were inhibited, whereas apoptosis was promoted. Luciferase reporter assay suggested that TUSC5 was a target gene of miR-3188. In addition, miR-3188 overexpression increased the p-p38 expression, while miR-3188 suppression decreased the p-p38 expression significantly. miR-3188 regulated breast cancer progression via the p38 MAPK signaling pathway. In conclusion, miR-3188 affects breast cancer cell proliferation, apoptosis, and migration by targeting TUSC5 and activating the p38 MAPK signaling pathway. miR-3188 may serve as a potential therapeutic agent for the treatment of breast cancer.

scholarly journals Long noncoding RNA 00976 promotes pancreatic cancer progression through OTUD7B by sponging miR-137 involving EGFR/MAPK pathway

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Shan Lei ◽  
Zhiwei He ◽  
Tengxiang Chen ◽  
Xingjun Guo ◽  
Zhirui Zeng ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Migration And Invasion ◽  
Potential Biomarker

Abstract Background Accumulation evidence indicates the vital role of long non-coding RNAs (lncRNAs) in tumorigenesis and the progression of malignant tumors, including pancreatic cancer (PC). However, the role and the molecular mechanism of long non-coding RNA 00976 is unclear in pancreatic cancer. Methods In situ hybridization (ISH) and qRT-PCR was performed to investigate the association between linc00976 expression and the clinicopathological characteristics and prognosis of patients with PC. Subsequently, linc00976 over-expression vector and shRNAs were transfected into PC cells to up-regulate or down-regulate linc00976 expression. Loss- and gain-of function assays were performed to investigate the role of linc00976 in proliferation and metastasis in vitro and vivo. ITRAQ, bioinformatic analysis and rescue assay were used to illustrate the ceRNA mechanism network of linc00976/miR-137/OTUD7B and its downstream EGFR/MAPK signaling pathway. Results linc00976 expression was overexpressed in PC tissues and cell lines and was positively associated with poorer survival in patients with PC. Function studies revealed that linc00976 knockdown significantly suppressed cell proliferation, migration and invasion in vivo and in vitro, whereas its overexpression reversed these effects. Based on Itraq results and online database prediction, Ovarian tumor proteases OTUD7B was found as a downstream gene of linc00976, which deubiquitinated EGFR mediates MAPK signaling activation. Furthermore, Bioinformatics analysis and luciferase assays and rescue experiments revealed that linc00976/miR137/OTUD7B established the ceRNA network modulating PC cell proliferation and tumor growth. Conclusion The present study demonstrates that linc00976 enhances the proliferation and invasion ability of PC cells by upregulating OTUD7B expression, which was a target of miR-137. Ultimately, OTUD7B mediates EGFR and MAPK signaling pathway, suggesting that linc00976/miR-137/OTUD7B/EGFR axis may act as a potential biomarker and therapeutic target for PC.

Melittin Suppresses VEGF-A-Induced Tumor Growth by Blocking VEGFR-2 and the COX-2-Mediated MAPK Signaling Pathway

2012 ◽  
Vol 75 (11) ◽  
pp. 1922-1929 ◽  
Author(s):  
Jeong-Eun Huh ◽  
Jung Won Kang ◽  
Dongwoo Nam ◽  
Yong-Hyeon Baek ◽  
Do-Young Choi ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Cox 2

scholarly journals Amelogenin Exon 5 Peptide Promotes Cell Proliferation and Osteogenic Differentiation in Human Dental Pulp Stem Cells

2019 ◽  
Vol 9 (20) ◽  
pp. 4425
Author(s):  
Hirohito Kato ◽  
Yoichiro Taguchi ◽  
Isao Yamawaki ◽  
Yaru Ruan ◽  
Qingchao Wu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Dental Pulp ◽  
Mapk Signaling ◽  
Dental Pulp Stem Cells ◽  
Mapk Signaling Pathway ◽  
Enamel Matrix ◽  
Dental Pulp Capping

Amelogenin is a complex enamel matrix protein that consists of various molecular-size proteins and amino acids. A spliced form of amelogenin was identified that included exons 2, 3, 5, 6, and 7. However, the biological function of amelogenin exon 5 on dental pulp remains unknown. We designed a synthetic amelogenin exon 5 encoded peptide (SP), which was based on a protein produced by cells in response to the enamel matrix derivative (EMD). We investigated the effect of the SP on potentiation of osteogenesis and its signal pathway in dental pulp stem cells (DPSCs). DPSCs are an important cell for pulp tissue homeostasis. DPSCs were cultured with SP to examine the effect of cell proliferation and osteogenic differentiation. We also investigated the mitogen-activated protein kinase (MAPK) signaling pathway. SP significantly enhanced cell proliferation and the expression of osteogenic differentiation. Moreover, SP promoted the expression of the MAPK signaling pathway. Therefore, amelogenin exon 5 might contribute to dental pulp capping.

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