scholarly journals Effects of microRNA-374 on proliferation, migration, invasion, and apoptosis of human SCC cells by targeting Gadd45a through P53 signaling pathway

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Xiao-Jing Li ◽  
Zhi-Feng Li ◽  
Jiu-Jiang Wang ◽  
Zhao Han ◽  
Zhao Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Normal Skin ◽  
Negative Control ◽  
Migration And Invasion ◽  
Caspase 9 ◽  
P53 Signaling ◽  
P53 Signaling Pathway ◽  
Skin Samples

The present study investigated the effects of microRNA-374 (miR-374) on human squamous cell carcinoma (SCC) cell proliferation, migration, invasion, and apoptosis through P53 signaling pathway by targeting growth arrest and DNA-damage-inducible protein 45 α (Gadd45a). Skin samples were collected from patients with skin SCC and normal skin samples. Expression of miR-374, Gadd45a, P53, P73, P16, c-myc, bcl-2, Bax, caspase-3, and caspase-9 were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. A431 and SCL-1 cells were divided into blank, negative control (NC), miR-374 mimics, miR374 inhibitors, siRNA–Gadd45a, and miR-374 inhibitors + siRNA–Gadd45a groups. Their proliferation, migration, invasion, cell cycle, and apoptosis were evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, scratch test, Transwell assay, and flow cytometry. SCC skin tissues exhibited decreased expression of miR-374, P73, P16, Bax caspase-3 and caspase-9, and increased levels of Gadd45a, P53, c-myc, and Bcl-2 compared with the normal skin tissues. The miR-374 inhibitors group exhibited decreased expression of miR-374, P73, P16, Bax caspase-3 and caspase-9, and increased expression of Gadd45a, P53, c-myc, and Bcl-2, enhanced cell proliferation, migration, and invasion, and reduced apoptosis compared with the blank and NC groups; the miR-374 mimics group followed opposite trends. Compared with the blank and NC groups, the miR-374 inhibitors + siRNA–Gadd45a group showed decreased miR-374 level; the siRNA–Gadd45a group showed elevated levels of P73, P16, Bax, caspase-3 and caspase-9, decreased levels of Gadd45a, P53, c-myc, and Bcl-2, reduced cell proliferation, migration, and invasion, and accelerated apoptosis. miR-374 induces apoptosis and inhibits proliferation, migration, and invasion of SCC cells through P53 signaling pathway by down-regulating Gadd45a.

Effect of SRY-Related High Mobility Group Box 9 on Extracellular Signal-Regulated Kinase/p38 Signaling Pathway in Glioma

2021 ◽  
Vol 11 (1) ◽  
pp. 171-175
Author(s):  
Tianlong Quan ◽  
Chunhua Zhang ◽  
Xin Song ◽  
Lu Wang
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Invasion ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
High Mobility ◽  
Negative Control ◽  
Glioma Cell Line ◽  
High Mobility Group ◽  
Control Group

As a common malignant tumor in neurosurgery, glioma is characterized as high incidence rate, easy to invade, metastasize and recurrent. It is difficult to treat and has a poor prognosis. The gliomas pathogenesis is complex and has not been fully resolved. Therefore, finding effective molecular targets for glioma is beneficial to improve therapeutic effect. The SRY-related high mobility group box 9 (SOX9) gene involves in mammalian development and is significantly increased in glioma. However, SOX9’s role in gliomas is unclear. The glioma cell line U87 was assigned into control group, scramble group that was transfected with siRNA negative control, and SOX9 siRNA group that was transfected with SOX9 siRNA followed by analysis of SOX9 mRNA and protein level by qPCR and Western blot, cell proliferation by MTT assay, cell apoptosis by Caspase 3 activity assay, cell invasion by Transwell assay, and MMP-9 level by ELISA. SOX9 siRNA transfection significantly downregulated SOX9 mRNA and protein expressions, inhibited U87 cell proliferation, enhanced Caspase 3 activity, suppressed cell invasion of U87, decreased the secretion of MMP-9 in the supernatant, and reduced ERK1/2 and P38 phosphorylation levels (P < 0.05). SOX9 can regulate the progression of glioma by regulating ERK/P38 signaling pathway, promoting cell apoptosis, inhibiting cell proliferation, and restraining cell invasion.

scholarly journals PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia

2020 ◽  
Vol 19 ◽  
pp. 153303382094231
Author(s):  
Bin Li ◽  
Jie Hu ◽  
Di He ◽  
Qi Chen ◽  
Suna Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Protein Phosphatase ◽  
Cell Apoptosis ◽  
Myeloid Leukemia ◽  
P53 Signaling ◽  
P53 Signaling Pathway ◽  
Acute Myeloid

Objectives: This study was to explore the effect of protein phosphatase, Mg2+/Mn2+ dependent 1D knockdown on proliferation and apoptosis as well as p38 MAPK/p53 signaling pathway in acute myeloid leukemia. Methods: The expression of protein phosphatase, Mg2+/Mn2+ dependent 1D was detected in acute myeloid leukemia cell lines including SKM-1, KG-1, AML-193, and THP-1 cells, and normal bone marrow mononuclear cells isolated from healthy donors. The knockdown of protein phosphatase, Mg2+/Mn2+ dependent 1D was conducted by transfecting small interfering RNA into AML-193 cells and KG-1 cells. Results: The relative messenger RNA/protein expressions of protein phosphatase, Mg2+/Mn2+ dependent 1D were higher in SKM-1, KG-1, AML-193, and THP-1 cells compared with control cells (normal bone marrow mononuclear cells). After transfecting protein phosphatase, Mg2+/Mn2+ dependent 1D small interfering RNA into AML-193 cells and KG-1 cells, both messenger RNA and protein expressions of protein phosphatase, Mg2+/Mn2+ dependent 1D were significantly reduced, indicating the successful transfection. Most importantly, knockdown of protein phosphatase, Mg2+/Mn2+ dependent 1D suppressed cell proliferation and promoted cell apoptosis in AML-193 cells and KG-1 cells. In addition, knockdown of protein phosphatase, Mg2+/Mn2+ dependent 1D enhanced the expressions of p-p38 and p53 in AML-193 cells and KG-1 cells. The above observation suggested that protein phosphatase, Mg2+/Mn2+ dependent 1D knockdown suppressed cell proliferation, promoted cell apoptosis, and activated p38 MAPK/p53 signaling pathway in acute myeloid leukemia cells. Conclusion: Protein phosphatase, Mg2+/Mn2+ dependent 1D is implicated in acute myeloid leukemia carcinogenesis, which illuminates its potential role as a treatment target for acute myeloid leukemia.

IGF- I induced growth and metatasis suppressed by calycosin via STAT3/ BATF2/ NF-κB /FOXM1 in colorectal cancer cells 

2021 ◽  
Author(s):  
Qun Wang ◽  
Weijun Lu ◽  
Li Lu ◽  
Guoliang Pi ◽  
Wu Dong De ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Caspase 3 ◽  
Nuclear Accumulation ◽  
Migration And Invasion ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
Caspase 9 ◽  
Colorectal Cancer Cells ◽  
Igf I

Abstract To determine whether up-regulation of BATF2 by calycosin suppresses IGF- I induced growth and metastasis in human CRC,Cells were cultured and treated with calycosin and IGF-I. Protein and mRNA levels were determined by western-blot and real-time PCR respectively. Cell migration and invasion were assessed by transwell experiments. Apoptosis was measured by Flow cytometry. Cell proliferation was evaluated by the MTT assay.Co-immunoprecipitation and luciferase assays were used to analyze the interaction between BATF2 and MAT2Aand FOXM1.Cytoimmunofluorescence staining was applied for β-catenin and FOXM1 cellular localization.As results,Calycosin induced the up-regulation of BATF2 antagonized by IGF- I via STAT3, STAT1and NF-κB pathways resulting in cell apoptosis promotion via increasing BAX/Bcl-2 ratio subsequent contribute to caspase-3 and caspase-9 release. IGF- I induced cell migration,invasion and EMT suppressed by calycosin via BATF2 to block FOXM1 mediated β-catenin nuclear accumulation in three CRC cells. IGF- I induced cell proliferation was inhibited by calycosin down-regulating MAT2A and FOXM1. IGF-I and calycosin impacted MAT2A on transcriptional level. BATF2 interated with MAT2A and FOXM1 directly.We believed up-regulation of BATF2 may be a practicable treatment strategy for suppression IGF-1 induced growth and metatasis in CRC.

DHRS12 inhibits the proliferation and metastasis of osteosarcoma via Wnt3a/β-catenin pathway

2020 ◽  
Vol 16 (11) ◽  
pp. 665-674
Author(s):  
Zhixian Xu ◽  
Wubing He ◽  
Tie Ke ◽  
Yongfa Zhang ◽  
Guifeng Zhang
Keyword(s):  
Cell Proliferation ◽  
Experimental Design ◽  
Caspase 3 ◽  
Biological Effects ◽  
Immunohistochemical Analysis ◽  
Migration And Invasion ◽  
Caspase 9 ◽  
Proliferation And Metastasis ◽  
Plasmid Transfection ◽  
Induced Apoptosis

Aim: This experimental design was based on DHRS12 to explore its biological effects on osteosarcoma (OS). Materials & methods: The expression level of endogenous DHRS12 was analyzed by immunohistochemical analysis. DHRS12 was overexpressed in MG-63 and HOS cells by plasmid transfection. Cell proliferation, invasion, migration, apoptosis and western blot were used in the experiment. Results: The expression of DHRS12 was significantly reduced in OS. Overexpression of DHRS12 inhibited the proliferation, migration and invasion of MG-63 and HOS cells and induced apoptosis of OS cells. Overexpression of DHRS12 upregulated Bax, Caspase 9 and Caspase 3. Overexpression of DHRS12 resulted in inactivation of the Wnt3a/β-catenin signaling pathway. Conclusion: Overexpression of DHRS12 inhibited the progression of OS via the Wnt3a/β-catenin pathway.

scholarly journals Ze-Qi-Tang Formula Induces Granulocytic Myeloid-Derived Suppressor Cell Apoptosis via STAT3/S100A9/Bcl-2/Caspase-3 Signaling to Prolong the Survival of Mice with Orthotopic Lung Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Zi-hang Xu ◽  
Yang-zhuangzhuang Zhu ◽  
Lin Su ◽  
Xue-yang Tang ◽  
Chao Yao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Suppressor Cell ◽  
Inhibitory Effect ◽  
Luminescence Signal ◽  
P53 Signaling ◽  
Myeloid Derived Suppressor Cell ◽  
Lung Cancer Model ◽  
P53 Signaling Pathway

Non-small-cell lung cancer (NSCLC) remains the most common malignancy with the highest morbidity and mortality worldwide. In our previous study, we found that a classic traditional Chinese medicine (TCM) formula Ze-Qi-Tang (ZQT), which has been used in the treatment of respiratory diseases for thousands of years, could directly inhibit the growth of human NSCLC cells via the p53 signaling pathway. In this study, we explored the immunomodulatory functions of ZQT. We found that ZQT significantly prolonged the survival of orthotopic lung cancer model mice by modulating the tumor microenvironment (TME). ZQT remarkably reduced the number of MDSCs (especially G-MDSCs) and inhibited their immunosuppressive activity by inducing apoptosis in these cells via the STAT3/S100A9/Bcl-2/caspase-3 signaling pathway. When G-MDSCs were depleted, the survival promotion effect of ZQT and its inhibitory effect on lung luminescence signal disappeared in tumor-bearing mice. This is the first study to illustrate the immunomodulatory effect of ZQT in NSCLC and the underlying molecular mechanism.

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