scholarly journals Tilianin inhibits the human ovarian cancer (PA-1) cell proliferation via blocking cell cycle, inducing apoptosis and inhibiting JAK2/STAT3 signaling pathway

2021 ◽  
Author(s):  
Chunqiu Xiong ◽  
Bingbing Yan ◽  
Suhua Xia ◽  
Fei Yu ◽  
Jingjing Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Human Ovarian Cancer ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

miR126-Mediated Signal Transducer and Activator of Transcription 3 Signaling Pathway Regulates the Malignant Biological Behavior of Pancreatic Cancer Cells

2020 ◽  
Vol 10 (8) ◽  
pp. 1199-1205
Author(s):  
Demao Kong ◽  
Xia Wang
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Plasmid Transfection ◽  
Low Expression

Background and purpose: As a type of non-coding genetic material widely existing in eukaryotes, a growing amount of research have confirmed that it have close connection with the occurrence and progression of various malignancies. MicroRNA126 is increased in non-small-cell lung cancer, liver cancer and gastric carcinoma. The up-regulation of miR126 in cervical cancer is closely associated with the clinical staging, histological grade, depth of invasion and early metastasis of the tumor, and it is also of great value in predicting the survival prognosis of the tumor. However, there is little known about the relationship between miR126 and pancreatic carcinoma. Therefore, this study explored the miR126-mediated STAT3 signaling pathway in medicating pancreatic cancer cell multiplication, migration, cell cycle and apoptosis in vitro . Methods: PANC-1 cell (human pancreatic cancer cell line) was selected for routine resuscitation and subculture. The experiment is grouped as: blank control group (NC group), empty plasmid transfection group (miR126-NC group), miR126mimic transfection group (overexpression Group) and miR126 inhibition plasmid transfection group (low expression group); cell viability of each group for 12 h, 24 h, 48 h and 72 h was detected using MTT assay. Wound healing assay was used to evaluated the ability of cell migration. Flow cytometry was performed to analyze cell cycle. The mRNA expression of Caspase-3 was determined by reverse transcription PCR (RT-PCR). STAT3 protein was evaluated by western blot. Results: miR126 overexpression significantly increased cell proliferation at 12 h, 24 h, 48 h, and 72 h, while the cell proliferation rates of the low expression group at each time point were significantly reduced in comparision with those of the NC group and the miR126-NC group (P < 0 05). miR126 overexpression significantly induced cell migration, while miR126 low-expression significantly inhibited cell migration (P < 0 05). miR126 overexpression significantly enhanced the percentage of G2/M, while the percentage of G2/M in the low-expressed group was remarkably reduced in comparision with those of the NC group and the miR126-NC group (P < 0 05). The mRNA expression of Caspase-3 was significantly inhibited in miR126 overexpression group, while the expression of Caspase-3 mRNA in the cells with miR126 low expression was remarkably increased (P < 0 05). The protein expression of STAT3 in miR126 overexpression group was notably up-regulated, while the expression level of STAT3 protein in the low expression group was prominently down-regulated (P <0 05). Conclusion: MiR126 overexpression may induces the STAT3 signaling pathway and then regulates cell proliferation, cell migration, cell cycle arrest and cell apoptosis in pancreatic carcinoma.

scholarly journals CircSOD2 induced epigenetic alteration drives hepatocellular carcinoma progression through activating JAK2/STAT3 signaling pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Zhongwei Zhao ◽  
Jingjing Song ◽  
Bufu Tang ◽  
Shiji Fang ◽  
Dengke Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Migration ◽  
Real Time ◽  
Signaling Pathway ◽  
Molecular Mechanism ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Signaling Axis

Abstract Background Emerging evidence suggests that circular RNAs play critical roles in disease development especially in cancers. Previous genome-wide RNA-seq studies found that a circular RNA derived from SOD2 gene was highly upregulated in hepatocellular carcinoma (HCC), however, the role of circSOD2 in HCC remains largely unknown. Methods The expression profiling of circSOD2 and microRNA in HCC patients were assessed by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR). SiRNA or CRISPR-CAS9 were used to silence gene expression. The biological function of circSOD2 in HCC was investigated using in vitro and in vivo studies including, trans-well cell migration, cell apoptosis, cell cycle, CCK8, siRNA interference, western blots, and xenograft mouse model. The underlying molecular mechanism was determined by Chromatin Immunoprecipitation quantitative real time PCR (ChIP-qPCR), bioinformatic analysis, biotin-pull down, RNA immunoprecipitation, 5-mc DNA pulldown and luciferase assays. Results In accordance with previous sequencing results, here, we demonstrated that circSOD2 was highly expressed in HCC tumor tissues compared with normal liver tissues. Mechanically, we showed that histone writer EP300 and WDR5 bind to circSOD2 promoter and trigger its promoter H3K27ac and H3K4me3 modification, respectively, which further activates circSOD2 expression. SiRNA mediated circSOD2 suppression impaired liver cancer cell growth, cell migration, prohibited cell cycle progression and in vivo tumor growth. By acting as a sponge, circSOD2 inhibits miR-502-5p expression and rescues miR-502-5p target gene DNMT3a expression. As a DNA methyltransferase, upregulated DNMA3a suppresses SOCS3 expression by increasing SOCS3 promoter DNA methylation. This event further accelerates SOCS3 downstream JAK2/STAT3 signaling pathway activation. In addition, we also found that activated STAT3 regulates circSOD2 expression in a feedback way. Conclusion The novel signaling axis circSOD2/miR-502-5p/DNMT3a/JAK2/STAT3/circSOD2 provides a better understanding of HCC tumorigenesis. The molecular mechanism underlying this signaling axis offers new prevention and treatment of HCC.

Dieckol attenuates cell proliferation in Molt-4 leukemia cells via modulation of JAK/STAT3 signaling pathway

2021 ◽  
Vol 17 (73) ◽  
pp. 45
Author(s):  
Juandong Wang ◽  
Ai Li ◽  
Li Zhang ◽  
VishnuPriya Veeraraghavan ◽  
SurapaneniKrishna Mohan
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Leukemia Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals TRIM27 promotes IL-6-induced proliferation and inflammation factor production by activating STAT3 signaling in HaCaT cells

2020 ◽  
Vol 318 (2) ◽  
pp. C272-C281
Author(s):  
Xiao Miao ◽  
Yanwei Xiang ◽  
Weiwei Mao ◽  
Yiran Chen ◽  
Qi Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Gene Set Enrichment Analysis ◽  
Cell Counting ◽  
Hacat Cells ◽  
Stat3 Signaling ◽  
Factor Production ◽  
Stat3 Signaling Pathway ◽  
Inflammation Factor ◽  
Psoriatic Lesions

The IL-6/STAT3 signaling pathway is required for the development of psoriatic lesions, and tripartite motif-containing 27 (TRIM27) is a protein inhibitor of activated STAT3 (PIAS3)-interacting protein that could modulate IL-6-induced STAT3 activation. However, whether TRIM27 is associated with the IL-6/STAT3 signaling pathway in psoriasis remains enigmatic. TRIM27 expression and gene set enrichment analysis in patients with psoriasis were determined using bioinformatics. Human keratinocyte HaCaT cells treated with recombinant protein IL-6 (rh-IL-6) were transduced with lentivirus silencing TRIM27 and/or PIAS3 or, otherwise, transduced with lentivirus expressing TRIM27 and/or lentivirus silencing STAT3, or MG132, a proteasome-specific protease inhibitor. Cell proliferation and inflammation factor production were measured using Cell Counting Kit-8 and ELISA, respectively. TRIM27, proliferation marker protein Ki-67 (Ki67), phospho-STAT3 (p-STAT3), STAT3, and PIAS3 expressions were determined using real-time quantitative PCR, immunofluorescence staining, or Western blot analysis. Coimmunoprecipitation combined with ubiquitination analysis was performed to explore the interaction between TRIM27 and PIAS3. In the present study, TRIM27 expression was increased in psoriatic lesions, associated with the IL-6 signaling pathway, and induced by rh-IL-6 in a time-dependent manner. The increased cell proliferation, inflammation factor production, and expression of Ki67 and of p-STAT3 relative to STAT3 induced by rh-IL-6 and TRIM27 overexpression were significantly inhibited by TRIM27 silencing and STAT3 silencing, respectively. More importantly, TRIM27 interacted with PIAS3, and its overexpression promoted PIAS3 ubiquitination in HaCaT cells. PIAS3 silencing also significantly promoted TRIM27-dependent and IL6-induced STAT3 activation, cell proliferation, and inflammation factor production. In conclusion, our results highlight that TRIM27 expression is significantly increased by IL-6 and suggest a TRIM27/STAT3-dependent mechanism for regulation of inflammation and proliferation-associated development of psoriasis.

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