miR-203 Regulates Proliferation and Apoptosis of Colorectal Cancer Cells Through Targeting DJ-1

2020 ◽  
Vol 10 (3) ◽  
pp. 365-370
Author(s):  
Qiupeng Du ◽  
Na Du ◽  
Chenchen Zhu ◽  
Qingqing Shang ◽  
Haiyan Mao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Pten Expression ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cells ◽  
Colorectal Cell ◽  
Sw480 Cells

Objective: To assess whether miR-203 regulates DJ-1 expression, affects colorectal cancer cells through PTEN-PI3K/AKT signaling. Methods: Colorectal cancer (CRC) tissues and adjacent tissues were collected followed by analysis of the level of miR-203, DJ-1 and PTEN. miR-203 and DJ-1 level was measured in HCT116, SW480 and normal colorectal cell NCM460. miR-203 mimic or miR-NC was transfected into HCT116 or SW480 cells followed by measuring the level of miR-203, DJ-1, PTEN, p-AKT as well as cell apoptosis and proliferation. Results: Compared with tumor adjacent tissues, tumor tissues showed significantly lower level of miR-203 and PTEN, and higher level of DJ-1. There is a targeted relationship between miR-203 and DJ-1. Compared with NCM460 cell, HCT116 and SW480 cells displayed significantly lower miR-203 level and higher DJ-1 expression. miR-203 mimic significantly reduced DJ-1 and p-AKT level, increased PTEN expression, cell apoptosis and inhibited cell proliferation. Conclusion: Lower miR-203 and higher DJ-1 level is found in CRC patients. Upregulation of miR-203 inhibits DJ-1 expression, increases PTEN expression, impairs PI3K/AKT signaling, inhibits CRC cell proliferation and promotes apoptosis.

miR-194 Regulates Cisplatin Resistance in Colorectal Cancer Cells Through Targeting Yes-Associated Protein

2020 ◽  
Vol 10 (2) ◽  
pp. 157-162
Author(s):  
Lei Wu ◽  
Si Cheng ◽  
Yong Meng ◽  
Yahui Huang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Expression Profiles ◽  
Resistant Cell Line ◽  
Control Group ◽  
Regulatory Relationship ◽  
Colorectal Cancer Cells ◽  
Sw480 Cells

Elevated Yes-associated protein (YAP1) expression is associated with colorectal cancer. Bioinfor-matics analysis showed a targeting relationship between miR-194 and YAP13′-UTR. Our study assessed miR-194’s role in proliferation, apoptosis, and CDDP resistance of colorectal cancer cells. The CDDP-resistant cell line SW480/CDDP was established and miR-194 and YAP1 level in parental SW480 cells and normal intestinal epithelial HCoEpiC cells was measured. SW480/CDDP cells were separated into control group, miR-NC group and miR-194 mimic group followed by analysis of miR-194 and YAP1 level, cell apoptosis and proliferation by flow cytometry. There was a targeted regulatory relationship between miR-194 and YAP1 mRNA. miR-194 was significantly upregulated in SW480/CDDP cells compared to SW480 cells and downregulated in SW480 cells compared to HCoEpiC cells. Whereas, opposite YAP1 expression profiles were found in SW480/CDDP, SW480 and HCoEpiC cells. miR-194 mimic significantly upregulated miR-194 in the SW480/CDDP cells, with decreased YAP1 expression, increased cell apoptosis, decreased cell proliferation and reduced IC50. Decreased miR-194 and increased YAP1 expression involve in CDDP resistance of colorectal cancer. Increase of miR-194 expression can inhibit colorectal cancer cell proliferation, promote apoptosis and reduce CDDP resistance by down-regulating YAP1 expression.

scholarly journals Activation of odorant receptor in colorectal cancer cells leads to inhibition of cell proliferation and apoptosis

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0172491 ◽  
Author(s):  
Lea Weber ◽  
Klaudia Al-Refae ◽  
Juliane Ebbert ◽  
Peter Jägers ◽  
Janine Altmüller ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Odorant Receptor ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cells

scholarly journals Effect of API-1 and FR180204 on cell proliferation and apoptosis in human DLD-1 and LoVo colorectal cancer cells

2016 ◽  
Vol 12 (4) ◽  
pp. 2463-2474 ◽  
Author(s):  
Atiye Seda Yar Saglam ◽  
Ebru Alp ◽  
Zubeyir Elmazoglu ◽  
Emine Sevda Menevse
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cells

Curcumin inhibits proliferation of hepatocellular carcinoma cells through down regulation of DJ-1

2020 ◽  
Vol 29 (1) ◽  
pp. 1-8
Author(s):  
Lina Han ◽  
Yu Wang ◽  
Shulun Sun
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Carcinoma Cells ◽  
Pten Expression ◽  
Hepatocellular Carcinoma Cells ◽  
Proliferation And Apoptosis

PTEN exerts tumor suppressor role through inhibiting PI3K/AKT signaling. DJ-1 plays an oncogenic role through negatively regulation of PTEN expression. Curcumin (Cur) is a phenolic compound extracted from a variety of plant roots, with multiple anti-tumor pharmacological effects. This study aims to investigate whether Cur plays a role in the regulation of DJ-1-PENT/PI3K/AKT signaling as well as the proliferation and apoptosis of hepatocellular carcinoma cells. Normal human hepatocyte HL-7702 and hepatocellular carcinoma cell lines SMMC-7721 and HepG2 were cultured followed by analysis of the expression of DJ-1 and PTEN. SMMC-7721 and HepG2 cells were treated with different concentrations of Cur (0, 5, 10 μM) followed by measuring cell proliferation by CCK-8, caspase-3 activity as well as DJ-1 expression by western blot. In addition, SMMC-7721 or HepG2 cells were divided into two groups: Cur+pcDNA3.1-Blank and Cur+pcDNA3.1-DJ-1 for analysis of the expression of DJ-1, PTEN and p-AKT, cell apoptosis and proliferation. Compared with HL-7702, SMMC-7721 and HepG2 cells displayed significantly higher DJ-1 expression and lower PTEN expression. Cur treatment significantly inhibited proliferation of SMMC-7721 and HepG2 cells, increased caspase-3 activity and downregulated DJ-1 expression. Transfection of pcDNA3.1-DJ-1 significantly increased DJ-1 and p-AKT expression, promoted cell proliferation, but decreased PTEN expression and cell apoptosis. In conclusion, Cur inhibits proliferation of hepatocellular carcinoma cells and PTEN/PI3K/AKT signaling pathway via the reduction of DJ-1 expression, which provides new insights to the anticancer effects of curcumin in hepatocellular carcinoma.

scholarly journals MSH2 is required for cell proliferation, cell cycle control and cell invasiveness in colorectal cancer cells

2012 ◽  
Vol 57 (20) ◽  
pp. 2580-2585
Author(s):  
Kai Shen ◽  
YingJiang Ye ◽  
KeWei Jiang ◽  
Bin Liang ◽  
XiaoDong Yang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Cycle Control ◽  
Colorectal Cancer Cells ◽  
Cell Invasiveness

scholarly journals Calcium Channel Protein ORAI1 Mediates TGF-β Induced Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Qingjie Kang ◽  
Xudong Peng ◽  
Xiangshu Li ◽  
Denghua Hu ◽  
Guangxu Wen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Transforming Growth Factor ◽  
Mesenchymal Transition ◽  
Colorectal Cancer Cells ◽  
Sw480 Cells ◽  
Sw620 Cells ◽  
Tgf Β1

Accumulating evidence suggested that calcium release-activated calcium modulator 1(ORAI1), a key calcium channel pore-forming protein-mediated store-operated Ca2+ entry (SOCE), is associated with human cancer. However, its role in colorectal cancer (CRC) progression has not been well studied. Epithelial-mesenchymal transition (EMT) is a multistep process that occurs during the progression of cancers and is necessary for metastasis of epithelial cancer. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that has been shown to induce EMT. In this study, we are aimed at exploring the effects of ORAI1 on TGF-β1-induced EMT process in CRC cells. Herein, we confirmed ORAI1 expression was higher in CRC tissues than in adjacent non-cancerous tissues by using immunohistochemical staining and Western blot analysis. Higher ORAI1 expression was associated with more advanced clinical stage, higher incidence of metastasis and shorter overall survival. We compared ORAI1 expression in SW480 and SW620 cells, two CRC cell lines with the same genetic background, but different metastatic potential. We found ORAI1 expression was significantly higher in SW620 cells which exhibited higher EMT characteristics. Furthermore, knockdown of ORAI1 suppressed the EMT of SW620 Cells. After induced the EMT process in SW480 cells with TGF-β1, we found treatment of TGF-β1 showed a significant increase in cell migration along with the loss of E-cadherin and an increase in N-cadherin and Vimentin protein levels. Also, TGF-β1 treatment increased ORAI1 expression and was closely associated with the increase of SOCE. Silencing ORAI1 significantly suppressed Ca2+ entry, reversed the changes of EMT-relevant marks expression induced by TGF-β1, and inhibited TGF-β1-mediated calpain activation and cell migration. Finally, we blocked SOCE with 2-APB (2-Aminoethyl diphenylborinate), a pharmacological inhibitor. Interestingly, 2-APB and sh-ORAI1 both exhibited similar inhibition effects to the SW480 cells. In conclusion, our results demonstrated that ORAI1 could mediate TGF-β-Induced EMT by promoting Ca2+ entry and calpain activity in Colorectal Cancer Cells.

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