p53 target miR-29c-3p suppresses colon cancer cell invasion and migration through inhibition of PHLDB2

2017 ◽  
Vol 487 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Geng Chen ◽  
Tong Zhou ◽  
Yang Li ◽  
Zhenxiang Yu ◽  
Liankun Sun
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Qi-Hong Jiang ◽  
Ai-Xiang Wang ◽  
Yan Chen

As a member of the ezrin-radixin-moesin (ERM) family, radixin is overexpressed in many tumor tissues. However, little is known about its role in the progression of colon cancer. So we here aimed to determine the function of radixin in colon cancer cell invasion. Interestingly, we found that the expression of radixin was significantly elevated in colon cancer cells. Knockdown of radixin suppressed the invasion and migration of colon cancer cells. Further, knockdown of radixin inhibited the activation of Rac1 and ERK1/2, and decreased the expression and secretion of MMP-7. In addition, Rac1-ERK signaling pathway was required for the radixin-promoted invasion and MMP-7 production. Together, our findings suggest that radixin enhances the invasion and migration of colon cancer cells. Activation of Rac1-ERK pathway and consequent upregulation of MMP-7 production may contribute to the function of radixin in the regulation of colon cancer cell invasion. Thus, radixin may act as a novel target for the diagnosis and treatment of colon cancer.


2017 ◽  
Vol 18 (8) ◽  
pp. 964-982 ◽  
Author(s):  
Jolien Bridelance ◽  
Zuzanna Drebert ◽  
Olivier De Wever ◽  
Marc Bracke ◽  
Ilse M. Beck

2020 ◽  
Vol 16 ◽  
Author(s):  
Vibhavana Singh ◽  
Rakesh Reddy ◽  
Antarip Sinha ◽  
Venkatesh Marturi ◽  
Shravani Sripathi Panditharadyula ◽  
...  

: Diabetes and breast cancer are pathophysiologically similar and clinically established diseases that co-exist with a wider complex similar molecular signalling and having similar set of risk factors. Insulin plays a pivotal role for invasion and migration of breast cancer cells. Several ethnopharmacological evidences light the concomitant anti-diabetic and anti-cancer activity of medicinal plant and phytochemicals against breast tumor of patients with diabetes. This present article reviewed the findings on medicinal plants and phytochemicals with concomitant anti-diabetic and anti-cancer effects reported in scientific literature to facilitate the development of dual-acting therapies against diabetes and breast cancer. The schematic tabular form of published literatures on medicinal plants (63 plants belongs to 45 families) concluded the dynamics of phytochemicals against diabetes and breast tumor that could be explored further for the discovery of therapies for controlling of breast cancer cell invasion and migration in patient with diabetes.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ding Zhu ◽  
Xueshuang Huang ◽  
Fang Liang ◽  
Lijing Zhao

This article has been retracted. Please see the Retraction Notice for more detail: 10.1186/s13048-020-00747-z


2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing-an-zi Wang ◽  
Yongxiu Yang ◽  
Xiaolei Liang

Abstract Background Although lncRNA CTBP1-AS2 has been functionally analyzed only in cardiomyocyte hypertrophy and diabetes, analysis of TCGA dataset revealed its downregulation in endometrial carcinoma (EC), indicating its involvement in EC. Results In this study we found that CTBP1-AS2 was downregulated in EC and correlated with poor survival. MiR-216a might form base pairs with CTBP1-AS2 based on RNA-RNA interaction, which was confirmed by luciferase activity assay. Interestingly, upregulation of PTEN was observed after CTBP1-AS2 overexpression. Transwell assay showed that CTBP1-AS2 and PTEN overexpression led to decreased cancer cell invasion and migration and reduced enhancing effects of miR-216a on cell invasion and migration. It was known that miR-216a targeted PTEN. Conclusion Therefore, CTBP1-AS2 may sponge miR-216a to upregulate PTEN, thereby suppressing endometrial cancer cell invasion and migration.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
JunYu Ren ◽  
Wenliang Li ◽  
Guoqing Pan ◽  
Fengchang Huang ◽  
Jun Yang ◽  
...  

Decreased expression of miR-142-3p was observed in human cancers. However, the function and mechanism of miR-142-3p in human colorectal cancer remain obscure. The expressions of miR-142-3p in human colorectal cancer tissues and cell lines were measured by RT-qPCR. The effects of miR-142-3p on cell invasion and migration were detected by transwell assays. The efficiency of aerobic glycolysis was determined by glucose consumption and lactate production. Dual-luciferase reporter assays were performed to confirm the correlation between miR-142-3p and pyruvate kinase isozyme M2 (PKM2). The level of PKM2 was assessed by western blotting. Our results showed that the expression of miR-142-3p was decreased both in human colorectal cancer tissues and in cells. Overexpression of miR-142-3p in cell line attenuated colorectal cancer cell invasion and migration. About the underlying mechanism, we found that miR-142-3p modulated aerobic glycolysis via targeting pyruvate kinase M2 (PKM2). In addition, we demonstrated PKM2 and PKM2-mediated aerobic glycolysis contributes to miR-142-3p-mediated colorectal cancer cell invasion and migration. Hence, these data suggested that miR-142-3p was a potential therapeutic target for the treatment of human colorectal cancer.


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