MK2206 overcomes the resistance of human liver cancer stem cells to sorafenib by inhibition of pAkt and upregulation of pERK

Tumor Biology ◽  
2015 ◽  
Vol 37 (6) ◽  
pp. 8047-8055 ◽  
Author(s):  
Beibei Zhai ◽  
Xiaofeng Zhang ◽  
Bin Sun ◽  
Lu Cao ◽  
Linlin Zhao ◽  
...  
2020 ◽  
Vol 28 (2) ◽  
pp. 572-586 ◽  
Author(s):  
Liyan Wang ◽  
Xiaonan Li ◽  
Wei Zhang ◽  
Yuxin Yang ◽  
Qiuyu Meng ◽  
...  

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Chen Wang ◽  
Xiaoxue Jiang ◽  
Xiaonan Li ◽  
Shuting Song ◽  
Qiuyu Meng ◽  
...  

Abstract Background The functions of HULC have been demonstrated in several cancers. However, its mechanism has not been elucidated in human liver cancer stem cells. Methods Liver cancer stem cells were isolated from Huh7 cells; gene infection and tumorigenesis test in vitro and in vivo were performed. Results We demonstrate that HULC promotes growth of liver cancer stem cells in vitro and in vivo. Mechanistically, HULC enhances the expression of Sirt1 dependent on miR675 and then induces the cellular autophagy through Sirt1. HULC enhances CyclinD1 and thereby increases pRB and inhibited P21 WAF1/CIP 1 via autophagy-miR675-PKM2 pathway in human liver cancer stem cells. Ultimately, our results demonstrate that CyclinD1 is required for the oncogenic functions of HULC in liver cancer stem cells. Conclusions It reveals the key molecular signaling pathways for HULC and provides important basic information for finding effective tumor therapeutic targets based on HULC.


2021 ◽  
Author(s):  
Shuting Song ◽  
Sijie Xie ◽  
Rushi Qin ◽  
Yanan Lu ◽  
Liyan Wang ◽  
...  

Abstract Background: Long noncoding RNAs have recently considered as central regulators in diverse biological processes and emerged as vital players controlling tumorigenesis. Although wild MEG3 acts as a suppressor in several cancers, the function of mutant MEG3 is also unclear during tumorigenesis.Methods: Lentivalus infection,RT-PCR,Western blotting and tumorigenesis test in vitro and in vivo were performed.Results: our results suggest that mutant MEG3 promotes the growth of human liver cancer stem cells in vivo and in vitro.Mechanistically, our results show that mutant MEG3 enhances acetylation modification of HistoneH4 on K16.Then, mutant MEG3 enhances the expression of SETD2 dependent on H4K16Ac.Moreover, mutant MEG3 increases the DNA damage repair through SETD2.Ultimately, mutant MEG3 increases the telomeras activity dependent on DNA damage repair.Strikingly,TERT determines the cancerous function of mutant MEG3 in liver cancer stem cells. Therefore, we shed light on the fact that targeting mutant MEG3 could be a viable approach for cancer treatment.Conclusions: these observations will play an important role in finding effective tumor treatment targets.


2021 ◽  
Vol 23 ◽  
pp. 310-323
Author(s):  
Xiaoxue Jiang ◽  
Libo Xing ◽  
Yingjie Chen ◽  
Rushi Qin ◽  
Shuting Song ◽  
...  

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Ruijiao Kong ◽  
Haidong Liu ◽  
Yi Shi ◽  
Qiuhong Man ◽  
Shanrong Liu

2010 ◽  
Vol 120 (9) ◽  
pp. 3326-3339 ◽  
Author(s):  
Naotsugu Haraguchi ◽  
Hideshi Ishii ◽  
Koshi Mimori ◽  
Fumiaki Tanaka ◽  
Masahisa Ohkuma ◽  
...  

2015 ◽  
Vol 125 (10) ◽  
pp. 3795-3808 ◽  
Author(s):  
Pingping Zhu ◽  
Yanying Wang ◽  
Lei He ◽  
Guanling Huang ◽  
Ying Du ◽  
...  

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