scholarly journals In vivo and in vitro inhibition of human liver cancer progress by downregulation of the μ-opioid receptor and relevant mechanisms

2013 ◽  
Vol 30 (4) ◽  
pp. 1731-1738 ◽  
Author(s):  
JIN LU ◽  
ZEFENG LIU ◽  
LINGLING ZHAO ◽  
HUIMIN TIAN ◽  
XIUHUA LIU ◽  
...  
2019 ◽  
Vol 39 (11) ◽  
pp. 5973-5982 ◽  
Author(s):  
SACHIKO OGASAWARA ◽  
YUTARO MIHARA ◽  
REIICHIRO KONDO ◽  
HIRONORI KUSANO ◽  
JUN AKIBA ◽  
...  

2006 ◽  
Vol 26 (8) ◽  
pp. 964-975 ◽  
Author(s):  
Hirohisa Yano ◽  
Sachiko Ogasawara ◽  
Seiya Momosaki ◽  
Jun Akiba ◽  
Sakiko Kojiro ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Hong-Ryul Jung ◽  
Hyun Mi Kang ◽  
Jea-Woon Ryu ◽  
Dae-Soo Kim ◽  
Kyung Hee Noh ◽  
...  

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.


2020 ◽  
Author(s):  
Xiaoxue Jiang ◽  
Liyan wang ◽  
sijie xie ◽  
Yingjie Chen ◽  
Shuting Song ◽  
...  

Abstract Background: MEG3 is abnormally down-regulated in most tumors and inhibits tumorigenesis. Methods: Gene infection, Western blotting and tumorigenesis test in vitro and in vivo were performed to analyze the signaling pathway. Results: MEG3 increased the loading of P300 and RNA polymerase II onto the promoter regions of P53. Notably, MEG3 increased the methylation of histone H3 at lysine 27 through increasing the interplay between PRC2 and histone H3. Furthermore, MEG3 inhibited the expression of TERT by increasing the H3K27me3 and decreasing the loading of RNA pol Ⅱ in TERT promoter regions. Moreover, MEG3 inhibit the activity of telomerase by reducing the binding of TERT to TERC competitively. In addition, MEG3 also increased the TERRA through reducing DNA methyltransferase DNMT3b binding to the promoter regions of TERRA competitively. Therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibited the activity of telomerase in hLCSCs.In particular, MEG3 shortened the length of telomere by blocking the formation of complex maintaining telomere length(POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere competitively, which was caused by increasing the interplay between P53 and HULC in hLCSCs.Strikingly, MEG3 inhibited the growth in vitro and in vivo of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2). Conclusions: our results demonstrated MEG3 inhibits the occurrence of human liver cancer and these findings provide an important insight into the prevention and treatment of human liver cancer.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaoxue Jiang ◽  
Liyan Wang ◽  
Sijie Xie ◽  
Yingjie Chen ◽  
Shuting Song ◽  
...  

Abstract Background MEG3 downregulated the expression in several tumors and inhibits human tumorigenesis. But so far, the mechanism of MEG3 in tumorigenesis is still unclear. Methods In gene infection, cellular and molecular technologies and tumorigenesis test in vitro and in vivo were performed, respectively. Results Our results indicate that MEG3 enhances the P53 expression by triggering the loading of P300 and RNA polymerase II onto its promoter regions dependent on HP1α. Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53. Furthermore, MEG3 inhibits the expression of TERT by increasing the H3K27me3 in TERT promoter regions, thereby inhibiting the activity of telomerase by reducing the binding of TERT to TERC. Furthermore, MEG3 also increases the expression of TERRA; therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibits the activity of telomerase in hLCSCs. Strikingly, MEG3 reduces the length of telomere by blocking the formation of complex maintaining telomere length (POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere by increasing the interplay between P53 and HULC. Ultimately, MEG3 inhibits the growth of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2). Conclusions Our results demonstrates MEG3 inhibits the occurrence of human liver cancer by blocking telomere, and these findings provide an important insight into the prevention and treatment of human liver cancer.


PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e83195 ◽  
Author(s):  
Hironori Kusano ◽  
Jun Akiba ◽  
Sachiko Ogasawara ◽  
Sakiko Sanada ◽  
Makiko Yasumoto ◽  
...  

2020 ◽  
Author(s):  
Xiaoxue Jiang ◽  
Liyan Wang ◽  
Sijie Xie ◽  
Yingjie Chen ◽  
Shuting Song ◽  
...  

Abstract Background: MEG3 is down-regulated expression in several tumors and inhibits human tumorigenesis. But so far, the mechanism of MEG3 in tumorigenesis is still unclear. Methods: Gene infection, cellular and molecular technologies and tumorigenesis test in vitro and in vivo were performed,respectively.Results: our results indicate that MEG3 enhances the P53 expression by triggering the loading of P300 and RNA polymerase II onto its promoter regions dependent on HP1α. Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53. Furthermore, MEG3 inhibits the expression of TERT by increasing the H3K27me3 in TERT promoter regions. Thereby, MEG3 inhibits the activity of telomerase by reducing the binding of TERT to TERC. Furthermore, MEG3 also increases the expression of TERRA ,therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibits the activity of telomerase in hLCSCs. Strikingly, MEG3 reduces the length of telomere by blocking the formation of complex maintaining telomere length(POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere by increasing the interplay between P53 and HULC. Ultimately, MEG3 inhibits the growth of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2). Conclusions: Our results demonstrates MEG3 inhibits the occurrence of human liver cancer by blocking telomere and these findings provide an important insight into the prevention and treatment of human liver cancer.


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