scholarly journals Aptamer-conjugated nanomaterials for specific cancer cell recognition and targeted cancer therapy

2014 ◽  
Vol 6 (4) ◽  
pp. e95-e95 ◽  
Author(s):  
Qiaoling Liu ◽  
Chen Jin ◽  
Yanyue Wang ◽  
Xiaohong Fang ◽  
Xiaobing Zhang ◽  
...  
2020 ◽  
Vol 117 (36) ◽  
pp. 22390-22401 ◽  
Author(s):  
Shuo Shi ◽  
Zhen-Zhen Yang ◽  
Sanhong Liu ◽  
Fan Yang ◽  
Haifan Lin

Targeted cancer therapy aims to achieve specific elimination of cancerous but not normal cells. Recently, PIWI proteins, a subfamily of the PAZ-PIWI domain (PPD) protein family, have emerged as promising candidates for targeted cancer therapy. PPD proteins are essential for small noncoding RNA pathways. The Argonaute subfamily partners with microRNA and small interfering RNA, whereas the PIWI subfamily partners with PIWI-interacting RNA (piRNA). Both PIWI proteins and piRNA are mostly expressed in the germline and best known for their function in transposon silencing, with no detectable function in mammalian somatic tissues. However, PIWI proteins become aberrantly expressed in multiple types of somatic cancers, thus gaining interest in targeted therapy. Despite this, little is known about the regulatory mechanism of PIWI proteins in cancer. Here we report that one of the four PIWI proteins in humans, PIWIL1, is highly expressed in gastric cancer tissues and cell lines. Knocking out the PIWIL1 gene (PIWIL1-KO) drastically reduces gastric cancer cell proliferation, migration, metastasis, and tumorigenesis. RNA deep sequencing of gastric cancer cell line SNU-1 reveals that KO significantly changes the transcriptome, causing the up-regulation of most of its associated transcripts. Surprisingly, few bona fide piRNAs exist in gastric cancer cells. Furthermore, abolishing the piRNA-binding activity of PIWIL1 does not affect its oncogenic function. Thus, PIWIL1 function in gastric cancer cells is independent of piRNA. This piRNA-independent regulation involves interaction with the UPF1-mediated nonsense-mediated mRNA decay (NMD) mechanism. Altogether, our findings reveal a piRNA-independent function of PIWIL1 in promoting gastric cancer.


2021 ◽  
Vol Volume 16 ◽  
pp. 2123-2136
Author(s):  
Shini Feng ◽  
Yajing Ren ◽  
Hui Li ◽  
Yunfei Tang ◽  
Jinyu Yan ◽  
...  

2020 ◽  
Author(s):  
Shuo Shi ◽  
Zhen-Zhen Yang ◽  
Sanhong Liu ◽  
Fan Yang ◽  
Haifan Lin

ABSTRACTTargeted cancer therapy aims to achieve specific elimination of cancerous but not normal cells. Recently, PIWI proteins, a subfamily of the PAZ-PIWI Domain (PPD) protein family, have emerged as promising candidates for targeted cancer therapy. PPD proteins are essential for small non-coding RNA pathways. The Argonaute subfamily partners with microRNA and small interfering RNA, whereas the PIWI subfamily partners with PIWI-interacting RNA (piRNA). Both PIWI proteins and piRNA are mostly expressed in the germline and best known for their function in transposon silencing, with no detectable function in mammalian somatic tissues. However, PIWI proteins become aberrantly expressed in multiple types of somatic cancers, thus gaining interest in targeted therapy. Despite this, little is known about the regulatory mechanism of PIWI proteins in cancer. Here we report that one of the four PIWI proteins in humans, PIWIL1, is highly expressed in gastric cancer tissues and cell lines. Knocking out PIWIL1 expression (PIWIL1-KO) drastically reduces gastric cancer cell proliferation, migration, metastasis, and tumorigenesis. RNA deep sequencing of gastric cancer cell line SNU-1 reveals that PIWIL1-KO significantly changes the transcriptome, causing the up-regulation of most of its associated transcripts. Surprisingly, few bona fide piRNAs exist in gastric cancer cells. Furthermore, abolishing the piRNA-binding activity of PIWIL1 does not affect its oncogenic function. Thus, PIWIL1 function in gastric cancer cells is independent of piRNA. This piRNA-independent regulation involves interaction with the UPF1-mediated nonsense-mediated mRNA decay (NMD) mechanism. Altogether, our findings reveal a novel and piRNA-independent function of PIWIL1 in promoting gastric cancer.SIGNIFICANCEPrecision medicine aims to cure cancer without affecting normal tissues. PIWI proteins provide a promising opportunity for precision medicine because they are normally expressed only in the testis for male fertility but gain expression in diverse types of cancers. Thus, inhibiting PIWI expression may stop cancer development (and spermatogenesis) without affecting normal body function. To establish causality between PIWI and cancer, we show here that the expression of PIWIL1, a human PIWI protein, promotes gastric cancer. Surprisingly, this oncogenic function does not require piRNA, the expected partner of PIWI proteins, but involves the nonsense-mediated mRNA decay mechanism. These findings reveal a new function and action mechanism of PIWI proteins in oncogenesis, guiding the identification of PIWI inhibitors to cure cancer.


2015 ◽  
Vol 22 (11) ◽  
pp. 1335-1347 ◽  
Author(s):  
Yan Gao ◽  
Jacson Shen ◽  
Lara Milane ◽  
Francis Hornicek ◽  
Mansoor Amiji ◽  
...  

2014 ◽  
Vol 20 (32) ◽  
pp. 5218-5244 ◽  
Author(s):  
A. Aerts ◽  
N.R.E.N. Impens ◽  
M. Gijs ◽  
M. D'Huyvetter ◽  
H. Vanmarcke ◽  
...  

2011 ◽  
Vol 11 (10) ◽  
pp. 983-992 ◽  
Author(s):  
Arthur E. Frankel ◽  
Carol Carter ◽  
Shu-Ru Kuo ◽  
Jung-Hee Woo ◽  
Jeremy Mauldin ◽  
...  

2014 ◽  
Vol 3 (2) ◽  
pp. 83-88 ◽  
Author(s):  
Maria Gazouli ◽  
Nikolitsa Nomikou ◽  
John F Callan ◽  
Efstathios P. Efstathopoulos

Sign in / Sign up

Export Citation Format

Share Document