PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease.

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PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease. / Boele, Joost; Persson, Helena; Shin, Jay W; Ishizu, Yuri; Newie, Inga; Sökilde, Rolf; Hawkins, Shannon M; Coarfa, Cristian; Ikeda, Kazuhiro; Takayama, Ken-Ichi; Horie-Inoue, Kuniko; Ando, Yoshinari; Burroughs, A Maxwell; Sasaki, Chihiro; Suzuki, Chizuru; Sakai, Mizuho; Aoki, Shintaro; Ogawa, Ayumi; Hasegawa, Akira; Lizio, Marina; Kaida, Kaoru; Teusink, Bas; Carninci, Piero; Suzuki, Harukazu; Inoue, Satoshi; Gunaratne, Preethi H; Rovira, Carlos; Hayashizaki, Yoshihide; de Hoon, Michiel J L.

In: Proceedings of the National Academy of Sciences, Vol. 111, No. 31, 2014, p. 11467-11472.

Research output: Contribution to journalArticle

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Boele, J, Persson, H, Shin, JW, Ishizu, Y, Newie, I, Sökilde, R, Hawkins, SM, Coarfa, C, Ikeda, K, Takayama, K-I, Horie-Inoue, K, Ando, Y, Burroughs, AM, Sasaki, C, Suzuki, C, Sakai, M, Aoki, S, Ogawa, A, Hasegawa, A, Lizio, M, Kaida, K, Teusink, B, Carninci, P, Suzuki, H, Inoue, S, Gunaratne, PH, Rovira, C, Hayashizaki, Y & de Hoon, MJL 2014, 'PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease.', Proceedings of the National Academy of Sciences, vol. 111, no. 31, pp. 11467-11472. https://doi.org/10.1073/pnas.1317751111

APA

CBE

Boele J, Persson H, Shin JW, Ishizu Y, Newie I, Sökilde R, Hawkins SM, Coarfa C, Ikeda K, Takayama K-I, Horie-Inoue K, Ando Y, Burroughs AM, Sasaki C, Suzuki C, Sakai M, Aoki S, Ogawa A, Hasegawa A, Lizio M, Kaida K, Teusink B, Carninci P, Suzuki H, Inoue S, Gunaratne PH, Rovira C, Hayashizaki Y, de Hoon MJL. 2014. PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease. Proceedings of the National Academy of Sciences. 111(31):11467-11472. https://doi.org/10.1073/pnas.1317751111

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Boele, Joost ; Persson, Helena ; Shin, Jay W ; Ishizu, Yuri ; Newie, Inga ; Sökilde, Rolf ; Hawkins, Shannon M ; Coarfa, Cristian ; Ikeda, Kazuhiro ; Takayama, Ken-Ichi ; Horie-Inoue, Kuniko ; Ando, Yoshinari ; Burroughs, A Maxwell ; Sasaki, Chihiro ; Suzuki, Chizuru ; Sakai, Mizuho ; Aoki, Shintaro ; Ogawa, Ayumi ; Hasegawa, Akira ; Lizio, Marina ; Kaida, Kaoru ; Teusink, Bas ; Carninci, Piero ; Suzuki, Harukazu ; Inoue, Satoshi ; Gunaratne, Preethi H ; Rovira, Carlos ; Hayashizaki, Yoshihide ; de Hoon, Michiel J L. / PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease. In: Proceedings of the National Academy of Sciences. 2014 ; Vol. 111, No. 31. pp. 11467-11472.

RIS

TY - JOUR

T1 - PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease.

AU - Boele, Joost

AU - Persson, Helena

AU - Shin, Jay W

AU - Ishizu, Yuri

AU - Newie, Inga

AU - Sökilde, Rolf

AU - Hawkins, Shannon M

AU - Coarfa, Cristian

AU - Ikeda, Kazuhiro

AU - Takayama, Ken-Ichi

AU - Horie-Inoue, Kuniko

AU - Ando, Yoshinari

AU - Burroughs, A Maxwell

AU - Sasaki, Chihiro

AU - Suzuki, Chizuru

AU - Sakai, Mizuho

AU - Aoki, Shintaro

AU - Ogawa, Ayumi

AU - Hasegawa, Akira

AU - Lizio, Marina

AU - Kaida, Kaoru

AU - Teusink, Bas

AU - Carninci, Piero

AU - Suzuki, Harukazu

AU - Inoue, Satoshi

AU - Gunaratne, Preethi H

AU - Rovira, Carlos

AU - Hayashizaki, Yoshihide

AU - de Hoon, Michiel J L

PY - 2014

Y1 - 2014

N2 - Next-generation sequencing experiments have shown that microRNAs (miRNAs) are expressed in many different isoforms (isomiRs), whose biological relevance is often unclear. We found that mature miR-21, the most widely researched miRNA because of its importance in human disease, is produced in two prevalent isomiR forms that differ by 1 nt at their 3' end, and moreover that the 3' end of miR-21 is posttranscriptionally adenylated by the noncanonical poly(A) polymerase PAPD5. PAPD5 knockdown caused an increase in the miR-21 expression level, suggesting that PAPD5-mediated adenylation of miR-21 leads to its degradation. Exoribonuclease knockdown experiments followed by small-RNA sequencing suggested that PARN degrades miR-21 in the 3'-to-5' direction. In accordance with this model, microarray expression profiling demonstrated that PAPD5 knockdown results in a down-regulation of miR-21 target mRNAs. We found that disruption of the miR-21 adenylation and degradation pathway is a general feature in tumors across a wide range of tissues, as evidenced by data from The Cancer Genome Atlas, as well as in the noncancerous proliferative disease psoriasis. We conclude that PAPD5 and PARN mediate degradation of oncogenic miRNA miR-21 through a tailing and trimming process, and that this pathway is disrupted in cancer and other proliferative diseases.

AB - Next-generation sequencing experiments have shown that microRNAs (miRNAs) are expressed in many different isoforms (isomiRs), whose biological relevance is often unclear. We found that mature miR-21, the most widely researched miRNA because of its importance in human disease, is produced in two prevalent isomiR forms that differ by 1 nt at their 3' end, and moreover that the 3' end of miR-21 is posttranscriptionally adenylated by the noncanonical poly(A) polymerase PAPD5. PAPD5 knockdown caused an increase in the miR-21 expression level, suggesting that PAPD5-mediated adenylation of miR-21 leads to its degradation. Exoribonuclease knockdown experiments followed by small-RNA sequencing suggested that PARN degrades miR-21 in the 3'-to-5' direction. In accordance with this model, microarray expression profiling demonstrated that PAPD5 knockdown results in a down-regulation of miR-21 target mRNAs. We found that disruption of the miR-21 adenylation and degradation pathway is a general feature in tumors across a wide range of tissues, as evidenced by data from The Cancer Genome Atlas, as well as in the noncancerous proliferative disease psoriasis. We conclude that PAPD5 and PARN mediate degradation of oncogenic miRNA miR-21 through a tailing and trimming process, and that this pathway is disrupted in cancer and other proliferative diseases.

U2 - 10.1073/pnas.1317751111

DO - 10.1073/pnas.1317751111

M3 - Article

VL - 111

SP - 11467

EP - 11472

JO - Proceedings of the National Academy of Sciences

T2 - Proceedings of the National Academy of Sciences

JF - Proceedings of the National Academy of Sciences

SN - 1091-6490

IS - 31

ER -