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Tumor elimination by clustered microRNAs miR-306 and miR-79 via non-canonical activation of JNK signaling

Zhaowei Wang, Xiaoling Xia, View ORCID ProfileTatsushi Igaki
doi: https://doi.org/10.1101/2022.02.11.480121
Zhaowei Wang
1State Key Laboratory of Biocontrol, School of Ecology, Sun Yat-sen University, Shenzhen, Guangdong, 518107, China
2Laboratory of Genetics, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyoku, Kyoto, 607-8501, Japan
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Xiaoling Xia
2Laboratory of Genetics, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyoku, Kyoto, 607-8501, Japan
3Guangzhou Key Laboratory of Insect Development Regulation and Application Research, Institute of Insect Science and Technology & School of Life Sciences, South China Normal University, Guangzhou, Guangdong, 510631, China
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Tatsushi Igaki
2Laboratory of Genetics, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyoku, Kyoto, 607-8501, Japan
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  • ORCID record for Tatsushi Igaki
  • For correspondence: igaki.tatsushi.4s@kyoto-u.ac.jp
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Abstract

JNK signaling plays a critical role in both tumor promotion and tumor suppression. Here, we identified clustered microRNAs (miRNAs) miR-306 and miR-79 as novel tumor-suppressor miRNAs that specifically eliminate JNK-activated tumors in Drosophila. While showing no significant effect on normal tissue growth, miR-306 and miR-79 strongly suppressed growth of multiple tumor models including malignant tumors caused by Ras activation and cell polarity defects. Mechanistically, these miRNAs commonly target the mRNA of an E3 ubiquitin ligase Drosophila ring finger protein 146 (dRNF146). We found that DRNF146 promotes degradation of tankyrase (Tnks), an ADP-ribose polymerase that promotes JNK activation in a non-canonical manner. Thus, downregulation of dRNF146 by miR-306 and miR-79 leads to hyper-enhancement of JNK activation. Our data show that, while JNK activity is essential for tumor growth, elevation of miR-306 or miR-79 overactivate JNK signaling to the lethal level via non-canonical JNK pathway and thus eliminate tumors, providing a new miRNA-based strategy against cancer.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted February 11, 2022.
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Tumor elimination by clustered microRNAs miR-306 and miR-79 via non-canonical activation of JNK signaling
Zhaowei Wang, Xiaoling Xia, Tatsushi Igaki
bioRxiv 2022.02.11.480121; doi: https://doi.org/10.1101/2022.02.11.480121
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Tumor elimination by clustered microRNAs miR-306 and miR-79 via non-canonical activation of JNK signaling
Zhaowei Wang, Xiaoling Xia, Tatsushi Igaki
bioRxiv 2022.02.11.480121; doi: https://doi.org/10.1101/2022.02.11.480121

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