Food-Derived Compounds Apigenin and Luteolin Modulate mRNA Splicing of Introns with Weak Splice Sites
Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widesp...
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| Published in | iScience Vol. 22; pp. 336 - 352 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
20.12.2019
Elsevier |
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| Abstract | Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)+ RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A)+ RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development.
[Display omitted]
•Food-derived compounds, apigenin and luteolin, modulate mRNA splicing•The treatment of these flavonoids causes numerous alternative splicing events•Splicing of introns with weak splice sites tend to be inhibited by these flavonoids•Tumorigenic cells are more sensitive to these flavonoids than non-tumorigenic cells
Molecular Biology |
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| AbstractList | Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)
+
RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A)
+
RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression
in vivo
that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development.
•
Food-derived compounds, apigenin and luteolin, modulate mRNA splicing
•
The treatment of these flavonoids causes numerous alternative splicing events
•
Splicing of introns with weak splice sites tend to be inhibited by these flavonoids
•
Tumorigenic cells are more sensitive to these flavonoids than non-tumorigenic cells
Molecular Biology Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)+ RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A)+ RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development. [Display omitted] •Food-derived compounds, apigenin and luteolin, modulate mRNA splicing•The treatment of these flavonoids causes numerous alternative splicing events•Splicing of introns with weak splice sites tend to be inhibited by these flavonoids•Tumorigenic cells are more sensitive to these flavonoids than non-tumorigenic cells Molecular Biology Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A) RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A) RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development. Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)+ RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A)+ RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development. : Molecular Biology Subject Areas: Molecular Biology Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)+ RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A)+ RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development.Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)+ RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than nontumorigenic cells, both for the nuclear poly(A)+ RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development. |
| Author | Yamanaka, Yasutaka Shibuya, Yasuyuki Kobayashi, Hisato Seno, Shigeto Kurata, Masashi Fujiwara, Naoko Fujita, Ken-ichi Miyamae, Yusaku Masuda, Seiji Takahashi, Nobuyuki |
| AuthorAffiliation | 6 Department of Nutritional Science and Food Safety, Tokyo University of Agriculture, Tokyo 156-8502, Japan 4 NODAI Genome Research Center, Tokyo University of Agriculture, Tokyo 156-8502, Japan 2 Department of Oral and Maxillofacial Surgery, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan 1 Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan 3 Department of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Osaka 565-0871, Japan 5 Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan |
| AuthorAffiliation_xml | – name: 6 Department of Nutritional Science and Food Safety, Tokyo University of Agriculture, Tokyo 156-8502, Japan – name: 5 Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan – name: 2 Department of Oral and Maxillofacial Surgery, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan – name: 4 NODAI Genome Research Center, Tokyo University of Agriculture, Tokyo 156-8502, Japan – name: 1 Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan – name: 3 Department of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Osaka 565-0871, Japan |
| Author_xml | – sequence: 1 givenname: Masashi surname: Kurata fullname: Kurata, Masashi organization: Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan – sequence: 2 givenname: Naoko surname: Fujiwara fullname: Fujiwara, Naoko organization: Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan – sequence: 3 givenname: Ken-ichi surname: Fujita fullname: Fujita, Ken-ichi organization: Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan – sequence: 4 givenname: Yasutaka surname: Yamanaka fullname: Yamanaka, Yasutaka organization: Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan – sequence: 5 givenname: Shigeto surname: Seno fullname: Seno, Shigeto organization: Department of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Osaka 565-0871, Japan – sequence: 6 givenname: Hisato surname: Kobayashi fullname: Kobayashi, Hisato organization: NODAI Genome Research Center, Tokyo University of Agriculture, Tokyo 156-8502, Japan – sequence: 7 givenname: Yusaku surname: Miyamae fullname: Miyamae, Yusaku organization: Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan – sequence: 8 givenname: Nobuyuki surname: Takahashi fullname: Takahashi, Nobuyuki organization: Department of Nutritional Science and Food Safety, Tokyo University of Agriculture, Tokyo 156-8502, Japan – sequence: 9 givenname: Yasuyuki surname: Shibuya fullname: Shibuya, Yasuyuki organization: Department of Oral and Maxillofacial Surgery, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan – sequence: 10 givenname: Seiji surname: Masuda fullname: Masuda, Seiji email: masuda@kais.kyoto-u.ac.jp organization: Division of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31809999$$D View this record in MEDLINE/PubMed |
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| Snippet | Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate... |
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| Title | Food-Derived Compounds Apigenin and Luteolin Modulate mRNA Splicing of Introns with Weak Splice Sites |
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