ArticleOncotarget2016
PICT-1 triggers a pro-death autophagy through inhibiting rRNA transcription and AKT/mTOR/p70S6K signaling pathway.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- The stress sensor GCN2 differentially controls ribosome biogenesis in colon cancer according to the nutritional context.Molecular oncology · 2024Article
- G-quadruplex ligands as potent regulators of lysosomes.Autophagy · 2023Article
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- UBTF facilitates melanoma progression via modulating MEK1/2-ERK1/2 signalling pathways by promoting GIT1 transcription.Cancer cell international · 2021Article
- NOP53 Suppresses Autophagy throughInternational journal of molecular sciences · 2021Article
- Cell-Penetrating Peptides Predicted From CASC3, AKIP1, and AHRR Proteins.Frontiers in pharmacology · 2021Article
- Role of Autophagy in Cancer Cell Response to Nucleolar and Endoplasmic Reticulum Stress.International journal of molecular sciences · 2020Review
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- Emerging Role of the Nucleolar Stress Response in Autophagy.Frontiers in cellular neuroscience · 2019Review
- The nucleolus, an ally, and an enemy of cancer cells.Histochemistry and cell biology · 2018Review
- Delphinidin induced protective autophagy via mTOR pathway suppression and AMPK pathway activation in HER-2 positive breast cancer cells.BMC cancer · 2018Article
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- New roles for Dicer in the nucleolus and its relevance to cancer.Cell cycle (Georgetown, Tex.) · 2017Review
- Apigenin-induced lysosomal degradation of β-catenin in Wnt/β-catenin signaling.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PICT-1 was originally identified as a tumor suppressor. Here, we found that PICT-1 overexpression triggered pro-death autophagy without nucleolar disruption or p53 accumulation in U251 and MCF7 cells. Truncated PICT-1 fragments 181-346 and 1-346, which partly or totally lack nucleolar localization, showed weaker autophagy-inducing effects than full-length PICT-1 and a well-defined nucleolar mutant (181-479). Furthermore, PICT-1 partly localizes to the nucleolar fibrillar center (FC) and directly binds to ribosomal DNA (rDNA) gene loci, where it interacts with upstream binding factor (UBF). Overexpression of PICT-1 or the 181-479 mutant, but not the 1-346 or 181-346 mutants, markedly inhibited the phosphorylation of UBF and the recruitment of rRNA polymerase I (Pol I) to the rDNA promoter in response to serum stimulation, thereby suppressing rRNA transcription, suggesting that rRNA transcription inhibition might be an important contributor to PICT-1-induced autophagy. This is supported by the finding that CX-5461, a specific Pol I inhibitor, also induced autophagy. In addition, both CX-5461 and PICT-1, but not the 1-346 or 181-346 mutants, significantly suppressed the activation of the Akt/mTOR/p70S6K signaling pathway. Our data show that PICT-1 triggers pro-death autophagy through inhibition of rRNA transcription and the inactivation of AKT/mTOR/p70S6K pathway, independent of nucleolar disruption and p53 activation.
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