ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
KLF16 enhances stress tolerance of colorectal carcinomas by modulating nucleolar homeostasis and translational reprogramming.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- SERHL regulates invasion and metastasis through KLF16-PLCB1/PRKCA signaling in gastric cancer cells.Genes & diseases · 2026Article
- Predictive modeling of signal-responsive cis-elements in human red blood cell precursors.Nucleic acids research · 2026Article
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
- Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus.Molecular cell · 2026Review
- Fibrillarin Contributes to the Oncogenic Characteristics of Colorectal Cancer Cells and Reduces Sensitivity to 5-Fluorouracil.Cancers · 2025Article
- Article
- Single-cell transcriptomics reveals dynamic reprogramming of testicular immunity inZoological research · 2025Article
- reDA: differential abundance testing on scATAC-seq data using random walk with restart.Bioinformatics (Oxford, England) · 2025Article
- Review
- Enhanced Oxidative Phosphorylation Driven by TACO1 Mitochondrial Translocation Promotes Stemness and Cisplatin Resistance in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reproducible processing of TCGA regulatory networks.GigaScience · 2025Article
- Review
- KLF16 promotes pancreatic adenocarcinoma cell proliferation and migration by positively regulating SMAD6.World journal of gastrointestinal oncology · 2022Article
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Translational reprogramming is part of the unfolded protein response (UPR) during endoplasmic reticulum (ER) stress, which acts to the advantage of cancer growth and development in different stress conditions, but the mechanism of ER stress-related translational reprogramming in colorectal carcinoma (CRC) progression remains unclear. Here, we identified that Krüppel-like factor 16 (KLF16) can promote CRC progression and stress tolerance through translational reprogramming. The expression of KLF16 was upregulated in CRC tissues and associated with poor prognosis for CRC patients. We found that ER stress inducers can recruit KLF16 to the nucleolus and increase its interaction with two essential proteins for nucleolar homeostasis: nucleophosmin1 (NPM1) and fibrillarin (FBL). Moreover, knockdown of KLF16 can dysregulate nucleolar homeostasis in CRC cells. Translation-reporter system and polysome profiling assays further showed that KLF16 can effectively promote cap-independent translation of ATF4, which can enhance ER-phagy and the proliferation of CRC cells. Overall, our study unveils a previously unrecognized role for KLF16 as an ER stress regulator through mediating translational reprogramming to enhance the stress tolerance of CRC cells and provides a potential therapeutic vulnerability.
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