ArticlePloS one2013
FK-16 derived from the anticancer peptide LL-37 induces caspase-independent apoptosis and autophagic cell death in colon cancer cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 150 citations in OpenAlex.
- Apoptosis Modulation by LL-37: From Mitochondrial Cell Death to Prosurvival Signaling.International journal of molecular sciences · 2026Review
- The potential of mitochondrial permeability transition-driven necrosis-related genes in prognostic evaluation of colorectal cancer patients.Frontiers in oncology · 2026Article
- Synthesis and evaluation of KR-12, an LL-37 fragment, and its short-chain fatty acid derivatives: selective cytotoxicity in colorectal cancer cells and anti-tumor efficacy in an azoxymethane/DSS-induced colitis-associated cancer mouse model.Pharmacological reports : PR · 2025Article
- Article
- Virtual Screening of Cathelicidin-Derived Anticancer Peptides and Validation of Their Production in the ProbioticInternational journal of molecular sciences · 2025Article
- Antimicrobial Peptides of the Cathelicidin Family: Focus on LL-37 and Its Modifications.International journal of molecular sciences · 2025Review
- Data-Driven Visualization of the Dynamics of Antimicrobial Peptides in Cell Death.Probiotics and antimicrobial proteins · 2025Review
- Exploring the potential of anticancer peptides as therapeutic agents for cancer treatment.Research in pharmaceutical sciences · 2025Review
- Origami of KR-12 Designed Antimicrobial Peptides and Their Potential Applications.Antibiotics (Basel, Switzerland) · 2024Review
- Antimicrobial Properties and Cytotoxicity of LL-37-Derived Synthetic Peptides to Treat Orthopedic Infections.Antibiotics (Basel, Switzerland) · 2024Article
- Comparative Study of the Potential Cell-Penetrating Peptide ∆M4 on Apoptosis Cell Signaling in A375 and A431 Cancer Cell Lines.Pharmaceutics · 2024Article
- DCTPep, the data of cancer therapy peptides.Scientific data · 2024Article
- From oncolytic peptides to oncolytic polymers: A new paradigm for oncotherapy.Bioactive materials · 2024Review
- Anticancer Mechanisms and Potential Anticancer Applications of Antimicrobial Peptides and Their Nano Agents.International journal of nanomedicine · 2024Review
- Application Value of Antimicrobial Peptides in Gastrointestinal Tumors.International journal of molecular sciences · 2023Review
- Recent advances and applications of peptide-agent conjugates for targeting tumor cells.Journal of cancer research and clinical oncology · 2023Review
- Resistance is futile: targeting multidrug-resistant bacteria withRSC chemical biology · 2023Review
- Novel cationic cryptides in Penaeus vannamei demonstrate antimicrobial and anti-cancer activities.Scientific reports · 2023Article
- Article
- Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.International immunopharmacology · 2023Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host immune peptides, including cathelicidins, have been reported to possess anticancer properties. We previously reported that LL-37, the only cathelicidin in humans, suppresses the development of colon cancer. In this study, the potential anticancer effect of FK-16, a fragment of LL-37 corresponding to residues 17 to 32, on cultured colon cancer cells was evaluated. FK-16 induced a unique pattern of cell death, marked by concurrent activation of caspase-independent apoptosis and autophagy. The former was mediated by the nuclear translocation of AIF and EndoG whereas the latter was characterized by enhanced expression of LC3-I/II, Atg5 and Atg7 and increased formation of LC3-positive autophagosomes. Knockdown of Atg5 or Atg7 attenuated the cytotoxicity of FK-16, indicating FK-16-induced autophagy was pro-death in nature. Mechanistically, FK-16 activated nuclear p53 to upregulate Bax and downregulate Bcl-2. Knockdown of p53, genetic ablation of Bax, or overexpression of Bcl-2 reversed FK-16-induced apoptosis and autophagy. Importantly, abolition of AIF/EndoG-dependent apoptosis enhanced FK-16-induced autophagy while abolition of autophagy augmented FK-16-induced AIF-/EndoG-dependent apoptosis. Collectively, FK-16 induces caspase-independent apoptosis and autophagy through the common p53-Bcl-2/Bax cascade in colon cancer cells. Our study also uncovered previously unknown reciprocal regulation between these two cell death pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.