ArticleOncotarget2017
NPC-26 kills human colorectal cancer cells via activating AMPK signaling.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The potential of mitochondrial permeability transition-driven necrosis-related genes in prognostic evaluation of colorectal cancer patients.Frontiers in oncology · 2026Article
- Targeting POLRMT by IMT1 inhibits colorectal cancer cell growth.Cell death & disease · 2024Article
- A Descriptive Whole-Genome Transcriptomics Study in a Stem Cell-Based Tool Predicts Multiple Tissue-Specific Beneficial Potential and Molecular Targets of Carnosic Acid.International journal of molecular sciences · 2023Article
- Identification of G protein subunit alpha i2 as a promising therapeutic target of hepatocellular carcinoma.Cell death & disease · 2023Article
- Autophagy-related signaling pathways are involved in cancer (Review).Experimental and therapeutic medicine · 2021Review
- PF-06409577 Activates AMPK Signaling and Inhibits Osteosarcoma Cell Growth.Frontiers in oncology · 2021Article
- AMPK-ERK/CARM1 Signaling Pathways Affect Autophagy of Hepatic Cells in Samples of Liver Cancer Patients.Frontiers in oncology · 2019Article
- Targeting Mitochondrial Ion Channels to Fight Cancer.International journal of molecular sciences · 2018Review
- Jujube leaf green tea extracts inhibits hepatocellular carcinoma cells by activating AMPK.Oncotarget · 2017Article
- Article
- Kaempferol induces autophagic cell death of hepatocellular carcinoma cells via activating AMPK signaling.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NPC-26 is novel mitochondrion-interfering compound. The current study tested its potential effect against colorectal cancer (CRC) cells. We demonstrated that NPC-26 induced potent anti-proliferative and cytotoxic activities against CRC cell lines (HCT-116, DLD-1 and HT-29). Activation of AMP-activated protein kinase (AMPK) signaling mediated NPC-26-induced CRC cell death. AMPKα1 shRNA knockdown or dominant negative mutation abolished NPC-26-induced AMPK activation and subsequent CRC cell death. NPC-26 disrupted mitochondrial function, causing mitochondrial permeability transition pore (mPTP) opening and reactive oxygen species (ROS) production. ROS scavengers (NAC or MnTBAP) and mPTP blockers (cyclosporin A or sanglifehrin A) blocked NPC-26-induced AMPK activation and attenuated CRC cell death. Significantly, intraperitoneal injection of NPC-26 potently inhibited HCT-116 tumor growth in severe combined immuno-deficient (SCID) mice. Yet, its anti-tumor activity was significantly weakened against AMPKα1-silenced HCT-116 tumors. Together, we conclude that NPC-26 kills CRC cells possibly via activating AMPK signaling.
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Registered trials
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.