ArticleOncogene2017
The lack of Raf-1 kinase feedback regulation enhances antiapoptosis in cancer cells.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Systemic therapy plus HAIC versus systemic therapy for hepatocellular carcinoma: a systematic review and meta-analysis.International journal of surgery (London, England) · 2025Pooled it
- Sorafenib Plus Hepatic Arterial Infusion Chemotherapy in Advanced Hepatocellular Carcinoma: A Systematic Review and Meta-analysis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Pooled it
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- The antipsychotic drug pimozide promotes apoptosis through the RAF/ERK pathway and enhances autophagy in breast cancer cells.Cancer biology & therapy · 2024Article
- Advancing hepatocellular carcinoma treatment with hepatic arterial infusion chemotherapy.World journal of gastrointestinal oncology · 2024Article
- Arterial chemotherapy for hepatocellular carcinoma in China: consensus recommendations.Hepatology international · 2024Article
- The worthy role of hepatic arterial infusion chemotherapy in combination with anti-programmed cell death protein 1 monoclonal antibody immunotherapy in advanced hepatocellular carcinoma.Frontiers in immunology · 2023Review
- Comparative effectiveness of interventional therapeutic modalities for unresectable hepatocellular carcinoma: A systematic review and network meta-analysis.Oncology letters · 2022Article
- Electroacupuncture-Regulated miR-34a-3p/PDCD6 Axis Promotes Post-Spinal Cord Injury Recovery in BothJournal of immunology research · 2022Article
- MicroRNA-29b regulates the radiosensitivity of esophageal squamous cell carcinoma by regulating the BTG2-mediated cell cycle.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2021Article
- Cost-Effectiveness Analysis of Hepatic Arterial Infusion of FOLFOX Combined Sorafenib for Advanced Hepatocellular Carcinoma With Portal Vein Invasion.Frontiers in oncology · 2021Article
- Sorafenib combined with embolization plus hepatic arterial infusion chemotherapy for inoperable hepatocellular carcinoma.World journal of gastrointestinal oncology · 2020Article
- Genes Involved in the PD-L1 Pathway Might Associate with Radiosensitivity of Patients with Gastric Cancer.Journal of oncology · 2020Article
- Sorafenib plus hepatic arterial infusion chemotherapy with oxaliplatin versus sorafenib alone for advanced hepatocellular carcinoma.Journal of interventional medicine · 2019Article
- Oncomirs Expression Profiling in Uterine Leiomyosarcoma Cells.International journal of molecular sciences · 2017Article
- A network-based predictive gene-expression signature for adjuvant chemotherapy benefit in stage II colorectal cancer.BMC cancer · 2017Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Raf-1 has an important role in cellular antiapoptosis. So far, there is no solid evidence that shows that Raf-1 mutation is associated with cancer development. In the course of further study of Raf-1 signaling, we have reported that Raf-1 hyperphosphorylation inhibits its kinase activity toward its downstream mitogen-activated protein kinase kinase 1/2 (MEK1/2) and proposed a model for negative feedback regulation of Raf-1. Here, we show that there is no hyperphosphorylation in some cancer cells, which results in increased kinase activity and enhances the antiapoptotic ability. Inhibition of either Raf-1 or ALG-2 (apoptosis-linked gene 2) expression results in apoptosis signal-regulating kinase 1/c-Jun N-terminal kinase (ASK1/JNK) signaling activation, and cell sensitivity to chemotherapeutic reagents, indicating that inhibition of ASK1/JNK apoptotic signaling by Raf-1 is mediated by ALG-2. A previous report indicated that extracellular signal-regulated kinase 1/2 (ERK1/2) were responsible for Raf-1 hyperphosphorylation. However, our evidence shows that when ERK1/2 are activated and the Raf-1 gene is not mutated, Raf-1 is not hyperphosphorylated in these cells, indicating that ERK1/2 are not responsible for the Raf-1 hyperphosphorylation in these cancer cell lines. Surprisingly, we also found that Raf-1 is not a necessary kinase for MEK1/2 activation under normal tissue culture conditions, but is required for MEK1/2 activation under apoptosis-inducing conditions. Our research demonstrates that although Raf-1 gene is not mutated, an abnormality of Raf-1 kinase feedback regulation enhances its antiapoptotic function, and Raf-1 can still be a pharmaceutical target to increase chemotherapy or radiotherapy sensitivity in these cancer cells.
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