ArticleCancer letters2021
KRAS-dependent cancer cells promote survival by producing exosomes enriched in Survivin.
Article in Cancer letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Nanotherapeutics to Overcome Chemotherapy Resistance in Ovarian Cancer.Pharmaceutical research · 2026Review
- The Role of Exosomal Biomarkers in the Monitoring of Bioactivation and Metabolite Clearance of Chemotherapeutics in Cancer Patients.Current drug metabolism · 2026Review
- Proteomics in pancreatic cancer.Biomarker research · 2025Review
- Colorectal Cancer Cells-Derived Exosomal PIK3CA Mutation DNA Promotes Tumor Metastasis by Activating Fibroblast and Affecting Tumor Metastatic Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Small extracellular vesicles (sEVs) in pancreatic cancer progression and diagnosis.Journal of controlled release : official journal of the Controlled Release Society · 2025Review
- The MEK inhibitor trametinib is effective in inhibiting the growth of canine oral squamous cell carcinoma.Scientific reports · 2025Article
- Exosomes: their role and therapeutic potential in overcoming drug resistance of gastrointestinal cancers.Frontiers in oncology · 2025Review
- Exosome applications for the diagnosis and treatment of pancreatic ductal adenocarcinoma: An update (Review).Oncology reports · 2025Review
- Endosomal Trafficking Bypassed by the RAB5B-CD109 Interplay Promotes Axonogenesis in KRAS-Mutant Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Opportunities for targeted therapies: trametinib as a therapeutic approach to canine oral squamous cell carcinomas.Research square · 2024Article
- Decoding the secrets of small extracellular vesicle communications: exploring the inhibition of vesicle-associated pathways and interception strategies for cancer treatment.American journal of cancer research · 2024Review
- Unlocking the Secrets of Extracellular Vesicles: Orchestrating Tumor Microenvironment Dynamics in Metastasis, Drug Resistance, and Immune Evasion.Journal of Cancer · 2024Review
- Alpha-hederin reprograms multi-miRNAs activity and overcome small extracellular vesicles-mediated paclitaxel resistance in NSCLC.Frontiers in pharmacology · 2024Article
- TEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors.Cancer research · 2023Article
- Liquid biopsy techniques and pancreatic cancer: diagnosis, monitoring, and evaluation.Molecular cancer · 2023Review
- Oncolytic adenovirus-mediated dual knockdown of survivin and OCT4 improves therapeutic efficacy in esophageal cancer.Annals of translational medicine · 2023Article
- KRAS Mutations in Solid Tumors: Characteristics, Current Therapeutic Strategy, and Potential Treatment Exploration.Journal of clinical medicine · 2023Review
- Pancreatic cancer and fibrosis: Targeting metabolic reprogramming and crosstalk of cancer-associated fibroblasts in the tumor microenvironment.Frontiers in immunology · 2023Review
- Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Functions and clinical applications of exosomes in pancreatic cancer.Molecular biology reports · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in KRAS frequently occur in human cancer and are especially prevalent in pancreatic ductal adenocarcinoma (PDAC), where they have been shown to promote aggressive phenotypes. However, targeting this onco-protein has proven to be challenging, highlighting the need to further identify the various mechanisms used by KRAS to drive cancer progression. Here, we considered the role played by exosomes, a specific class of extracellular vesicles (EVs) derived from the endocytic cellular trafficking machinery, in mediating the ability of KRAS to promote cell survival. We found that exosomes isolated from the serum of PDAC patients, as well as from KRAS-transformed fibroblasts and pancreatic cancer cells, were all highly enriched in the cell survival protein Survivin. Exosomes containing Survivin, upon engaging serum-starved cells, strongly enhanced their survival. Moreover, they significantly compromised the effectiveness of the conventional chemotherapy drug paclitaxel, as well as a novel therapy that combines an ERK inhibitor with chloroquine, which is currently in clinical trials for PDAC. The survival benefits provided by oncogenic KRAS-derived exosomes were markedly reduced when depleted of Survivin using siRNA or upon treatment with the Survivin inhibitor YM155. Taken together, these findings demonstrate how KRAS mutations give rise to exosomes that provide a unique form of intercellular communication to promote cancer cell survival and therapy resistance, as well as raise interesting possibilities regarding their potential for serving as therapeutic targets and diagnostic markers for KRAS-dependent cancers.
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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.