ArticleJournal of experimental & clinical cancer research : CR2019
Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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Who cites it
111 citing papers in PubMed.
- Preliminary results from a phase II trial of spatially fractionated radiotherapy combined with immunotherapy and anti-angiogenic therapy in patients with bulky solid tumors: early evidence of promising efficacy and favorable safety.Radiation oncology (London, England) · 2026Trial
- Multiomics profiling and experiments in preclinical models revealed RAD51-IN-1 as a synergistic potentiator of anlotinib sensitivity.Science advances · 2026Trial
- Sintilimab and anlotinib with gemcitabine plus cisplatin in advanced biliary tract cancer: SAGC a randomized phase 2 trial.Nature communications · 2025Trial
- Effectiveness and safety of anlotinib with or without S-1 in the treatment of patients with advanced hepatocellular carcinoma in a Chinese population: a prospective, phase 2 study.Radiology and oncology · 2023Trial
- Anlotinib plus etoposide and cisplatin/carboplatin as first-line therapy for extensive-stage small cell lung cancer (ES-SCLC): a single-arm, phase II study.Investigational new drugs · 2022Trial
- Clinical Application of Anlotinib Combined with Docetaxel: Safe and Effective Treatment for Lung Carcinoma.Disease markers · 2022Trial
- The pivotal role of SCD1 in digestive cancers: Bridging lipid metabolic reprogramming and programmed cell death (Review).International journal of oncology · 2026Review
- Diosgenin Attenuates Angiogenesis via Targeting Src/STAT3 Signaling Pathway to Treat Non-Small Cell Lung Cancer.Chinese journal of integrative medicine · 2026Article
- Breaking senescence restriction: MAFK-AREG axis promotes NSCLC cells to resist doxorubicin.Oncology letters · 2026Article
- Integrating QSAR-Machine Learning, Biochemical Assays, and Molecular Dynamics for the Discovery of JAK2 Inhibitors in Cervical Cancer.Journal of chemical information and modeling · 2026Article
- SPOCK1 acts as a negative regulator of ferroptosis in non-small cell lung cancer.NPJ precision oncology · 2026Article
- Captivating Synergistic, Dose-Dependent Anticancer Effects of Tumor-Regulation Modulators Chloroquine and Ivermectin Completely Abolished by an Opposing Modulator, Deoxycholic Acid, in Hamster Fibrosarcoma: In Vivo, In Vitro, and Literature Review.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Exploration of the mechanism of anlotinib in reversing PD-1 immunotherapy resistance: insights from single-cell sequencing.Cancer gene therapy · 2026Article
- Targeting serine synthesis pathway to reverse paclitaxel resistance in NSCLC with combination of paclitaxel and anlotinib.Journal of experimental & clinical cancer research : CR · 2026Article
- Integrating the hallmarks of cancer into autophagy: a perspective from underlying mechanisms to therapeutic strategies.Theranostics · 2026Review
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- A novel PNIPAM-Modified polyurethane/carboxymethyl cellulose photo-thermoresponsive hydrogel loaded with gemcitabine to suppress esophageal cancer cells via VEGF-mediated angiogenic pathway inhibition.Journal of biological engineering · 2025Article
- Autophagy inhibition potentiates anti-cancer activity of Sunitinib in kidney cancer cells.Biology direct · 2025Article
- AURKA promotes angiogenesis in uveal melanoma via activation of the JAK2/STAT3/VEGFA signaling pathway.Cancer cell international · 2025Article
- Tumor suppressor SLC9A2 inhibits colorectal cancer metastasis and reverses immunotherapy resistance by suppressing angiogenesis.Journal of experimental & clinical cancer research : CR · 2025Article
51 more citing papers are in PubMed but not listed here.
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15 authors.
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Abstract
backgroundThe efficacy and safety of multikinase inhibitor anlotinib have been confirmed in the treatment of advanced non-small cell lung cancer (NSCLC). However, the direct functional mechanisms of tumor lethality mediated by anlotinib were not fully elucidated, and the underlying mechanisms related to resistance remain largely elusive.
methodsCell viability, colony formation, apoptosis and tumor growth assays were performed to examine the effect of anlotinib on lung cancer cells in vitro and in vivo. The punctate patterns of LC3-I/II were detected by confocal microscopy. HUVECs motility was detected using Transwell and scratch wound-healing assay. To visualize the microvessels, tubular formation assay was performed. The expression of LC3-I/II and beclin-1 and the changes of JAK2/STAT3/VEGFA pathway were detected by western blotting. The VEGFA levels in tumor supernatant were measured by ELISA.
resultsAnlotinib treatment decreased cell viability and induced apoptosis in Calu-1 and A549 cells. Moreover, anlotinib induced human lung cancer cell autophagy in a dose- and time-dependent manner. Blocking autophagy enhanced the cytotoxicity and anti-angiogenic ability of anlotinib as evidenced by HUVECs migration, invasion, and tubular formation assay. Co-administration of anlotinib and chloroquine (CQ) further reduced VEGFA level in the tumor supernatant, compared with that of anlotinib or CQ treatment alone. When autophagy was induced by rapamycin, the JAK2/STAT3 pathway was activated and VEGFA was elevated, which was attenuated after deactivating STAT3 by S3I-201. Further in vivo studies showed that anlotinib inhibited tumor growth, induced autophagy and suppressed JAK2/STAT3/VEGFA pathway, and CQ enhanced this effect.
conclusionAnlotinib induced apoptosis and protective autophagy in human lung cancer cell lines. Autophagy inhibition further enhanced the cytotoxic effects of anlotinib, and potentiated the anti-angiogenic property of anlotinib through JAK2/STAT3/VEGFA signaling.
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