ArticleCells2020
AXL Controls Directed Migration of Mesenchymal Triple-Negative Breast Cancer Cells.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- AXL is associated with STAT3 activation in breast cancer.Molecular and clinical oncology · 2026Article
- AXL receptor tyrosine kinase regulates Golgi organization and function via an adhesion-Arf1 signalling axis in breast and lung cancer cell lines.Biology open · 2026Article
- Emerging Protein Targets in Triple-Negative Breast Cancer: Beyond Conventional Therapy.Cancers · 2026Review
- Differential AXL expression and Arf1 regulation control stiffness-dependent Golgi organization in breast cancer cells.Journal of cell science · 2026Article
- RTK AXL and its Isoforms: Regulation and Implications in Cancer.Current medicinal chemistry · 2026Review
- Trastuzumab-Conjugated pH-Sensitive Micelles Exhibit Antitumor Activity and Induce Mesenchymal-to-Epithelial Transition in Triple-Negative Breast Cancer Cell Lines.Pharmaceutics · 2025Article
- Targeting AXL can effectively overcome c-Met-induced therapeutic resistance in renal cancer and promote tumor cell death through increased oxidative stress.Cancer letters · 2025Article
- Current status and innovative developments of CAR-T-cell therapy for the treatment of breast cancer.Cancer cell international · 2025Review
- Distinct tumor architectures and microenvironments for the initiation of breast cancer metastasis in the brain.Cancer cell · 2024Article
- Nuclear translocation of Axl contributes to the malignancy of oral cancer cells.Journal of dental sciences · 2024Article
- Triple‑negative breast cancer cells that survive ionizing radiation exhibit an Axl‑dependent aggressive radioresistant phenotype.Experimental and therapeutic medicine · 2023Article
- circ-0000512 inhibits PD-L1 ubiquitination through sponging miR-622/CMTM6 axis to promote triple-negative breast cancer and immune escape.Journal for immunotherapy of cancer · 2023Article
- miR-613 suppresses renal cell carcinoma proliferation, invasion and migration by regulating the AXL/AKT pathway.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Distinct tumor architectures for metastatic colonization of the brain.bioRxiv : the preprint server for biology · 2023Article
- Article
- Inhibitory effect of the novel tyrosine kinase inhibitor DCC-2036 on triple-negative breast cancer stem cells through AXL-KLF5 positive feedback loop.Cell death & disease · 2022Article
- Endocytic trafficking of GAS6-AXL complexes is associated with sustained AKT activation.Cellular and molecular life sciences : CMLS · 2022Article
- 20 (S)-ginsenoside Rh2 inhibits colorectal cancer cell growth by suppressing the Axl signaling pathway in vitro and in vivo.Journal of ginseng research · 2022Article
- Review
- CAR-T Cell Therapy for Breast Cancer: From Basic Research to Clinical Application.International journal of biological sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer with high risk of relapse and metastasis. TNBC is a heterogeneous disease comprising different molecular subtypes including those with mesenchymal features. The tyrosine kinase AXL is expressed in mesenchymal cells and plays a role in drug resistance, migration and metastasis. We confirm that AXL is more expressed in mesenchymal TNBC cells compared to luminal breast cancer cells, and that its invalidation impairs cell migration while having no or little effect on cell viability. Here, we found that AXL controls directed migration. We observed that AXL displays a polarized localization at the Golgi apparatus and the leading edge of migratory mesenchymal TNBC cells. AXL co-localizes with F-actin at the front of the cells. In migratory polarized cells, the specific AXL inhibitor R428 displaces AXL and F-actin from the leading edge to a lateral area localized between the front and the rear of the cells where both are enriched in protrusions. In addition, R428 treatment disrupts the polarized localization of the Golgi apparatus towards the leading edge in migratory cells. Immunohistochemical analysis of aggressive chemo-resistant TNBC samples obtained before treatment reveals inter- and intra-tumor heterogeneity of the percentage of AXL expressing tumor cells, and a preference of these cells to be in contact with the stroma. Taken together, our study demonstrates that AXL controls directed cell migration most likely by regulating cell polarity.
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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.