ArticleOncotarget2017
Rab coupling protein mediated endosomal recycling of N-cadherin influences cell motility.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- A systematic computational analysis of the endosomal recycling pathway in glioblastoma.Biochemistry and biophysics reports · 2024Article
- Endosomal recycling inhibitors downregulate estrogen receptor-alpha and synergise with endocrine therapies.Breast cancer research and treatment · 2024Article
- YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression.Oncogene · 2024Article
- YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression.Research square · 2023Article
- The small GTPase ARF3 controls invasion modality and metastasis by regulating N-cadherin levels.The Journal of cell biology · 2023Article
- Article
- Glypican 4 regulates planar cell polarity of endoderm cells by controlling the localization of Cadherin 2.Development (Cambridge, England) · 2021Article
- Rab11-FIP1 mediates epithelial-mesenchymal transition and invasion in esophageal cancer.EMBO reports · 2021Article
- Vesicle trafficking pathways that direct cell migration in 3D matrices and in vivo.Traffic (Copenhagen, Denmark) · 2018Review
- Rab11 family expression in the human placenta: Localization at the maternal-fetal interface.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rab coupling protein (RCP) is a Rab GTPase effector that functions in endosomal recycling. The RCP gene is frequently amplified in breast cancer, leading to increased cancer aggressiveness. Furthermore, RCP enhances the motility of ovarian cancer cells by coordinating the recycling of α5β1 integrin and EGF receptor to the leading edge of migrating cells. Here we report that RCP also influences the motility of lung adenocarcinoma cells. Knockdown of RCP inhibits the motility of A549 cells in 2D and 3D migration assays, while its overexpression enhances migration in these assays. Depletion of RCP leads to a reduction in N-cadherin protein levels, which could be restored with lysosomal inhibitors. Trafficking assays revealed that RCP knockdown inhibits the return of endocytosed N-cadherin to the cell surface. We propose that RCP regulates the endosomal recycling of N-cadherin, and in its absence N-cadherin is diverted to the degradative pathway. The increased aggressiveness of tumour cells that overexpress RCP may be due to biased recycling of N-cadherin in metastatic cancer cells.
Indexed as
Identifiers
What OpenQuestion holds
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.