ArticleOncology letters2018
Rab-like protein 1 A is upregulated by cisplatin treatment and partially inhibits chemoresistance by regulating p53 activity.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- The interrelated roles of RAB family proteins in the advancement of neoplastic growth.Frontiers in oncology · 2025Review
- The oncogenic potential of Rab-like protein 1A (RBEL1A) GTPase: The first review of RBEL1A research with future research directions and challenges.Journal of Cancer · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rab-like protein 1 A (RBEL1A), which is a predominant isoform of RBEL1, has been identified to serve an important function in breast tumorigenesis and may be upregulated in breast tumor cells. RBEL1A may block the transcriptional activity of p53, which is important in the induction of cisplatin sensitivity. Previous studies supported the association between the induction of chemoresistance and the inhibition of p53 by RBEL1A. However, the response of RBEL1A to chemotreatment and its interaction with p53 remains to be investigated. The present study revealed that the cisplatin treatment induced the expression of RBEL1A in MCF-7 cells. Consistent with previous studies, the present study demonstrated that cisplatin treatment and RBEL1A overexpression blocked the oligomerization of p53 in MCF-7 cells and led to a decrease of the transcriptional activity of p53 and its downstream target gene p21. Additionally, upregulation of RBEL1A decreased the protein level of p53 by promoting the ubiquitination of p53. A cytotoxicity assay demonstrated that upregulation of RBEL1A partially contributed to chemosensitivity via inhibiting p53 in MCF-7 cells. A pG13L (p53-responsive reporter plasmid) luciferase reporter and co-immunoprecipitation assay revealed that upregulation of RBEL1A led to an inhibition of the transcriptional activity of p53 or its target gene p21. Analysis of cellular proliferation, cell cycle and invasion also confirmed the regulatory activity of RBEL1A on the malignancy of breast cancer cells. Taken together, these results suggest that the induction of RBEL1A following cisplatin treatment may partially inhibit chemosensitivity in a p53-dependent manner.
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