ArticleOncology letters2020
Knockdown of SAR1B suppresses proliferation and induces apoptosis of RKO colorectal cancer cells.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Advances in the basic function of the small GTPase SAR1B and its regulatory role in the biological behavior of tumor cells (Review).Molecular and clinical oncology · 2026Review
- Crosstalk between dysregulated amino acid sensing and glucose and lipid metabolism in colorectal cancer.Frontiers in oncology · 2025Review
- Using period analysis to timely assess and predict 5-year relative survival for colorectal cancer patients in Taizhou, eastern China.Cancer medicine · 2023Article
- Over-expression of SRD5A3 and its prognostic significance in breast cancer.World journal of surgical oncology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is the third most commonly diagnosed cancer worldwide. SAR1 gene homolog B (SAR1B) is a GTPase that has been reported to have a central role in the regulation of lipid homeostasis and is associated with numerous diseases. However, its role in cancer, particularly in CRC, remains unclear. The present study revealed that SAR1B was overexpressed in CRC samples and this was associated with shorter overall survival time in patients with CRC. Colony formation, cell proliferation and flow cytometry assays were conducted to evaluate the functions of SAR1B in CRC. It was reported that SAR1B may be associated with tumorigenesis of CRC. Knockdown of SAR1B suppressed cell proliferation and induced significant apoptosis of RKO cells. Furthermore, microarray analysis was performed to identify the potential targets of SAR1B in CRC. Bioinformatics analysis revealed that SAR1B was significantly involved in regulating 'TGF-β signaling', 'paxillin signaling', 'cell cycle regulation by BTG family proteins' and 'IGF-1 signaling'. These results suggested that SAR1B may be considered a potential prognostic biomarker and therapeutic target for CRC.
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Registered trials
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