ArticleJournal of clinical laboratory analysis2024
RACK1 promotes the occurrence and progression of cervical carcinoma.
Article in Journal of clinical laboratory analysis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 2 citations in OpenAlex.
- The Association Between RACK1 Gene Polymorphisms rs1279736 and rs3756585 in Uterine Cervical Cancer with the Risk Factor of HPV: A Focus on Squamous Cell Carcinoma (SCC).Iranian journal of pathology · 2025Article
- Ribosomal rodeo: wrangling translational machinery in gynecologic tumors.Cancer metastasis reviews · 2024Review
- RACK1 promotes the occurrence and progression of cervical carcinoma.Journal of clinical laboratory analysis · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRACK1 has been identified as a multifunctional cytosolic protein, and plays a pivotal role in multiple biological responses involved in several kinds of tumors, while its effect in cervical cancer has not been well elucidated yet. The study aimed to investigate the role of RACK1 in cervical cancer occurrence and progression.
methodsThe expression of RACK1 in cervical specimens was measured by immunohistochemical staining and Western blot assay. Transgenic mice were used to detect the role of RACK1 in modulating tumorigenesis in vivo. Cervical carcinoma cell lines were used to explore the underlying mechanisms of RACK1 on the behaviors of tumor cells in vitro.
resultsWe found that RACK1 expression was upregulated in cancer tissues compared with adjacent tissues, and its expression was gradually increased from cervictis, and cervical intraepithelial neoplasis (CIN) to carcinoma. Genetic overexpression of RACK1 facilitated tumor formation and growth in nude mice. Mechanism studies disclosed that RACK1 over-expression prolonged the G
conclusionsTaken together, we concluded that RACK1 stimulates tumorigenesis and progression of cervical cancer via modulating the proliferation of tumor cells, implying that targeting RACK1 may serve as a promising method for cervical cancer therapy.
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Registered trials
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