Open Access

ARTICLE

Bioinformatics comprehensive analysis confirmed the potential involvement of SLC22A1 in lower-grade glioma progression and prognosis

by JING HUI^1,2, NANA SUN³, YONG LIU⁴, CHUNBO YU^1,2, YONG KE⁴, YONG CAO⁴, ANXIAO YU⁴, QINGHONG KONG^1,2,*, YUN LIU^1,2,4,*

1 Guizhou Provincial College-Based Key Lab for Tumor Prevention and Treatment with Distinctive Medicines, Zunyi Medical University, Zunyi, 563000, China
2 College of Basic Medicine, Zunyi Medical University, Zunyi, 563000, China
3 Department of Dermatology, Guizhou Province Cosmetic Plastic Surgery Hospital, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China
4 School of Forensic Medicine, Zunyi Medical University, Zunyi, 563000, China

* Corresponding Authors: QINGHONG KONG. Email: ; YUN LIU. Email:

BIOCELL 2024, 48(5), 803-815. https://doi.org/10.32604/biocell.2024.047122

Received 25 October 2023; Accepted 05 March 2024; Issue published 06 May 2024

Abstract

Background: Although it has been established that the human Solute Carrier Family 22 (SLC22) functions as a cationic transporter, influencing cellular biological metabolism by modulating the uptake of various cations, its impact on cancer prognosis remains unclear. Methods: We conducted a comprehensive analysis utilizing data from The Cancer Genome Atlas (TCGA) and other databases to assess the prognostic value and functional implications across various tumors. Silence of SLC22A1 RNA in glioma U251 cells was performed to access the impact of SLC22A1 on lower-grade glioma (LGG) progression. Results: Our findings demonstrated a significant correlation between SLC22A1 expression and the survival time of patients with various cancers (p < 0.05). Importantly, we found the potential involvement of SLC22A1 in occurrence and progress of certain cancers, with a pronounced impact on LGG. Further examination of the SLC22A1-LGG relationship revealed its status as an independent risk factor for LGG, suggesting its potential involvement in regulating diverse immune pathways and metabolic activities. Chinese Glioma Genome Atlas (CGGA) data supported the reliability of the risk score as a prognostic and recurrence indicator, emphasizing the accuracy of the nomograph (1, 3, and 5-year-AUC >0.8). Cell proliferation and clone formation experiment proved that decreased expression of SLC22A1 in glioma U251 cells inhibited glioma cell growth. Conclusion: Our findings suggest SLC22A1 has huge prospects as a promising biomarker and therapeutic target for LGG prognosis. SLC22A1 has only been proved to support cellular function previously. Our findings demonstrated a robust connection between the tumor microenvironment and functional proteins that maintain basal cell metabolism, which gifts unique tumor immune characteristics of gliomas. Additionally, we provide a highly practical prediction model for estimating the survival rate of LGG patients.

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