揭示 SLC35F3 在肺腺癌中的神秘作用

IF 1.9 4区 医学 Q3 RESPIRATORY SYSTEM Clinical Respiratory Journal Pub Date : 2024-10-16 DOI:10.1111/crj.70023
Yiwang Ye, Feihu Long, Wei Yue, Zichun Wei, Jianyi Yang, Yuancai Xie
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引用次数: 0

摘要

背景溶质运载家族 35 成员 F3(SLC35F3)在肺腺癌(LUAD)中的作用仍不清楚。为了填补这一空白,我们采用生物信息学分析和实验验证进行了一项研究。 方法 本研究旨在通过分析癌症基因组图谱(TCGA)数据库中的数据,研究 SLC35F3 在各种癌症类型中的表达模式,尤其关注 LUAD,以评估其临床相关性。研究还探讨了SLC35F3的潜在调控机制,包括它与免疫浸润、肿瘤突变负荷(TMB)和LUAD中药物敏感性的相互作用。调查包括分析 LUAD 细胞单细胞测序中 SLC35F3 的表达、研究 LUAD 中 SLC35F3 的基因变异以及使用定量实时 PCR (qRT-PCR) 评估细胞系中 SLC35F3 的表达。 结果 在泛癌症和 LUAD 中均观察到 SLC35F3 的异常表达。在 LUAD 患者中,SLC35F3 表达的显著增加与性别相关(p < 0.001),并与较差的总生存期(OS)相关(p = 0.020)。SLC35F3的表达被确定为LUAD患者的一个独立预后决定因素(p = 0.032)。SLC35F3与细胞周期等多种通路相关。在 LUAD 中,SLC35F3 的表达与免疫浸润、TMB 和某些药物相关。结果表明,SLC35F3 在 LUAD 组织和细胞系中均有明显上调。 结论 SLC35F3可作为LUAD患者的预后生物标志物和免疫治疗靶点。 临床试验注册 不适用。
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Unveiling the Enigmatic Role of SLC35F3 in Lung Adenocarcinoma

Background

The role of solute carrier family 35 member F3 (SLC35F3) in lung adenocarcinoma (LUAD) remains unclear. To address this gap, we conducted a study employing bioinformatics analysis and experimental validation.

Methods

This study aimed to examine the expression patterns of SLC35F3 in various cancer types, particularly focusing on LUAD, by analyzing data from the Cancer Genome Atlas (TCGA) database to evaluate its clinical relevance. The research also explored potential regulatory mechanisms of SLC35F3, including its interactions with immune infiltration, tumor mutational burden (TMB), and drug sensitivity in LUAD. The investigation included analyzing SLC35F3 expression in single-cell sequencing of LUAD cells, examining genetic variations of SLC35F3 in LUAD, and assessing SLC35F3 expression in cell lines using quantitative real-time PCR (qRT-PCR).

Results

The aberrant expression of SLC35F3 was observed in both pan-cancer and LUAD. In LUAD patients, a statistically significant increase in SLC35F3 expression was correlated with gender (p < 0.001) and was associated with poorer overall survival (OS) (p = 0.020). The expression of SLC35F3 was identified as an independent prognostic determinant in patients with LUAD (p = 0.032). SLC35F3 exhibited associations with various pathways, including cell cycle and more. SLC35F3 expression demonstrated correlations with immune infiltration, TMB, and some drugs in LUAD. Results indicated significant upregulation of SLC35F3 in both LUAD tissues and cell lines.

Conclusions

SLC35F3 may serve as a prognostic biomarker and immunotherapeutic target for patients with LUAD.

Clinical Trial Registration

Not applicable.

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来源期刊
Clinical Respiratory Journal
Clinical Respiratory Journal 医学-呼吸系统
CiteScore
3.70
自引率
0.00%
发文量
104
审稿时长
>12 weeks
期刊介绍: Overview Effective with the 2016 volume, this journal will be published in an online-only format. Aims and Scope The Clinical Respiratory Journal (CRJ) provides a forum for clinical research in all areas of respiratory medicine from clinical lung disease to basic research relevant to the clinic. We publish original research, review articles, case studies, editorials and book reviews in all areas of clinical lung disease including: Asthma Allergy COPD Non-invasive ventilation Sleep related breathing disorders Interstitial lung diseases Lung cancer Clinical genetics Rhinitis Airway and lung infection Epidemiology Pediatrics CRJ provides a fast-track service for selected Phase II and Phase III trial studies. Keywords Clinical Respiratory Journal, respiratory, pulmonary, medicine, clinical, lung disease, Abstracting and Indexing Information Academic Search (EBSCO Publishing) Academic Search Alumni Edition (EBSCO Publishing) Embase (Elsevier) Health & Medical Collection (ProQuest) Health Research Premium Collection (ProQuest) HEED: Health Economic Evaluations Database (Wiley-Blackwell) Hospital Premium Collection (ProQuest) Journal Citation Reports/Science Edition (Clarivate Analytics) MEDLINE/PubMed (NLM) ProQuest Central (ProQuest) Science Citation Index Expanded (Clarivate Analytics) SCOPUS (Elsevier)
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